One concerned supplements said to enhance adenosine triphosphate output in mitochondria. Dubois notes that just because the supplement may stimulate mitochondrial function does not mean it will noticeably increase energy in humans. He also points out that there are no randomized clinical trials proving the benefits of this therapy.

Then he discusses several historical examples of promising theories that did not stand up to scientific evaluation, such as dietary cholesterol and cardiovascular disease. At one time eating eggs, especially the yellow, was widely believed to lead to an increase in cardiovascular problems. Subsequent large-scale studies demonstrated that consumption of eggs has little negative effect on the heart.

On another topic, Dubois says that the use of cardiac stents did not outperform standard medical approaches in preventing heart attacks. The same negative result was found when detailed studies published in the New England Journal of Medicine found the use of cement injected for vertebroplasty performed no better than a placebo.

Dubois also discusses ideas based on scientific studies that were overhyped without rigorous human trials. One famous example was the hypothesis by Nobel Prize winner Linus Pauling, PhD, that vitamin C would prevent colds. Subsequent Cochrane Reviews contradicted this opinion.

DuBois asserts that studies need to address the following questions before a therapy is recommended for wide use:

1. Has it been tested in people?
2. Who profits?
3. Are claims measurable and reproducible?

He also suggests the use of placeboes and appropriate randomized controlled trials before scientific conclusions are made on how significant the benefit is to the general population.

The ability to admit that uncertainty remains is also key to transparency. While anecdotal evidence has a place, only studies done on human beings with careful controls can tell us what actually works. Experts who tout a compelling mechanism or armed with laboratory data on mice or human antidotal data do not reach the level of actionable evidence. Dubois ends by stating the next time a supplement or therapy seems too good to be true, take a pause.

In an era where mechanisms are marketed as miracles, clinicians must resist the pull of plausibility and demand proof grounded in rigorous human trials. Before embracing the next promising therapy, pause compelling theory is never a substitute for reproducible evidence.

Reference

1. Dubois B. Beyond the hype: why good theories aren’t good medicine. Sensible Medicine. Available at sensible-med.com/p/beyond-the-hype-why-good-theories?utm_source=publication-search. Accessed February 13, 2026.

From Decisions in Dentistry. February/March 2026;12(1):5.

Cloud-based practice management technologies are transforming dental care delivery through enhanced communication, coordination, and engagement between patients and providers. These platforms improve accessibility, documentation accuracy, and workflow efficiency, ultimately contributing to improved oral health outcomes. The global cloud-based dental practice management software market was valued at $721 million in 2023, with an anticipated annual growth rate of 11.4% through 2030.¹ As adoption increases, oral health professionals are discovering that cloud-based systems strengthen both operational efficiency and the patient–provider relationship by supporting consistent, transparent communication.

The modern dental landscape is undergoing rapid technological transformation. Practices can integrate digital tools to streamline administrative functions, improve clinical documentation, and enhance patient interactions. Central among them, cloud-based practice management systems have emerged. By connecting communication, scheduling, billing, and record management within a single interface, these systems help reduce redundancies and improve accuracy.

Historically, practices used on-site servers and fragmented systems that required manual updates and localized access. This often resulted in communication delays, data loss, and security vulnerabilities. Technicians had to address operational hiccups in person, which further postponed patient care and increased overhead costs.

Today, cloud-based systems centralize data and provide secure, remote access for both providers and patients. The transition to cloud-based technology also reflects larger trends in healthcare toward interoperability and patient empowerment.¹ Patients expect the same digital convenience from their healthcare providers that they experience elsewhere. They value seamless communication, self-service options, and transparency regarding costs and outcomes. Oral health professionals who meet these expectations through technology can increase engagement, compliance, and satisfaction.

In addition, cloud-based platforms align with regulatory standards that emphasize patient data security and continuity of care. They offer enhanced encryption and automated backup features that protect patient information and ensure compliance with Health Insurance Portability and Accountability Act of 1996 (HIPAA) guidelines.^1,2 Balancing accessibility and security provides evidence-based, coordinated care without compromising patient trust.

Unified Communication Systems

Cloud-based communication platforms combine phone, text, and email correspondence on one secure system. This allows staff to manage all patient communication from a centralized location, improving consistency and responsiveness. Team members can access patient records, appointment histories, and emergency notes from any authorized device. Delayed or inconsistent messages can otherwise lead to scheduling errors, confusion, and dissatisfaction. Newer systems ensure that these interactions are automatically logged and retrievable, providing administrative efficiency and legal protection. Comprehensive documentation of patient communication is invaluable in risk management and malpractice defense.²

Patient satisfaction is influenced by effective communication, or lack thereof. Surveys found that up to 59% of patients would consider switching providers if their communication expectations were not met.³ Providing multiple channels, including text reminders, email updates, and direct phone outreach, allows patients to use the mode of interaction they prefer. This personalization enhances engagement and creates a perception of accessibility and respect. This is especially true for multigenerational practices, where different age groups have distinct preferences and comfort levels with technology. Younger patients gravitate toward digital-first options, while older patients value live phone support or in-person clarification.^1,3 That adaptability reduces frustration but also builds trust, reinforcing that the practice is attentive to individual needs.

Moreover, these systems ease administrative workload by reducing reliance on external vendors and simplifying message tracking. Emergency calls can be routed through one platform, granting clinicians immediate access to medical histories, medication lists, and scheduling tools. This ensures accurate, informed responses even after office hours. The integration of automated communication, documentation, and scheduling results in a more organized, accountable, and patient-friendly workflow.

Patient Portals and Digital Engagement

Patient portals have improved access to health information. In dentistry, patients can now review treatment plans, sign consent forms, and receive pre- and post-operative instructions without ever stepping foot in a physical practice. This is particularly helpful in rural settings, where access is already limited and services are often rendered in one visit to save on travel and time, requiring most of the patient onboarding to be completed correctly and in advance.

In the digital era, patients are encouraged to take a more active role in their oral health. Between 2018 and 2022, national portal usage rose from 38% to 57%, reflecting growing patient interest in online healthcare management.⁴ Cloud-based portals better integrate clinical, financial, and educational materials in one place. Patients can securely download radiographs, pay balances, and review upcoming appointments without any formal interactions. A systematic literature review suggests that portal engagement correlates with improved treatment adherence and satisfaction.⁵ Patients have a greater understanding of their oral health conditions and report higher trust in their providers when using these portals.

Encouragement from the dental team significantly increases these portal adoption rates.⁴ Staff should be trained to introduce portals during check-in or as part of treatment discussions to highlight their convenience and security. These repeated nods reinforce the portal’s role as an essential part of the practice’s experience. Over time, this normalizes portal use, helping patients view it not as an optional add-on, but as a trusted, convenient extension of their care.

Digital engagement also supports accountability and transparency. Timestamped audit trails record when documents are sent, opened, or acknowledged. These records provide verifiable evidence of communication and ensure that patient instructions are clear and accessible to all parties. In addition to reducing paper waste, portals minimize the volume of administrative calls, allowing staff to focus on higher-value clinical tasks.

Online Scheduling and Operational Efficiency

Traditional appointment scheduling methods are time-consuming and depend on staff availability. Cloud-based scheduling systems offer real-time booking capabilities that align with the patient’s expectations for convenience. These platforms allow patients to view available time slots, select providers, and book appointments without calling the office. Practices can even set custom parameters for online scheduling, controlling which types of visits can be self-booked and when.⁶ This ensures that production goals and provider availability remain balanced. Notifications of confirmed or canceled appointments are instant, allowing staff to adapt schedules dynamically.

Online scheduling particularly benefits high-volume general and periodontal practices with recurring dental hygiene appointments. Patients are more likely to schedule and keep appointments when given multiple options. Research in hospital settings found that the introduction of online scheduling reduced unfilled appointments by 5.8% within 1 year.⁷ When combined with text message reminders, the no-show rate declined further, improving overall practice productivity.

This hybrid scheduling model ensures inclusivity across age groups. While younger generations value autonomy and speed, older patients often prefer direct interaction. Cloud-based systems allow practices to accommodate both preferences seamlessly. By reducing administrative bottlenecks and optimizing appointment flow, online scheduling contributes to improved revenue and patient satisfaction.

Billing and Financial Communication

The billing process can be a major source of frustration for both patients and staff. Cloud-based payment systems streamline financial communication through text-to-pay options and automated billing reminders. Patients receive secure links to settle balances electronically, eliminating the need for mailed statements or manual follow-up calls. Financial analyses showed that nearly 45% of patients missed payments due to miscommunication with their healthcare provider.⁸ Cloud-based billing tools address this issue by automating reminders, reducing delays, and allowing patients to pay at their convenience. The psychological barrier associated with in-person or phone payments is also reduced, helping patients avoid feelings of embarrassment or anxiety when reviewing their finances.

These tools also strengthen revenue cycle management by reducing the time between service delivery and payment. These transactions are automatically recorded in the practice ledger, eliminating data entry errors and minimizing security threats from fraudulent electronic payment systems. Reputable cloud-based platforms comply with HIPAA and Payment Card Industry Data Security Standard guidelines to safeguard financial data.⁹ Transactions are encrypted, protecting against unauthorized access or data breaches. Patients who perceive payment systems as secure are also more likely to remain loyal to a given practice.⁸

Offering flexible payment methods, including debit, credit, health saving accounts/flexible spending accounts, and digital wallet options, improves the financial experience by meeting individuals where they are most comfortable. Clear cost estimates, real-time balance updates, and accessible online receipts reduce uncertainty, empowering patients to take a more active role in managing their care. For the practice, this transparency not only strengthens patient relationships but also aligns day-to-day business operations with a broader commitment to patient-centered ethics and financial clarity.

Future Opportunities

The integration of cloud-based systems signifies a cultural change within dental care delivery. While the benefits are well documented, implementation requires careful planning. Staff adoption is one of the most common barriers. Successful transition demands comprehensive training to ensure all team members understand how to use new systems effectively. Change management strategies, including stepwise implementation and ongoing support, can mitigate resistance. Practices should designate a digital coordinator to oversee adoption and provide peer training.

Cost considerations also play a role. While cloud systems typically reduce long-term expenses associated with information technology maintenance, the initial investment can be significant, upwards of $50,000 in upfront costs for one-time licensing and installation services. Subsequent subscriptions can be $200 to $500 per month, depending on ongoing needs for data migration, implementation and onboarding, training, and extra features.¹⁰ Practices should evaluate return on investment by tracking key performance indicators such as appointment fill rate, payment turnaround time, and patient retention.^1,10

Ethical concerns related to privacy and data security must also be addressed. Although these systems employ advanced encryption, providers remain responsible for maintaining compliance with state and federal regulations. Clear protocols for password management, device security, and access permissions are essential.

From a patient’s perspective, digital communication should enhance, not replace personal interaction. Over-reliance on automation may risk depersonalization of care. Ideally, technological efficiency should be balanced by warmth and empathy. Artificial intelligence and predictive analytics are poised to further personalize patient communication and care planning. They can identify patterns in patient behavior, forecast appointment cancellations, and tailor recare reminders based on risk profiles.

Integration with wearable health technology and mobile applications may soon allow continuous monitoring of oral health indicators such as salivary pH or bruxism patterns.¹ Such developments will deepen the connection between patients and providers, moving dentistry toward a model of preventive, data-driven care. As these innovations unfold, the role of the oral health professional will expand beyond technical expertise. Dental clinicians will increasingly act as digital stewards, guiding patients through a technologically enriched environment while preserving existing personal relations.

Conclusions

Cloud-based dental management systems have reshaped how practices communicate, schedule, and manage finances. They provide a secure, efficient, and patient-centered framework for care delivery that aligns with modern expectations. By embracing these tools responsibly, oral health professionals can enhance engagement, improve outcomes, and strengthen the integrity of their practice operations.

Ultimately, while technology serves as the framework, human connection remains the cornerstone of dentistry. When they are used to foster understanding and trust, both patients and providers benefit from a more connected and compassionate experience.

References

1. Grand View Research. Cloud-Based Dental Practice Management Software Market 2024-2030. Available at grandviewresearch.com/industry-analysis/cloud-based-dental-practice-management-software-market-report. Accessed February 23, 2026.
2. Mahan Law Dental Attorneys and Practice Advisors. Dental Record Keeping and Documentation Best Practices for Malpractice Defense. Available at https://mahandentallaw.com/dental-record-keeping-and-documentation-best-practices-for-malpractice-defense. Accessed February 23, 2026.
3. Gasdia T. Healthcare communication trends: Nearly 70% of patients prefer conversational messaging over basic texting. Available at https://artera.io/blog/healthcare-communication-trends. Accessed February 23, 2026.
4. Assistant Secretary for Technology Policy. Individuals’ access and use of patient portals and smartphone health apps, 2024. Available at healthit.gov/data/data-briefs/individuals-access-and-use-patient-portals-and-smartphone-health-apps-2024. Accessed February 23, 2026.
5. Carini E, Villani L, Pezzullo A, et al. The impact of digital patient portals on health outcomes, system efficiency, and patient attitudes: Updated systematic literature review. J Med Internet Res. 2021;23:e26189.
6. CareStack. Online dental scheduling software. Available at https://carestack.com/dental-software/features/online-scheduling. Accessed February 23, 2026.
7. Betancor PK, Boehringer D, Jordan J, et al. Efficient patient care in the digital age: Impact of online appointment scheduling in a medical practice and a university hospital on the “no-show” rate. Front Digit Health. 2025:1567397.
8. Dental Intelligence. How text-to-pay options in dental intelligence can help you collect more. Available at dentalintel.com/blog-posts/how-text-to-pay-options-in-dental-intelligence-can-help-you-collect-more. Accessed February 23, 2026.
9. Meegle. Cloud-Based Scheduling Platforms. Available at meegle.com/en_us/topics/intelligent-scheduling/cloud-based-scheduling-platforms. Accessed February 23, 2026.
10. Mahanam B. Your 2025 guide to choosing cloud-based dental practice software. Available at overjet.com/blog/your-2025-guide-to-choosing-cloud-based-dental-practice-software?utm_source=chatgpt.com. Accessed February 23, 2025.

From Decisions in Dentistry. February/March 2026;12(1):9-12.

Dental implants do not just fail. We fail them — through a disregard of biological, restorative, and maintenance principles.¹ True implant success tests the resilience of the peri-implant apparatus. Because implants lack a periodontal ligament, exhibit collagen fibers aligned parallel rather than perpendicular to their surface, and host a unique microbiome in which fewer than 10% of species overlap with periodontal niches, they function within their own ecological and immunologic environment.^1,2 This environment is acutely sensitive to both patient self-care and the quality of professional maintenance.

A growing clinical consensus indicates that peri-implant diseases are largely preventable when risk factors are properly managed and robust maintenance protocols are followed.^1,3 Without such support, dysbiotic biofilm accumulates, provoking rapid inflammatory change, implant surface degradation, and nonlinear bone loss.³ Peri-implantitis progresses faster than periodontitis, with lesions nearly twice as large and driven by more aggressive cytokine profiles.³ Early and ongoing recare can safeguard implants from this destructive sequelae. Yet it is the standard of maintenance that shapes their prognoses.

Emerging research has refined the understanding of material-tissue interactions, revealing that titanium is not inert; when its protective dioxide layer is disrupted, ions and particles are released, amplifying a local inflammatory reaction known as metallosis.^3,4 Tribocorrosion from improper hand or power instrumentation can initiate or accelerate tissue breakdown, making surface-safe debridement essential.

Risk Factors Impacting Maintenance

Active or previous periodontitis captures the biological, mechanical, behavioral, and environmental factors that undermine implant health. Numerous longitudinal studies confirm that patients with successfully treated periodontitis had higher rates of peri-implant mucositis, bone loss, and implant failure than periodontally healthy individuals.^3,5 In fact, without maintenance, tissue level implants had a 15-fold increased risk of peri-implant bone loss in periodontally compromised patients in a 20-year follow-up.⁵ Even with successful treatment, these patients remain vulnerable to biological complications, underscoring the importance of structured, ongoing maintenance for implants.

This inherent vulnerability reinforces the role of soft tissue phenotype, as the peri-implant complex depends on sufficient, resilient mucosal tissue to buffer change. Thin mucosal tissues provide less protection against mechanical forces, poor prosthetic design, and plaque accumulation.^1,6 Wider bands of keratinized mucosa are generally associated with improved patient comfort, reduced inflammation, and more stable marginal bone levels, though controversial.^3,6

An often-cited meta-analysis revealed that sites with insufficient keratinized tissue are more prone to bleeding, discomfort during brushing, and biofilm retention, all of which can precipitate disease progression.⁶ When a peri-implant tissue deficiency is identified, augmentation procedures may be performed before implant placement, loading, or during peri-implantitis therapy.

Suboptimal prosthetic designs further complicate maintenance, creating situations where clinicians are unable to diagnose or manage disease effectively. Overcontoured crowns, emergence profiles exceeding 30°, prosthetic splinting, open contacts, and deep restorative margins impede hygiene access and collect biofilm.⁷

A recent systematic review and meta-analysis found strongly associated overcontoured prostheses to peri-implantitis prevalence, with some reports above 80%.⁷ Remnants from cement-retained restorations can trigger persistent inflammation with their detection becoming more difficult among deeper margins or multiple or splinted units.^3,7 Maintenance therefore begins with a well-designed restoration from a properly placed implant.

From there, broader influences come into play. Cigarette smoking, for example, impairs both perioperative and long-term treatment outcomes with a dose-dependent response.^2,3 A 2024 meta-analysis associated vaping with negative esthetic, clinical, and radiographic parameters; it is gaining popularity among young adults.⁸ Even with discontinued use, disease susceptibility may only begin to re-approximate the risk of a nonsmoker after 21 years.^2,3 Early intervention and cessation can be life-changing and should be discussed during subsequent maintenance visits.⁹

Attention must also be given to systemic factors, which exert equally significant biological pressures. Obesity and uncontrolled type 2 diabetes mellitus (T2DM) create a chronically pro-inflammatory, dysregulated host environment that undermines peri-implant health. Findings from the Academy of Osseointegration and American Academy of Periodontology Consensus on Prevention and Management of Peri-Implant Diseases and Conditions suggest that obesity does not consistently reduce implant survival but is associated with deeper peri-implant pockets, more bleeding on probing, and greater marginal bone loss, increasing the risk of peri-implant diseases.³

Poorly controlled T2DM slows and impairs osseointegration, leading to early implant failure and complications compared to healthy or well-controlled patients.^3,9 Nutritional counseling can broaden the impact of recare, supporting not only oral health but mental and systemic wellness.

Yet across all categories, one powerful and modifiable factor remains: adherence to routine professional maintenance. Because even with these comorbidities, patients who were maintained every 3 to 6 months had better therapeutic outcomes.^1,3,5,9 These findings demonstrate that maintenance is not merely beneficial but essential, functioning as the primary defense against disease initiation and escalation.

Maintenance and Self-Care Protocols

Implant maintenance necessitates a shift from traditional instrumentation to more biologically compatible techniques. High-abrasion polishing pastes, stainless steel curettes, and certain ultrasonic tips can scratch or strip the protective dioxide layer of an integrated implant, potentially releasing metal particles and altering cellular responses via metallosis.^2,4,9 Low-abrasion air-polishing techniques with erythritol powder via guided biofilm therapy consistently demonstrated high effectiveness with minimal surface disruption.^4,10 A 2025 randomized clinical trial comparing erythritol-based air polishing with ultrasonic debridement using a polyetheretherketone insert found both modalities reduced probing depths and bleeding on probing, but air polishing achieved patient-preferred comfort with less instrumentation time and greater surface decontamination.¹¹

Self-care instruction should then complement professional therapy. Patients must be taught techniques compatible with their implant prosthesis. For many, conventional wax or unwaxed floss may not be appropriate, as it can lodge around misfit abutments and exposed threads, acting as plaque-retentive foreign bodies in the peri-implant sulcus.¹² Water flossers, by contrast, offer improved plaque removal in both supragingival and subgingival spaces and are more practical for multiple and full-arch implant restorations on a low-to-medium setting.^12,13

Removable locator- and bar-retained implant-assisted overdentures require daily cleaning and periodic replacement of worn attachments. Patients should be encouraged to debride the intaglio surface with a specialized electric brush head, then rinse it in an antimicrobial solution.¹⁴ Fixed full-arch restorations demand meticulous self-care with similar brushing and interproximal aids and should then be removed every 18 months, on average, for complete evaluation and debridement.^13,14 These maintenance routines, though time-intensive, protect difficult-to-reach mucosal tissues beneath larger prosthetic surfaces.

Maintenance should extend through every phase of treatment, independent of the final prosthesis. Because healing follows a predictable biological sequence, implant debridement and recare should be timed to align with each stage as follows:

• Two weeks. Inflammation is prevalent, as the epithelial seal is still forming around the implant collar.¹⁵ Gentle biofilm disruption and reinforcement of self-care with a hygiene team prevent its early breakdown.
• Six to eight weeks. Woven bone remodeling and connective-tissue organization accelerate along the implant body.¹⁵ Localized debridement prevents deeper plaque penetration and ensures all restorative steps occur in a healthy, stable environment.
• Twelve weeks. Lamellar bone has matured and osseointegration is sufficiently established.¹⁵ Radiographs and gentler clinical measurements should be taken to guide long-term maintenance planning and self-care, with more thorough surface debridement.

Personalized maintenance reduces probing depths, bleeding, and other negative indices, especially for already ailing implants or periodontal patients.^1,9,14 Large cohort data continue to confirm higher implant survival rates among patients who remain in regular maintenance programs.^5,14 Implant maintenance is indispensable in preventing disease recurrence and maintaining stability, especially when 60% of treated diseased implants relapse, requiring secondary intervention or removal, in as little as 1 year.¹⁶

Case Report

The following case outlines the management of a failing dentition through comprehensive periodontal and implant therapy. A 59-year-old man presented to a private practice dissatisfied with his smile and experiencing increasing discomfort in the posterior region secondary to long-standing, untreated periodontitis (Figures 1-16). His medical history was noncontributory aside from a penicillin allergy. He reported smoking one pack of cigarettes daily for at least 20 years.

The patient expressed concern about losing additional teeth without a definitive plan in place. Clinical examination revealed generalized pink-red, edematous, and poorly attached periodontal tissues with heavy plaque, calculus, and debris accumulation throughout. Probing depths ranged from 4 to 10 mm with profuse bleeding on probing and/or suppuration. Cone-beam computed tomography (CBCT) imaging revealed generalized moderate-to-severe horizontal bone loss with isolated vertical defects and periapical or furcal lesions.

After a thorough evaluation and discussion of treatment options, a comprehensive plan was developed and informed consent was obtained. Although a removable, implant-assisted prosthesis would have been ideal given his periodontal and smoking histories, the patient declined any removable solution and accepted the associated risks. He agreed to a strict maintenance program. Intraoral scans, CBCT imaging, photographs, and videos, collected as part of his initial consultation, were sent to the laboratory to digitally plan same-day implant placement in the maxillary arch and next-day loading.

1. Initial debridement and self-care instruction with the dental hygiene team was performed to reduce inflammation, lower the bacterial load, and reinforce proper oral hygiene.
2. Digital implant planning for fabrication of tooth-borne reduction and osteotomy guides was completed to ensure implant positioning and accuracy.
3. Full-mouth periodontal and implant therapy was initiated to remove hopeless teeth, control periodontal infection, and prepare the arches for implant-supported rehabilitation.

• Extraction of all remaining maxillary teeth and implant placement for next-day conversion using a digital workflow were carried out to remove nonrestorable teeth and provide an immediate functional and esthetic restoration.
• Osseous resective surgery #19 to 30 with extractions and bone grafting of #18; #31 was performed to correct periodontal defects, remove hopeless teeth, and regenerate adequate bone for periodontal stability.

4. Follow-up visits with localized debridement using guided biofilm therapy at 2, 6, and 12 weeks were scheduled to control biofilm during healing and support peri-implant health.
5. A final integration check and delivery of the final prototype by the restorative dentist were completed to verify implant integration, confirm abutment stability, and finalize the prosthetic design.
6. Periodontal maintenance every 3 months was prescribed to monitor tissue health, maintain implant stability, and prevent recurrence of periodontal disease.

His initial debridement was performed by the dental hygienist, emphasizing the importance of long-term maintenance and patient compliance from treatment onset. He was given a pressure-controlled electric toothbrush with specialized heads, stabilized chlorine dioxide rinse, and a water flosser. Oral hygiene instructions were reviewed and demonstrated at this and subsequent visits. They were provided in written and video formats for improved compliance.

All remaining maxillary teeth were extracted, and alveolar ridge reduction was completed using a prefabricated printed guide to achieve appropriate prosthetic space. Bone-level implants were placed with the aid of a tooth-borne guide for initial osteotomy preparation. Following abutment selection and placement using a denture trough guide, photogrammetry was performed to verify implant position and angulation remotely with the laboratory. Extraction sockets were grafted, flaps were repositioned, and resorbable sutures were placed. A final intraoral scan was taken to initiate fabrication of a milled provisional restoration to enhance form and function. Osseous resective surgery was then completed from #19-30, along with extraction and grafting of hopeless teeth #18 and #31.

The patient returned the next day for delivery of the interim full-arch maxillary restoration. Oral hygiene protocols were reinforced, and he was scheduled for subsequent follow-ups at 2, 6, and 12 weeks for guided biofilm therapy and evaluation. At the final integration check, radiographs confirmed satisfactory healing, and abutments were torqued to their final values. Updated intraoral scans and photogrammetry records were sent to the laboratory to fabricate the final prototype to be delivered by the restorative dentist.

The patient continues to be seen every 3 months for periodontal maintenance. With consistent follow-up, improved oral hygiene practices, and his growing sense of agency and ownership over his oral health, the patient is expected to achieve stable long-term function despite the significant risk factors present at the start of treatment.

Future Directions

A structured post-operative schedule at 2, 6 to 8, and 12 weeks, followed by maintenance every 3 to 6 months depending on risk, reflects tissue healing and is especially important in full-arch implant therapy, where extensive prosthetic surfaces increase hygiene challenges. Early recare enables clinicians to identify inflammation, open contacts, prosthetic convexities, or residual cement before they contribute to irreversible bone loss. Although clinical experience supports this approach, high-quality evidence remains limited. More robust research is needed to evaluate how specific maintenance intervals influence inflammatory markers, microbial changes, radiographic bone stability, and long-term implant survival. Even so, maintenance is as essential to implant therapy as the implant it supports.

References

1. Wang HL, Avila-Ortiz G, Monje A, et al. AO/AAP consensus on prevention and management of peri-implant diseases and conditions: Summary report. J Periodontol. 2025;96:519-541.
2. Schwarz F, Derks J, Monje A, Wang HL. Peri-implantitis. J Clin Periodontol. 2018;45(Suppl 20):S246-S266.
3. Galarraga-Vinueza ME, Pagni S, Finkelman M, Schoenbaum T, Chambrone L. Prevalence, incidence, systemic, behavioral, and patient-related risk factors and indicators for peri-implant diseases: An AO/AAP systematic review and meta-analysis. J Periodontol. 2025;96:587-633.
4. Kotsakis G, Olmedo D. Peri-implantitis is not periodontitis: Microbiome-biomaterial interactions. Periodontol 2000. 2021;86:231-240.
5. Roccuzzo A, Imber JC, Marruganti C, Salvi GE, Ramieri G, Roccuzzo M. Clinical outcomes of dental implants in patients with and without history of periodontitis: A 20-year prospective study. J Clin Periodontol. 2022;49:1346-1356.
6. Lin GH, Chan HL, Wang HL. The significance of keratinized mucosa on implant health: a systematic review. J Periodontol. 2013;84:1755-67.
7. Lin GH, Lee E, Barootchi S, Rosen PS, Curtis D, Kan J, Wang HL. The influence of prosthetic designs on peri-implant bone loss: An AO/AAP systematic review and meta-analysis. J Periodontol. 2025;96:634-651.
8. Guney Z, Altingoz SM, Has H, Serdar MA, Kurgan S. The impact of electronic cigarettes on peri-implant health: A systematic review and meta-analysis. J Dent. 2024;143:104883.
9. Mojaver S, Zad A, Sarmiento H, Fiorellini JP. Efficacy of supportive peri-implant therapy in the management of peri-implant mucositis and peri-implantitis: A systematic review. J Am Dent Assoc. 2025;S0002-8177:00497-0.
10. Ravidà A, Dias DR, Lemke R, Rosen PS, Bertolini MM. Efficacy of decontamination methods for biofilm removal from dental implant surfaces and reosseointegration: an AAP/AO systematicreview on peri-implant diseases and conditions. Int J Oral Maxillofac Implants. 2025;4:91-160.
11. Maiorani C, Butera A, Pérez-Albacete Martínez C, et al. Effectiveness of erythritol-based air polishing and ultrasonic instrumentation with peek inserts in peri-implant maintenance: a randomized clinical trial including different prosthetic materials. Dent J (Basel). 2025;13:235.
12. Tütüncüoğlu S, Cetinkaya BO, Pamuk F, et al. Clinical and biochemical evaluation of oral irrigation in patients with peri-implant mucositis: a randomized clinical trial. Clin Oral Investig. 2022;26:659-671.
13. Maghsoudi P, Valkenburg C, Ter Gunne LP, van der Weijden FGA. Retrospective evaluation of peri-implant maintenance in patients with implant-supported fixed prostheses. Int J Dent. 2025;2025:9920951.
14. Araújo TG, Moreira CS, Neme RA, Luan H, Bertolini M. Long-term implant maintenance: a systematic review of home and professional care strategies in supportive implant therapy. Braz Dent J. 2024;35:e246178.
15. Salvi GE, Bosshardt DD, Lang NP, et al. Temporal sequence of hard and soft tissue healing around titanium dental implants. Periodontol 2000. 2015;68:135-52.
16. Monje A, Barootchi S, Rosen PS, Wang HL. Surgical- and implant-related factors and onset/progression of peri-implant diseases: An AO/AAP systematic review. J Periodontol. 2025;96:542-561.

From Decisions in Dentistry. February/March 2026;12(1):14-19.

Today, dental lasers are used for both soft and hard tissue procedures. When evaluating dental lasers, three concepts should be considered. The first is the target tissue chromophore(s) for the specific laser wavelength. A chromophore is the substance that absorbs laser energy allowing work to be done to the intended tissue. In soft tissue, the primary chromophores are hemoglobin, melanin, and water. In teeth and bone, the primary chromophores are water and hydroxyapatite.

The second concept is the depth of tissue penetration of laser energy, which depends on the laser’s wavelength and the proportion of light absorbed in the target tissue. Laser energy absorbed in water has a very shallow depth of tissue penetration.

The third concept is the type of photo effect (photoacoustic or photothermal) that occurs when light waves are converted to working energy. Knowledge of this effect will help determine appropriate thermal relaxation intervals and tissue cooling methods.

Visible and near infrared wavelengths are not absorbed in water, penetrate more deeply, and are primarily suited for soft tissue and photobiomodulation (PBM) procedures. Alternatively, near and midinfrared wavelengths are absorbed in water, penetrate less deeply, and are equally adept in soft and hard tissue procedures. Table 1 provides information on which lasers are indicated for different procedures.

Periodontal Diseases

One of the most widely used applications for dental lasers is in the treatment of periodontal diseases. This multistep process includes scaling and root planing to debride and disinfect sulcular epithelium (neodymium-doped yttrium aluminum garnet [Nd:YAG], diode), remove calculus and smear layer on root surfaces (erbium-doped yttrium aluminum garnet [Er:YAG]), and promote fibrin clot formation and coagulation (Nd:YAG, diode) collectively promoting epithelial reattachment. Nd:YAG and diode lasers are minimally absorbed by water, allowing deep tissue penetration and efficient removal and disinfection of diseased epithelium through absorption by hemoglobin and melanin. The shock waves created in water molecules from Er:YAG laser energy assist in calculus removal and elimination of the smear layer on root surfaces.

When using Nd:YAG, longer pulse durations of 650 microseconds stimulate fibrin clot formation. When diseased tissue lining the pocket is eliminated with debridement and laser, the fibrin clot functions as a scaffold for new tissue growth.¹

Surgery and implant recovery

Creating a temporary space or mote around a crown or cavity preparation to isolate gingival margins is a routine procedure in the general dentist’s office. Lasers provide an attractive alternative to the placement of gingival retraction cord. To accomplish adequate troughing, the laser is used to surgically remove tissue while providing hemostasis. Erbium and carbon dioxide (CO₂) lasers surgically remove tissue because of their absorption in water, but do not have the hemostatic effect that diode and Nd:YAG lasers provide. This is due to the absorption in hemoglobins and melanin and the photothermal tissue interaction that create coagulation. The result is a clean operating field with minimal trauma to the surrounding tissues and less postoperative discomfort. Figure 1 shows diode troughing and Figure 2 features CO₂ troughing.

Lasers can be utilized for other surgical procedures such as frenectomies, gingivectomies, and biopsies. The precision of laser cuts promotes quick healing with less scarring and post-operative pain. Diode, Nd:YAG, and, to a lesser degree, CO₂ lasers (Figure 3) coagulate as they cut, eliminating the need for sutures. When using erbium lasers for surgical procedures, additional methods for hemostasis should be considered. For biopsy procedures, the extent of collateral tissue damage must be managed and the type of laser used reported to the pathologist.

When uncovering a dental implant, a laser that will reflect off the implant’s metal surface while absorbed by soft tissue chromophores, such as water, hemoglobin, or melanin, is required. Erbium and CO₂ lasers are reflected off metal and absorbed in water.² In addition, the shallow depth of tissue penetration and minimal collateral damage make these lasers obvious choices for implant recovery (Figure 4).³ Photothermal tissue effects from diode and Nd:YAG lasers are dangerous to use around metal implants, as the heat generated can be fatal to osteocytes and cause irreversible thermal damage to the implant surface.^4,5

Hemostasis

Oral health professionals encounter soft tissue bleeding routinely. The photothermal effects and absorption in hemoglobins and melanin make diode and Nd:YAG lasers highly effective for hemostasis and are frequently used in periodontal therapy. Erbium and CO₂ lasers are designed for rapid tissue cutting due to their absorption in water. Only the CO₂ laser’s photothermal effect coagulates blood vessels for adequate hemostasis and is often used in conjunction with operative procedures.

Depigmentation/De-epithelialization

Amalgam tattoos and melanin pigmentation can be removed with diode, Nd:YAG, erbium, and CO₂ lasers. Diode and Nd:YAG laser energy is absorbed by dark pigments, resulting in tissue ablation. Conversely, erbium and CO₂ light energy is absorbed by water in soft tissues, and the affected pigmented tissue is ablated as an intended side effect.

Low energy ablation therapy/de-epithelialization occurs at the epithelial surface and is not classified as ablation or PBM, rather the photothermal surface effect increases blood flow to the treated area resulting in faster healing. This can be accomplished with erbium and CO₂ lasers and can be helpful in treatment of oral conditions such as lichen planus and spongiotic gingivitis (Figure 5).⁶

Snoring

Erbium and CO₂ lasers can be used in a nonablative process to minimize snoring. Er:YAG lasers create subablative micropulses that initiate two processes.⁷ First, an indirect triggering effect by short duration heat shocking of the epithelium. Second is a direct slow thermal injury of the connective tissues. The result is neocollagenesis and the remodeling of collagen. This leads to firmer soft palate tissue and reduced vibrations. CO₂ laser energy is applied to the soft palate, which creates cross-linking of collagen, causing it to contract. In its contracted form, collagen will reform stronger cross-linkages. Once treated, the soft palate is stiffer and less likely to vibrate.⁸

Photobiomodulation

PBM is used to reduce inflammation and promote healing.⁹ Its effectiveness depends on wavelength and energy density. Diodes and Nd:YAG are not absorbed in water; they penetrate deep into tissues to initiate biochemical responses in mitochondria. Optimal wavelengths are 660 to 1064 nm and dosages range from 4 to 8 J/cm². PBM is used to stimulate healing for aphthous ulcers, temporomandibular disorders, extractions, soft tissue surgeries, and post-operative pain management following tooth extraction or implant placement. PBM can significantly reduce both healing time and amount of pain experienced.¹⁰

Cavity Preparations and debonding crowns

CO₂ and Er:YAG lasers offer a highly effective option for a variety of hard tissue procedures including cavity preparations. Compared to rotary handpieces, lasers differ in three aspects. First, when using a laser, the practitioner relies on visual cues for cutting efficiency vs tactile sensations created by a bur. Distance to the target and hand speed are variables to master as these lasers operate in a noncontact mode approximately 10 mm above the tooth structure. Second, dental burs are usually end-cutting and side-cutting while lasers are end-cutting only. Third, these lasers are often able to perform most procedures, including class II cavity preparations without local anesthesia. This is especially advantageous for pediatric and highly anxious patients.

CO₂ and erbium lasers are absorbed in water and hydroxyapatite. Er:YAG laser energy is almost 100x more absorbed in water than hydroxyapatite while CO₂ laser energy is almost 100x more absorbed in hydroxyapatite than water. The result is that both lasers can manipulate tooth structure and bone; erbium by photoacoustic interaction, and CO₂ by photothermal reaction.

Water spray is used with erbium lasers primarily to hydrate tooth structure ensuring efficient cutting while keeping the tooth cool even though the photoacoustic effect generates minimal heat. The photoacoustic interaction creates explosions in enamel and dentin ejecting tooth particles that create the preparation. The photothermal tissue interaction of CO₂ with tooth structure ablates or vaporizes enamel and dentin creating the tooth preparation. Water spray is used to reduce heat and minimize thermal damage to pulpal tissues. Both lasers are effective in removing enamel and dentin but for quite varied reasons (Figures 6-8).

The removal of bonded crowns can be time consuming and requires multiple burs with rotary handpieces. Erbium laser energy is transmitted through ceramic materials and is absorbed in the cement layer beneath. Laser energy disrupts the chemical bond present between the tooth and the cement, and the cement and the crown. After 3 to 5 minutes when the laser energy is painted on all surfaces of the crown, a scaler may be used to dislodge the crown if needed. On rare occasions when the crown is not dislodged and when a rotary handpiece is needed, the bonded crowns are easily removed. Zirconia crowns with a higher yttria content are associated with a decreased crown retrieval time.¹¹ Unlike erbium lasers, CO₂ lasers are not able to debond crowns but can be used to section and remove a crown. Due to the lack of tactile sensation and the brightness of the ablation, rotary handpieces are considered more effective.

Endodontics

Erbium lasers are also useful in endodontic procedures because of their photoacoustic effects. Once the irrigating solution has been introduced to the canal system, these lasers may deploy two different techniques to assist endodontic procedures.

First, photon-induced photoacoustic streaming (PIPS) creates nonthermal photoacoustic waves within the cleaning and debriding solutions introduced in the canal, effectively cleaning canals and subcanals and freeing dentinal tubules of the smear layer.¹² During obturation, sealer can reach portions of the canal anatomy that would be occluded without the use of erbium lasers. Second, Er:YAG lasers are used to improve debridement and disinfection creating synchronized pairs of ultra-short pulses, generating an accelerated collapse of laser-induced bubbles. This leads to enhanced shockwave emission even inside the narrowest root canals, known as shock wave-enhanced emission photoacoustic streaming (SWEEPS).¹² PIPS is often compared to a single shotgun while SWEEPS is compared to an automatic gun.

Tooth Hypersensitivity

Diodes, Nd:YAG, erbium, and CO₂ lasers can all address hypersensitivity. Hypotheses on the mechanisms of action, however, differ. Some surmise that protein on the surface of the tooth structure is coagulated without altering the surface of the tooth structure itself, indicating that lasers melt the surface of the tubules and create a frozen smear layer.¹³ Others suggest plasma inside the tooth structure precipitates, altering the activity of the nerve fiber.¹⁴ Laser power settings are generally 10x lower than surgical settings, which prevent irreversible damage to the tooth surfaces. In comparing the effectiveness of Nd:YAG laser vs diode, Nd:YAG was found to be better at long-term hypersensitivity reduction¹⁵ while other studies have shown that Er:YAG is effective at long-term dentin desensitizing.

Peri-Implantitis

Laser therapy should be considered in conjunction with mechanical debridement of the ailing implant. However, long-term data on using lasers of any variety to treat peri-implantitis are not available. Current treatment of peri-implantitis includes removing the inflamed/granulation tissue, removing diseased cortical bone, decontaminating the implant surface, and stimulating new bone growth. Use of diode or Nd:YAG lasers is contraindicated due to the risk of thermal damage to the implant surface and surrounding bone and should only be considered at the end of treatment to stimulate a fibrin clot.

Erbium and CO₂ laser energy is reflected off dental implant surfaces and can be safely used to remove granulation tissue, decorticate the pocket, and debride and decontaminate the implant surface. CO₂ lasers provide adequate water spray, minimizing photothermal effects and erbium lasers keeps bone hydrated. Photoacoustic effects associated with Er:YAG lasers have also been shown to clean biofilm from narrow geometries inaccessible to instrumentation on implant surfaces.¹⁶

Future Applications

New applications and wavelengths are constantly being evaluated for use in dentistry. A blue light diode laser (445 nm) is offers unique antimicrobial effects and the ability to use an uninitiated tip. The 445 nm wavelength has a much higher affinity for hemoglobins than 950 to 970 nm wavelengths and can operate at a fraction of the power output. The result is a clean fast cut with lower thermal collateral damage to surrounding tissues.¹⁷ Erbium lasers are used for surgical removal of bone during extractions followed by disinfection of the socket prior to grafting and/or implant placement. Outcomes are expected to be favorable vs nonlased sockets. Today PBM is used in orthodontics to accelerate tooth movement. Studies show dramatic decreases in overall treatment time. High-intensity laser therapy is also being evaluated for stimulation of healing and pain management.

References

1. Wang HL, Avila-Ortiz G, Monje A, et al. AO/AAP consensus on prevention and management of peri-implant diseases and conditions: Summary report. J Periodontol. 2025;96:519-541.
2. Schwarz F, Derks J, Monje A, Wang HL. Peri-implantitis. J Clin Periodontol. 2018;45(Suppl 20):S246-S266.
3. Galarraga-Vinueza ME, Pagni S, Finkelman M, Schoenbaum T, Chambrone L. Prevalence, incidence, systemic, behavioral, and patient-related risk factors and indicators for peri-implant diseases: An AO/AAP systematic review and meta-analysis. J Periodontol. 2025;96:587-633.
4. Kotsakis G, Olmedo D. Peri-implantitis is not periodontitis: Microbiome-biomaterial interactions. Periodontol 2000. 2021;86:231-240.
5. Roccuzzo A, Imber JC, Marruganti C, Salvi GE, Ramieri G, Roccuzzo M. Clinical outcomes of dental implants in patients with and without history of periodontitis: A 20-year prospective study. J Clin Periodontol. 2022;49:1346-1356.
6. Lin GH, Chan HL, Wang HL. The significance of keratinized mucosa on implant health: a systematic review. J Periodontol. 2013;84:1755-67.
7. Lin GH, Lee E, Barootchi S, Rosen PS, Curtis D, Kan J, Wang HL. The influence of prosthetic designs on peri-implant bone loss: An AO/AAP systematic review and meta-analysis. J Periodontol. 2025;96:634-651.
8. Guney Z, Altingoz SM, Has H, Serdar MA, Kurgan S. The impact of electronic cigarettes on peri-implant health: A systematic review and meta-analysis. J Dent. 2024;143:104883.
9. Mojaver S, Zad A, Sarmiento H, Fiorellini JP. Efficacy of supportive peri-implant therapy in the management of peri-implant mucositis and peri-implantitis: A systematic review. J Am Dent Assoc. 2025;S0002-8177:00497-0.
10. Ravidà A, Dias DR, Lemke R, Rosen PS, Bertolini MM. Efficacy of decontamination methods for biofilm removal from dental implant surfaces and reosseointegration: an AAP/AO systematicreview on peri-implant diseases and conditions. Int J Oral Maxillofac Implants. 2025;4:91-160.
11. Maiorani C, Butera A, Pérez-Albacete Martínez C, et al. Effectiveness of erythritol-based air polishing and ultrasonic instrumentation with peek inserts in peri-implant maintenance: a randomized clinical trial including different prosthetic materials. Dent J (Basel). 2025;13:235.
12. Tütüncüoğlu S, Cetinkaya BO, Pamuk F, et al. Clinical and biochemical evaluation of oral irrigation in patients with peri-implant mucositis: a randomized clinical trial. Clin Oral Investig. 2022;26:659-671.
13. Maghsoudi P, Valkenburg C, Ter Gunne LP, van der Weijden FGA. Retrospective evaluation of peri-implant maintenance in patients with implant-supported fixed prostheses. Int J Dent. 2025;2025:9920951.
14. Araújo TG, Moreira CS, Neme RA, Luan H, Bertolini M. Long-term implant maintenance: a systematic review of home and professional care strategies in supportive implant therapy. Braz Dent J. 2024;35:e246178.
15. Salvi GE, Bosshardt DD, Lang NP, et al. Temporal sequence of hard and soft tissue healing around titanium dental implants. Periodontol 2000. 2015;68:135-52.
16. Monje A, Barootchi S, Rosen PS, Wang HL. Surgical- and implant-related factors and onset/progression of peri-implant diseases: An AO/AAP systematic review. J Periodontol. 2025;96:542-561.

From Decisions in Dentistry. February/March 2026;12(1):20-23.

Untreated oral diseases create a considerable economic burden, stemming from both high treatment costs and losses in workforce productivity. In 2019, a representative sample of 194 countries spent $387 billion to treat oral diseases, while losing $323 billion in productivity, a total cost of $710 billion (Figure 2).² Oral diseases can also impact overall health and well-being, contributing to rising healthcare costs.

The magnitude of the economic costs, along with a sharp decline in the quality of life for people with caries, demands innovative solutions. Today, fluoride remains the consensus choice for caries prevention. Results from over 70 global clinical studies conclude that fluoride reduces decayed, missing, and filled tooth surfaces (DMFS) by 24% in children.³ A meta-review of 40 studies reported that fluoride, either from dentifrice or water supplementation, prevents 29% of caries on the tooth crown and 22% of caries on the root surface.⁴

Arginine is an oral prebiotic that increases the pH of biofilms and the oral environment when metabolized by oral bacteria (Figure 3), whereas fluoride acts directly on the tooth surface to strengthen enamel and promote remineralization.⁵ A naturally occurring semi-essential amino acid, arginine is found in many foods such as meats, dairy products, and even in breast milk.

Arginine’s potential as an anticaries agent was first recognized in the 1980s. Early work found that the pH of dental plaque varied based on the proportion of arginolytic bacteria present. This pH-modulating effect was later linked to ammonia production by oral bacteria during arginine metabolism. This process increases the buffering capacity of saliva, and may increase the ammonia-producing capacity of the oral microbiome, generally.⁶

The first clinical study of arginine’s effectiveness as an anti-caries agent was conducted in Venezuela in the early 2000s. In this study, adolescents used an arginine dentifrice over 2 years. Arginine supplementation was associated with a significant decrease in the mean DMFS score.⁷ A subsequent study using arginine mints as a supplement over a 1-year period also reported a significant decrease in the DMFS score.⁸

Numerous studies conducted combining fluoride and arginine (1.5%) have demonstrated the additive effect of these two caries preventive agents in enhancing remineralization and in reducing early carious lesions. Research shows this dual intervention leads to a 50% reduction in early carious lesion size^9,10 and up to 20% less new cavities as measured by decayed, missing, and filled teeth (DMFT) vs fluoride toothpaste after 2 years of use.^11,12

The results of a recent 2-year clinical trial in China among 6,000 children, aged 10-14, across three centers, comparing two concentrations of arginine (1.5% and 8%) dentifrice with a 1,450 ppm sodium fluoride (NaF) control, identified a dose-response relationship between arginine and caries reduction. Compared to the NaF control, the 8% arginine dentifrice significantly reduced DMFS scores by 26%, and DMFT scores by 25.3% at 2 years. DMFS and DMFT scores for the lower arginine concentration (1.5%) were not statistically different from those of the NaF control group at 2 years.¹³

A recent 1-year phase 2 clinical trial in the US confirmed the efficacy of arginine. The trial enrolled 2,025 children, aged 10-14, across nine centers. Three arginine concentrations, 1.5%, 4%, or 8.0% were tested. A control group used a 0.24% (1,100 ppm) sodium fluoride dentifrice without arginine. A consistent decreasing dose-response trend in incremental DMFS and DMFT occurred over the study period, but it was not statistically significant. DMFS and DMFT increments were most favorable for the 1.5% arginine dentifrice, followed by the 4% dentifrice, and then the 8% dentifrice.

The contrasting results between the arginine alone vs fluoride trials are likely driven by differences in study design. The power of the studies was vastly different with approximately 2,000 subjects per group in the China study vs 500 subjects per group in the US study.

Central to these differences are the study duration and baseline caries experience; the China trial spanned 2 years with a lower disease burden (DMFS < 1), while the phase 2 US trial was a shorter, 1-year study involving participants with more advanced baseline disease (DMFS < 2). These discrepancies in length and initial severity can significantly alter the sensitivity of a trial to detect differences in treatment efficacy.

While other methodological variations like center count and pandemic recruitment strategies occurred, the interaction between study length and disease experience remains the most probable explanation for the differing results.

Fluoride alone has not eliminated tooth decay. Therefore, new and innovative evidence-based caries preventive actives must be identified that can complement the work that has been done solely by fluoride over the past 50 plus years. There are very few complex chronic diseases like caries that are managed by a single approach.

Fluoride and arginine have different mechanisms of action that can help to address the global burden of caries along with lifestyle changes that reduce sugar consumption and emphasize the importance of self-care in the management of caries. Arginine dentifrices alone or in conjunction with fluoride could offer novel approaches to reduce the caries economic burden while improving the quality of life for everyone.

Contact

Colgate Palmolive
https://www.colgatepalmolive.com/en-us/contact-us
800-468-6502

Acknowledgments

I would like to express my gratitude to the numerous investigators involved in the US clinical trial along with their dedicated staff members: Benett Amaechi, Domenick Zero, Marcelle Nascimento, Augusto Elias-Boneta, Violet Haraszthy, Meelin Dian Chin Kit-Wells, Yiming Li, David Hershkowitz, Hatice Hasturk, Raffi Miller, Andrea Zandona, Mabi Singh, and Gerard Kugel. I would also like to acknowledge the statistician for the US Phase 2 study, Howard Proskin, and the hardworking members of the R&D, clinical and regulatory teams at Colgate-Palmolive. Finally, I would like to thank Erin Kello for summarizing the clinical evidence used in the preparation of this clinical insights article.

References

1. World Health Organization. Global Oral Health Status Report: Towards Universal Health Coverage for Oral Health by 2030. Available at who.int/publications/i/item/9789240061484. Accessed February 18, 2026.
2. World Economic Forum. The Economic Rationale for a Global Commitment to Invest in Oral Health. Available at https://www.weforum.org/publications/the-economic-rationale-for-a-global-commitment-to-invest-in-oral-health/. Accessed February 18, 2026.
3. Marinho VC, Higgins JP, Sheiham A, Logan S. Fluoride toothpastes for preventing dental caries in children and adolescents. Cochrane Database Syst Rev. 2003;2003:CD002278.
4. Griffin SO, Regnier E, Griffin PM, Huntley V. Effectiveness of fluoride in preventing caries in adults. J Dent Res. 2007;86:410-415.
5. Nascimento MM, Alvarez AJ, Huang X, et al. Metabolic profile of supragingival plaque exposed to arginine and fluoride. J Dent Res. 2019;98:1245-1252.
6. Burne RA. Anti-caries mechanisms of action of arginine. In: Arginine and the Healthy Oral Microbiome. Proceedings from a Colgate Symposium: Arginine–A Breakthrough Technology Fighting the Caries Epidemic. Available at https://pages.ada.org/jadaplus_arginine/anti-caries-mechanisms-of-action-of-arginine. Accessed February 18, 2026.
7. Acevedo AM, Machado D, Rivera LE, Wolff M, Kleinberg I. The inhibitory effect of an arginine bicarbonate/calcium carbonate (CaviStat^®)-containing dentifrice on the development of dental caries in Venezuelan school children. J Clin Dent. 2005;16:63-70.
8. Acevedo AM, Montero M, Rojas-Sanchez F, et al. Clinical evaluation of the ability of CaviStat in a mint confection to inhibit the development of dental caries in children. J Clin Dent. 2008;19:1-8.
9. Yin W, Hu DY, Li X, et al. The anti-caries efficacy of a dentifrice containing 1.5% arginine and 1450 ppm fluoride as sodium monofluorophosphate assessed using Quantitative Light-induced Fluorescence (QLF). J Dent. 2013;41(Suppl 2):S22-28.
10. Yin W, Hu DY, Fan X, et al. A clinical investigation using quantitative light-induced fluorescence (QLF) of the anticaries efficacy of a dentifrice containing 1.5% arginine and 1450 ppm fluoride as sodium monofluorophosphate. J Clin Dent. 2013;24(Spec no A):A15-22.
11. Li X, Zhong Y, Jiang X, et al. Randomized clinical trial of the efficacy of dentifrices containing 1.5% arginine, an insoluble calcium compound and 1450 ppm fluoride over two years. J Clin Dent. 2015;26:7-12.
12. Kraivaphan P, Amornchat C, Triratana T, et al. Two-year caries clinical study of the efficacy of novel dentifrices containing 1.5% arginine, an insoluble calcium compound and 1,450 ppm fluoride. Caries Res. 2013;47(6):582-590.
13. Yin W, Zhou Z, Huang RZ, et al. Arginine dentifrices and childhood caries prevention: a randomized clinical trial. JDR Clin Trans Res. 2025:23800844251361471.

From Decisions in Dentistry. February/March 2026;12(1):24-25.

Autoimmune (AI) diseases are chronic inflammatory disorders marked by the presence of autoantibodies and dysfunction in both innate and adaptive immunity. This dysfunction results in end-organ damage and clinical disease manifestations.^1,2 The innate immune response triggers adaptive immune responses and proliferation of innate immune cells such as macrophages, granulocytes, and dendritic cells. These release inflammatory factors stimulating the infiltration of T and B cells.

The hallmark of AI disease is the presence of autoantibodies that target organ tissue, leading to cytotoxic reactions resulting in tissue damage, and cell death.³ Approximately 15 million people in the United States, or 4.6%, have an AI disease. Of those individuals, 34% have more than one AI disease.^2,3 Women are twice as likely as men to be diagnosed with an autoimmune disease, accounting for 63% of cases compared to 37% in men.^2,3

Immune system dysfunction is due to proinflammatory environmental agents such as diet, smoking, xenobiotic contacts, infections, obesity, sleep deprivation, stress, and air pollution, as well as family history of AI diseases.^2,3 Screening for an AI disease involves an antinuclear antibody (ANA) test. The higher the ANA titers, the greater the probability of developing an AI disease. Due to potential false positives, further antibody testing and clinical evaluation are required.³

The five most common AI diseases in the US are rheumatoid arthritis (RA), psoriasis, type I diabetes, Graves disease (GD), and autoimmune thyroiditis.⁴ Each AI disease is associated with distinct oral manifestations that may be early indicators of disease onset and progression.

Rheumatoid Arthritis

RA is the most common inflammatory arthritis characterized by the proliferation of synovial fluid within joints (Figure 1). The wrists, proximal interphalangeal joints, and meta-carpophalangeal joints are the most frequently affected. Symptoms may last for 6 weeks or more. Risk factors associated with RA are older age with a peak onset between ages 30 and 50, family history of RA, female sex, and smoking. The autoantibodies present in patients with RA include rheumatoid factor and anticitrullinated protein antibody.⁵

Oral manifestations of RA include periodontitis, xerostomia, secondary Sjögren syndrome, oral candidiasis, and temporomandibular joint disorder. The most common is periodontitis characterized by attachment and bone loss due to a microbial shift from Gram-positive to Gram-negative species such as Porphyromonas gingivalis, P. aggregatibacter, and P. actinomycetemcomitans. This shift causes the release of inflammatory cytokines and metalloproteinases resulting in tissue and bone loss.⁶ Both RA and periodontitis show an overexpression of pro-inflammatory cytokines such as interleukin (IL) 1-beta, tumor necrosis factor-alpha (TNF)-α, IL-6 and IL-8.⁷

Xerostomia is the second most common oral manifestation, affecting up to 50% of patients with RA and is often associated with decreased parotid gland function. The symptoms include dryness, burning sensation, difficulty swallowing, and decreased or loss of taste sensation. Xerostomia increases the risk of other oral conditions such as caries, periodontitis, candidiasis, and oral malodor.⁶ When xerostomia is accompanied with dry eyes it may indicate secondary Sjögren syndrome, which affects 21% of individuals with RA.⁸ Management strategies for xerostomia and Sjögren syndrome include frequent sipping of water, chewing gum, and using saliva substitutes or salivary stimulants such as pilocarpine or cevimeline.⁹

Oral candidiasis, an opportunistic fungal infection, is a common sequela in patients with xerostomia. Oral candidiasis is caused by Candida albicans, a fungus present in 30% to 60% of immunocompetent adults. Oral candidiasis is typically asymptomatic and appears as white or erythematous lesions. White lesions are easily removed with gauze, leaving an erythematous mucosal surface. These lesions present most often on the tongue, labial and buccal mucosa, gingival tissues, hard and soft palate, and the oropharynx. The different types of white lesions include pseudomembranous candidiasis, acute atrophic candidiasis, and chronic atrophic candidiasis.

Pseudomembranous candidiasis presents in a third of total cases and is seen mostly in immunocompromised patients using topical steroids. Most commonly seen on the palate, acute atrophic candidiasis is more common among those with uncontrolled diabetes. Chronic atrophic candidiasis, also known as denture stomatitis, occurs under dentures in 65% of cases due to a poor fit, prolonged denture use, and poor oral hygiene.

Oral candidiasis can also present as erythematous lesions including angular cheilitis, median rhomboid glossitis, and linear gingival erythema. Angular cheilitis arises due to a moist environment at the commissures of the mouth. Median rhomboid glossitis is very rare, affecting less than 1% of individuals and presents as an erythematous patch in the center of the tongue due to atrophy of filiform papillae. Atrophy can occur due to smoking or use of inhaled steroids. Linear gingival erythema is seen in patients with human immunodeficiency virus as an erythematous line over the gingival margin of single or multiple teeth. Symptoms include burning sensation, oral bleeding, and changes in taste.

The first line treatment for mild presentations of oral candidiasis is a topical antifungal, with nystatin being the most prescribed. For patients with diabetes, nystatin oral rinse or clotrimazole troches should be avoided due to their high sucrose content. An alternative is triazoles (fluconazole or itraconazole).¹⁰

Psoriasis

Psoriasis is a chronic inflammatory skin disease that presents as scaly plaques (Figure 2).¹¹ Up to 3% of the population or 4.5. million people are affected by this disease with symptoms beginning before the age of 40.^12,13 There are several types of psoriasis including plaque, inverse, guttate, pustular, erythrodermic, and nail psoriasis. Of these types, plaque psoriasis is the most common and affects up to 80% to 90% of individuals. The most frequently areas affected are the elbows, knees, face, scalp, fingernails and toenails, genitals, lower back, palms, and feet.¹⁰

Oral manifestations associated with psoriasis include benign migratory glossitis, fissured tongue, periodontitis, intraoral psoriasis, and chronic atrophic candidiasis. Benign migratory glossitis, also known as geographic tongue, is the most common, affecting approximately 10% of individuals with fissured tongue often accompanying it. If symptomatic, geographic tongue can be treated with oral rinses containing anesthetics, topical corticosteroids, antihistamines, vitamin A, and zinc supplements.¹⁴

Both psoriasis and periodontitis share pathophysiologic features including neutrophil and cytokine presence, along with IL-17 and TNF-α.¹⁵ Intraoral psoriasis appears as either small, white papules that bleed when scraped or as red and white plaques. The most common locations are the lips, tongue, palate, buccal mucosa and gingiva.¹³

Type 1 Diabetes

Type 1 diabetes is characterized by an immune-mediated destruction of pancreatic beta cells that leads to insulin deficiency. The disease pathophysiology is composed of three stages: destruction of beta cells, beta cell dysfunction, and symptomatic hyperglycemia.

In the first stage, the beta cells are destroyed but fasting glucose levels are normal and there are no symptoms. In the second stage, more beta cell dysfunction occurs, leading to dysglycemia or an impaired fasting glucose (100 to 125 mg/dL), impaired glucose tolerance, and glycated hemoglobin (HbA1C) of 5.7% to 6.4%. The last stage presents with symptomatic hyperglycemia (≥ 200 mg/dL), fasting glucose (126 mg/dL) and HbA1C ≥ 6.5%. If left untreated, ketoacidosis, a life-threatening condition, occurs causing hyperglycemia, ketonuria, and electrolyte imbalance. The symptoms of ketoacidosis include fruity smelling breath, lethargy, and coma.¹⁶

Type 1 diabetes affects about 304,000 children and adolescents and 1.7 million adults or 5% to 10% of the population.^16,17 More common among men (0.64%) than women (0.46%), type 1 diabetes causes polyuria or frequent urination, polydipsia or frequent need to drink water, and unintentional weight loss.¹⁸ Treatment requires replacement of insulin through daily injections or continuous subcutaneous insulin through an insulin pump.¹⁶

The oral manifestations associated with type 1 diabetes include periodontitis, oral mucosal diseases, xerostomia, burning mouth, and taste disturbances.^19,20 The function of normal immune cells, including neutrophils, monocytes, and macrophages, are impaired. Neutrophil impairment adherence, chemotaxis, and phagocytosis are dysfunctional, which lead to diminished bacterial killing and an increase in periodontal destruction. Monocytes normally produce TNF-α; however, in those with type 1 diabetes, they produce more TNF-α than normal, resulting in further periodontal destruction.¹⁹

The oral mucosal diseases associated with type 1 diabetes include oral lichen planus (OLP), recurrent aphthous stomatitis (RAS), and oral candidiasis.²⁰ The six clinical subtypes of OLP are reticular, papular, plaque, atrophic, erosive, and bullous. Of these subtypes, the most common are reticular, erosive, and plaque.

The reticular type presents as a white lacy network on the buccal mucosa also referred to as Wickham striae. The erosive type presents as erythematous ulcerations while the plaque type appears as white keratotic papules. OLP presents bilaterally and appears most commonly on the buccal mucosa, tongue, and gingiva. The first line treatment is topical corticosteroids in either a gel form, such as triamcinolone acetonide, or a rinse (eg, dexamethasone).²¹

The three subgroups of RAS are minor aphthous ulcers, major aphthous ulcers, and herpetiform aphthous ulcers. Minor aphthous ulcers are the most common type, accounting for 80% of patients with RAS.²² They present as small round lesions with an erythematous halo covered by a grey-white pseudomembrane. The ulcers are 5 mm or less in diameter and present on nonkeratinized tissue including buccal and labial mucosa and the floor of the mouth.

Major aphthous ulcer type impact about 10% of those with RAS.²² The ulcers are larger in size measuring greater than 10 mm in diameter and last 5 to 10 weeks. These ulcers can present anywhere in the oral cavity and the oropharynx.

Herpetiform aphthous ulcers are the least common, appearing in 1% to 10% of patients with RAS.²² The ulcers are numerous and small, measuring 2 to 3 mm in diameter. They can appear on keratinized and nonkeratinized tissues.²²

Xerostomia and burning mouth syndrome are other common oral manifestation of type 1 diabetes. Xerostomia not only contributes to an increased caries risk. but also raises the risk for oral candidiasis. Patients experiencing xerostomia may have a burning sensation or a change in taste.²³ In a third of adults with type 1 diabetes, taste dysfunction occurs, inhibiting the ability to maintain a healthy diet, leading to poor glycemic control.²⁰

Thyroid Autoimmune Diseases

The thyroid gland is the largest endocrine gland in the body and is located directly inferior to the larynx. The thyroid is essential for the synthesis and secretion of thyroid hormones and iodine homeostasis.²⁴ The thyroid produces hormones that are 90% inactive thyroxine (T4) and 10% active triiodothyronine (T3). T4 is a prohormone of T3 and is converted peripherally in the liver, kidneys, and brain.²⁵

The thyroid also houses the parathyroid gland, which releases calcitonin, an essential hormone for bone health. When functioning normally, the hypothalamus releases thyrotropin, releasing hormone (TRH), which stimulates the pituitary gland to release thyroid stimulating hormone (TSH). TSH stimulates the thyroid to release T3 and T4.²⁴ When T3 and T4 levels increase, the release of TRH and TSH decreases through a negative feedback loop. This, in turn, decreases T3 and T4 secretion and iodine uptake.²⁵ These thyroid hormones play an important role in body temperature regulation, heart rate, digestive rate, muscle contraction, and metabolism.²⁴ When the thyroid is functioning incorrectly, diseases such as Graves disease (GD) and Hashimoto thyroiditis (HT) can arise.

Graves Disease

GD is defined as an overactivity of the thyroid gland also known as hyperthyroidism.²⁶ The disease is caused by thyroid-stimulating immunoglobulin (TSI) also known as thyroid stimulating antibody (TSAb). TSI binds to the TSH receptor on the thyroid cell membrane, leading to thyroid hormone synthesis T3 and T4 and thyroid gland growth. As a result, TSH is low and T3 and T4 levels are elevated.²⁷

GD affects one in 100 Americans and is more commonly seen in women over the age of 30. A family history of GD, HT, or other autoimmune disorders such as vitiligo, autoimmune gastritis, TID, and RA, increase the likelihood of a GD diagnosis. Symptoms include weight loss, rapid and irregular heartbeat, nervousness, irritability, insomnia, muscle weakness, sweating, goiter, and ophthalmopathy.²⁶

The most common oral manifestations associated with hyperthyroidism are increased caries risk, periodontitis, enlargement of extraglandular thyroid tissue seen on the lateral posterior tongue, maxillary or mandibular osteoporosis, accelerated tooth eruption, and burning mouth syndrome.²⁸

Autoimmune Thyroiditis

Autoimmune thyroiditis, or HT, is an underactivity of the thyroid gland or hypothyroidism (Figure 3).²⁹ The disease is caused by the formation of antithyroid antibodies, thyroid peroxidase, thyroglobulin, and T-cell activation that attack the thyroid tissue, causing progressive fibrosis.^30,31 As a result, TSH is elevated and T3 and T4 are low.³¹

HT is four to 10 times more common in women than in men. While the disease can manifest in teens and young women, it is mostly seen between the ages of 30 and 50. Individuals are more likely to develop the disease if other autoimmune diseases are present such as celiac disease, lupus, Sjögren syndrome, RA, and type 1 diabetes. Symptoms include fatigue, weight gain, cold intolerance, joint and muscle pain, constipation, dry skin, irregular menstrual periods, and slow heart rate. Individuals with HT are treated with levothyroxine sodium.²⁹

The most common oral manifestations associated with hypothyroidism are macroglossia or enlarged tongue, dysgeusia or altered taste sensation, periodontitis, delayed tooth eruption, altered tooth morphology, and delayed wound healing.²⁸ Patients with HT are likely to develop cardiovascular and metabolic disorders, which are associated with poor periodontal health.

The commonality between HT and periodontal diseases is the presence of inflammation and T helper cells, Th1 and Th17. HT also presents with vascular endothelial dysfunction, which impairs blood flow and nutrient delivery to the periodontal tissues. Patients with HT may have decreased bone density, exacerbating bone loss seen with periodontitis.³¹

Conclusion

With the rise in prevalence of autoimmune diseases in the US, oral health professionals must be able to accurately identify, understand, and treat the most common oral pathologies associated with the top five AI diseases. By recognizing the oral manifestations early, oral health professionals play a vital role in ensuring accurate diagnosis, timely intervention, and improved patient outcomes through comprehensive care.

References

1. Abajina M, Abend, AH, Avasarala J, et al. Estimation of prevalence of autoimmune diseases in the United States using electronic health record data. J Clin Invest. 2025;135:e178722.
2. Miller FW. The increasing prevalence of autoimmunity and autoimmune diseases: an urgent call to action for improved understanding, diagnosis, treatment, and prevention. Curr Opin Immunol. 2022;80:102266.
3. Jiang D, Shi J, Su Q, Xiang Y, Zhang M. The role of inflammation in autoimmune disease: a therapeutic target. Front Immunol. 2023;14:1267091.
4. De Widt L. New study calculates autoimmune disease prevalence in U.S. Available at /newsnetwork.mayoclinic.org/discussion/new-study-calculates-autoimmune-disease-prevalence-in-u-s/. Accessed February 13, 2026.
5. Wasserman AM. Diagnosis and management of rheumatoid arthritis. Am Fam Physician. 2011;84:1246-1252.
6. Abubakr OA, Hamdy MA, Mohamed MA, Youssef AM. Dental and oral manifestations of rheumatoid arthritis: is it related to general disease activity? J Med Sci Res. 2023;6:15-24.
7. Cugno M, Gualtierotti R, Marzano AV, Spadari F. Main oral manifestations in immune-mediated and inflammatory rheumatic diseases. J Clin Med. 2019:8;21.
8. Sjögren’s Foundation. Overlapping diseases. Available at sjogrens.org/living-with-sjogrens/overlapping-diseases#:~:text=Graves%20disease%20and%20Hashimoto%20thyroiditis,Autoimmune%20Thyroid%20Disease%20and%20Sjögren’s. Accessed February 13, 2026.
9. Blum MA, Carsons SE. Sjögren syndrome. Available at ncbi.nlm.nih.gov/books/NBK431049/. Accessed February 14, 2026.
10. Brizuela M, Raja A, Taylor M. Oral Candidiasis.Treasure Island, Florida: StatPearls. 2025.
11. Cleveland Clinic. Psoriasis. Available at my.clevelandclinic.org/health/diseases/6866-psoriasis. Accessed Febuary 13, 2026.
12. Adamska K, Adamski Z, Dorocka-Bobkowska B, Olejnik M. Oral health status of psoriatic patients managed with modern biological therapy. Postepy Dermatol Alergol. 2021;39:1151-1156.
13. Brown GC, Dreyer LN. Oral manifestations of psoriasis clinical presentation and management. N Y State Dent J. 2012;78:14-18.
14. Carla V, Carlos A, Carneiro S. Geographic tongue and psoriasis: clinical, histopathological, immunohistochemical and genetic correlation – a literature review. An Bras Dermatol. 2016;91:410-421.
15. Farag YMK, Hussein M, Sonis S. Psoriasis and oral health in adult United States population: a cross-sectional study. BMC Oral Health. 2023;23:66.
16. Lucier J, Mathias PM. Type 1 diabetes. Available at ncbi.nlm.nih.gov/books/NBK507713. Accessed February 13, 2026.
17. American Diabetes Association. Statistics About Diabetes. Available at diabetes.org/about-diabetes/statistics/about-diabetes. Accessed February 13, 2026.
18. United States Centers for Disease Control and Prevention. Prevalence of diagnosed diabetes in adults by diabetes type – United States, 2016. Available at cdc.gov/mmwr/volumes/67/wr/mm6712a2.htm#:~:text=The%20prevalence%20of%20type%201%20diabetes%20was%20higher%20among%20men,%25)%20(p%3C0.01). Accessed February 13, 2026.
19. Indurkar MS, Indurkar S, Maurya AS. Oral manifestations of diabetes. Clin Diabetes. 2016;34:54-57.
20. Vernillo AT. Dental considerations for the treatment of patients with diabetes mellitus. J Am Dent Assoc. 2003;134:24-33.
21. Raj G, Raj M. Oral lichen planus. Available at ncbi.nlm.nih.gov/books/NBK578201. Accessed February 13, 2026.
22. Chatterjee K, Plewa MC. Recurrent apthous stomatitis. Available at ncbi.nlm.nih.gov/books/NBK431059/. Accessed February 13, 2026.
23. Rohani B. Oral manifestations in patients with diabetes mellitus. World J Diabetes. 2019;10:485-489.
24. Achanta A, Kasbage SD. Oral manifestations of thyroid disorders. J Res Med Dent Sci. 2022;10:12-16.
25. Armstrong M, Asuka E, Fingeret A. Physiology, thyroid function. Available at ncbi.nlm.nih.gov/books/NBK537039/. Accessed February 13, 2026.
26. National Institute of Diabetes and Digestive and Kidney Diseases. Graves’ Disease. Available at niddk.nih.gov/health-information/endocrine-diseases/graves-disease. Accessed February 13, 2026.
27. Bhusal K, Pockhrel B. Graves’ Disease. Available at ncbi.nlm.nih.gov/books/NBK448195/. Accessed February 13, 2026.
28. Bathla M, Chandna S. Oral manifestations of thyroid disorders and its management. Indian J Endocrinol Metab. 2011;15:S113-S116.
29. National Institute of Diabetes and Digestive and Kidney Diseases. Hashimoto’s Disease. Available at niddk.nih.gov/health-information/endocrine-diseases/hashimotos-disease. Accessed February 13, 2026.
30. Kaura J, Jialal I. Hashimoto thyroiditis. Available at ncbi.nlm.nih.gov/books/NBK459262/. Accessed February 13, 2026.
31. Morais A, Resende M, Pereira J. Association between hashimoto’s thyroiditis and periodontal disease: a narrative review. Acta Med Port. 2016;29:651-657.

From Decisions in Dentistry. February/March 2026;12(1):28-31.

Periodontal diseases, a leading cause of tooth loss worldwide,  are chronic, multifactorial inflammatory conditions that compromise the supporting structures of the teeth.¹ Beyond the local implications of periodontal diseases, research increasingly highlights a close link between periodontal diseases and systemic conditions such as diabetes mellitus, cardiovascular disease, and hypertension.² In the field of periodontal medicine, researchers have described how oral inflammation contributes to systemic health via shared biological pathways (especially chronic inflammation and immune dysregulation).³

Diabetes affects 21 million Americans, including more than 9% of adults.⁴ Approximately 6 million United States adults have the disease but remain undiagnosed.⁵ Increasing annually in the US, the prevalence of diabetes varies by age and racial category, and is more common among older adults, American Indian/Alaska Native populations, Hispanic individuals, and non-Hispanic Black people.

The incidence of diabetes is also increasing annually. In 2002, 1.3 million new cases of diabetes were diagnosed, an increase of 500,000 annually since 1998, when incidence stood at 800,000.⁵

The rise in prevalence and incidence of diabetes is directly related to increasing obesity rates in the US.⁵ Type 2 diabetes comprises about 85% to 90% of all diabetes diagnoses, whereas type 1 diabetes constitutes 5% to 10% of patients. Gestational diabetes and secondary forms of diabetes associated with other conditions, such as pancreatic disease, drug therapies, and endocrine disorders, account for the remainder of cases.⁶

One significant modifiable factor that affects both periodontal diseases and systemic health is nutrition. A patient’s diet plays a key role in regulating immune function, controlling inflammation, and shaping the oral microbiome.¹ Studies suggest that deficiencies in key anti-inflammatory nutrients (vitamin D, antioxidants, and omega-3 fatty acids) weaken the host’s immune responses and delay periodontal healing.^1,7 Moreover, diets high in refined sugars, processed foods, and pro-inflammatory fats are associated with worsening periodontal and systemic conditions.^3,8

A cross-sectional study reported obesity and poor dietary habits as risk factors for periodontal diseases.⁷ These findings reinforce the conviction that nutrition is a common denominator influencing oral health and metabolic status.² Therefore, understanding the complex interactions between diet, periodontal tissues, and systemic health is essential for advancing both preventive and therapeutic strategies in dentistry. Oral health professionals have a unique opportunity to assess patients’ nutritional habits and offer personalized recommendations to enhance their oral and overall health outcomes.

Nutrition and Immune Modulation

A bidirectional relationship exists between oral health and nutrition. On one hand, dietary choices influence the integrity of oral tissues, while on the other, the health of the oral cavity affects nutrient intake. Diets high in sugar significantly increase the risk of dental caries. Although the complex nature of periodontal diseases makes it challenging to pinpoint a direct correlation with diet, growing evidence suggests a strong connection. For instance, evidence shows that individuals adhering to a pro-inflammatory diet — high consumption of processed foods and added sugars — have a higher prevalence of periodontitis.^3,7 Conversely, anti-inflammatory diets, such as the Mediterranean diet, are associated with better periodontal outcomes.

The OsteoPerio Study demonstrated that individuals adhering to high-quality dietary patterns (characterized by abundant intake of fruits, vegetables, whole grains, and lean proteins) exhibited significantly reduced risk of moderate to severe periodontitis. Importantly, these associations persisted after statistical adjustment for potential confounders, including age, smoking status, and body mass index, underscoring the independent influence of diet on periodontal health. This evidence substantially reinforces the conceptual framework that diet constitutes a critical and modifiable determinant in the pathogenesis and advancement of periodontal diseases.^9,10

The progression of periodontal diseases is closely linked to the host’s susceptibility. In the early stages of lesions, the host releases pro-inflammatory cytokines, such as interleukin (IL)-1, IL-2, IL-4, and IL-8 and tumor necrosis factor-alpha (TNF-α), which contribute to irreversible clinical attachment loss and tissue breakdown.^2,3,7,11

The systemic implications of oral inflammation highlight the importance of nutrition in modulating immune response.^2,7 Studies show a significant association between periodontal disease and hypertension, with interactive effects involving smoking and age.^2,7 Literature supports the need for interdisciplinary care to address systemic inflammation and reduce oral inflammatory burden.^3,7,8 Oral health professionals can assess dietary habits and offer personalized guidance to lower periodontal disease risk.⁷ Interprofessional collaboration among dental providers, nutritionists, and medical professionals should be part of treatment planning to help control inflammation.^7,8

Vitamin D and Dietary Patterns

Emerging evidence highlights the crucial role of diet and micronutrients in preventing and managing periodontal diseases.^1,3,8 Because periodontal diseases are a host immune response to bacteria, vitamin D contributes to periodontal health by supporting bone metabolism and regulating host immune responses to oral pathogens.¹

Maintaining adequate serum levels of vitamin D may reduce the risk and severity of periodontal diseases by decreasing inflammatory markers and enhancing the innate immune response.^10,12 Similarly, the broader impact of dietary patterns on periodontal health has also been studied.³ Multiple cross-sectional studies revealed that individuals following a pro-inflammatory diet, characterized by high consumption of red meat, refined grains, and sugars, had significantly higher rates of periodontitis.^3,9,10,12

In contrast, diets rich in fruits, vegetables, whole grains, and omega-3 fatty acids were associated with periodontal health.^3,9,10 High consumption of vitamin D-rich foods is often associated with anti-inflammatory dietary patterns. An anti-inflammatory diet includes fatty fish and nutrient-rich products, suggesting a synergistic effect in diminishing periodontal inflammation. Evidence from clinical trials indicates that adherence to an anti-inflammatory dietary pattern can significantly reduce gingival inflammation and contribute to improved periodontal outcomes.^3,9,10,13 This connection highlights the importance of comprehensive dietary assessments in dental settings.

Obesity and Metabolic Risk Factors

Beyond micronutrients, broader metabolic conditions, such as obesity, further illustrate the connection between systemic inflammation and oral health. The release of pro-inflammatory cytokines contributes to a chronic, low-grade inflammatory state. Individuals with obesity often exhibit poor dietary habits (rich in highly processed, pro-inflammatory foods) that further exacerbate periodontal tissue breakdown.⁷

Recent epidemiological findings demonstrate that individuals adhering to pro-inflammatory dietary patterns not only have higher rates of periodontitis but also tend to present with elevated body mass index. This supports the hypothesis that obesity mediates the relationship between dietary inflammation and periodontal risk.^9,10,12,14 The combination of nutritional deficiencies, systemic inflammation, and immune dysregulation creates an oral environment that is detrimental for susceptible hosts. These findings emphasize the need for oral health professionals to consider patients’ metabolic status during the initial periodontal evaluation. An all-encompassing approach not only promotes periodontal health but also addresses broader public health concerns such as cardiovascular disease and diabetes.³

Diabetes and Periodontitis

The interplay between periodontal diseases and diabetes has long been recognized. Epidemiological studies and clinical trials reveal that patients with diabetes who have poor glycemic control are more likely to experience periodontitis than those with controlled diabetes or without the disease. Conversely, periodontitis negatively affects diabetes management.

Studies have also investigated the biological mechanisms that link both conditions.¹⁵ Periodontal pathogens can invade gingival epithelial cells, survive intracellularly, and alter immune responses, leading to immune evasion and systemic inflammation. Periodontitis compromises the oral epithelial barrier, allowing bacterial products and pro-inflammatory mediators into circulation.¹⁶ This systemic dissemination may exacerbate diabetes and cardiovascular disease. Recognizing this bidirectional relationship is essential for optimal patient care in clinical practice.¹⁷

Periodontitis and Hypertension

Research suggests a significant association between moderate to severe periodontitis and hypertension, independent of traditional risk factors including age, smoking, and obesity. This link is believed to arise from chronic periodontal inflammation, contributing to systemic endothelial dysfunction and arterial stiffness (key mechanisms that drive elevated blood pressure).²

These findings underscore the need for integrated care models that bridge the clinical gap between dentistry and general medicine.² Oral health professionals should incorporate routine screening for hypertension risk factors. Additionally, they should collaborate with primary care providers to ensure comprehensive management of patients presenting with periodontal diseases. Providers should understand that the bidirectional relationship between periodontal health and hypertension can serve as a motivator for adherence to both oral hygiene and systemic health recommendations.^2,18

Proper management of periodontal inflammation lowers hypertension progression and its cardiovascular sequelae. This highlights the value of periodontal therapy as part of a comprehensive approach to reducing systemic inflammatory burden.² In practice, personalized treatment plans that address modifiable lifestyle factors, including smoking cessation, nutritional counseling, and weight management may help improve outcomes. By recognizing periodontal diseases as inflammatory markers, oral health professionals can take on a more proactive role in identifying individuals at risk. In turn, facilitating early interventions improves quality of life and reduces healthcare burdens for the patient.

Population-Based Care

Older adults face unique challenges related to oral health and nutrition, often due to natural aging processes that affect their ability to consume and/or maintain adequate nutrition.^8,19 Factors, such as tooth loss, dry mouth, and decreased chewing efficiency, can impair food intake and lead to malnourishment. This nutritional deficiency may contribute to weakened immune function and a decline in general health. Early interventions would be beneficial for older adults in addressing this nutritional deficiency, particularly by providing dietary recommendations tailored to include softer, nutrient-dense foods in addition to thorough oral health evaluations.^8,19 Managing these complex needs requires coordinated care among oral health professionals, geriatricians, dietitians, and caregivers.⁸

Effective strategies to reduce oral health disparities at the community level include nutrition education, access to whole foods, and culturally appropriate strategies to engage local populations effectively. These promote sustainable changes that help prevent oral diseases and improve overall nutrition by addressing broader social and environmental factors that influence diet and oral health. However, these efforts should be combined with proper clinical care that addresses the disease, not just its symptoms.

Dietary Inflammatory Screening Tool

The early identification of pro-inflammatory dietary habits enables patient-centered care and facilitates timely referral to nutrition specialists.^3,7,8 To facilitate this approach, a simplified dietary inflammatory index (DII) screening tool can be employed in clinical settings. This tool evaluates patients’ frequency of intake of common pro- and anti-inflammatory foods.^15,16 It allows clinicians to quickly identify individuals whose dietary patterns may contribute to heightened systemic and oral inflammation.^15,16 The simplified DII screening consists of:^20,21

1. Pro-inflammatory foods include red and processed meats, refined grains, sugary beverages, fried foods, sweets, high-fat dairy, and trans fats.
2. Anti-inflammatory foods include leafy greens, fruits (especially berries and citrus), fatty fish rich in omega-3 fatty acids, nuts, olive oil, whole grains, and legumes.

Patients report their weekly consumption frequency of these food groups, and the responses are scored to estimate the overall inflammatory load. Higher scores indicate a predominantly pro-inflammatory diet, whereas lower scores suggest an anti-inflammatory dietary pattern.

Patients with elevated DII scores can be counseled on the benefits of adopting anti-inflammatory dietary habits to reduce periodontal inflammation and support systemic health.^20,21 Oral health professionals can refer these patients for detailed nutritional assessment and personalized intervention. Integration of this screening into periodontal evaluations promotes a holistic, interdisciplinary approach that addresses modifiable lifestyle factors alongside conventional periodontal therapy.

A 2024 clinical trial validated the application of the DII in periodontal settings. The study demonstrated that individuals with high DII scores exhibited elevated clinical and molecular markers of gingival inflammation. Personalized nutritional counseling based on DII profiles led to measurable improvements in periodontal health, including reductions in inflammatory cytokines and changes in subgingival microbial composition.^9,15,20

Conclusion

Evidence suggests that periodontal diseases extend beyond local oral pathology to influence systemic health. The two-way relationship between periodontal and systemic health underscores the importance of viewing oral health as an integral part of overall patient care.¹³

Dietary patterns lacking essential micronutrients promote inflammation both locally in the periodontium and systemically.^3,9 Poor nutrition exacerbates inflammation, accelerating periodontal destruction and metabolic dysregulation.³ Obesity is linked with both periodontitis and systemic diseases, reinforcing shared pathophysiological mechanisms rooted in chronic inflammation.² Although current literature identifies a strong association between nutrition and periodontal health, a significant gap remains. Periodontal medicine lacks well-designed randomized controlled trials evaluating the causality of anti-inflammatory vitamins or supplementation on healing. It remains unclear whether deficiencies in anti-inflammatory nutrients are causal or simply share risk factors with periodontal diseases. Accurate measurement of this relationship would help design effective interventions. Future research should explore the effects of these specific micronutrients on clinical periodontal outcomes.

There is a clear need for integrated healthcare approaches that dissolve traditional boundaries between medical and dental care. Early detection of systemic risk factors through routine screenings and comprehensive patient assessments is only achieved through interprofessional collaboration. Nutritional counseling embedded within dental visits offers a feasible strategy to address modifiable risk factors holistically.

Clinically, identifying periodontal diseases as indicators of systemic health status can lower patient risk and guide personalized treatment plans. For individuals with chronic conditions, effective periodontal therapy may not only preserve oral health but also contribute to better systemic disease management by reducing inflammatory markers and improving clinical outcomes.²

Empowering patients through in-office education about the significant connections between oral hygiene, diet, lifestyle, and overall health is a crucial component in adherence to this positive lifestyle. As the link between nutrition and inflammation becomes evident, integrating dietary considerations into periodontal care is necessary. A deeper understanding of this connection offers a critical opportunity to shift from reactive treatment to proactive care that addresses the root causes of disease. Informed behavioral changes foster the patient’s adherence to treatment and mitigate disease progression across all domains.

References

1. Grant WB, van Amerongen BM, Boucher BJ. Periodontal disease and other adverse health outcomes share risk factors, including dietary factors and vitamin D status. Nutrients. 2023;15:2787.
2. Li Y, Yuan X, Zheng Q, et al. The association of periodontal disease and oral health with hypertension, NHANES 2009–2018. BMC Public Health. 2023;23:16012.
3. Altun E, Walther C, Borof K, et al. Association between dietary pattern and periodontitis—A cross-sectional study. Nutrients. 2021;13:4167.
4. Mokdad AH, Ford ES, Bowman BA, et al. The continuing increase of diabetes in the U.S. Diabetes Care. 2001;24:412.
5. United States Centers for Disease Control and Prevention. National Diabetes Fact Sheet. Available at cdc.gov/diabetes/pubs/estimates.htm. Accessed February 18, 2026.
6. Mealey BL, Oates TW. Diabetes mellitus and periodontal diseases. J Periodontol. 2006;77:1289-1303.
7. Liu L, Xia LY, Gao YJ, et al. Association between obesity and periodontitis in US adults: NHANES 2011–2014. Obes Facts. 2023;17:47-58.
8. Chan AKY, Tsang YC, Lo ECM, et al. Diet, nutrition, and oral health in older adults: a review of the literature. Dent J (Basel). 2023;11:222.
9. Yue Y, Hovey KM, LaMonte MJ, Wactawski-Wende J, Andrews CA, Millen AE. Association between dietary patterns and periodontal disease: the OsteoPerio Cohort Study. J Periodontol. 2023;94:622-634.
10. Reis C, Serrano HM, Marques FM, et al. Impact of dietary inflammatory index on gingival health: a randomized clinical trial with clinical, microbial, and cytokine assessments. J Periodontol. 2024;95:95-104.
11. Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza’s Clinical Periodontology. 14th ed. New York: Elsevier; 2021.
12. Dietrich T, Nunn M, Dawson-Hughes B, Bischoff-Ferrari HA. Association between serum concentrations of 25-hydroxyvitamin D and gingival inflammation. J Periodontol. 2005;76:1914-1920.
13. Woelber JP, Tennert C, Bremer K, et al. Influence of an anti-inflammatory diet on gingivitis. J Clin Periodontol. 2019;46:270-280
14. Alhassani AA, Hu FB, Li Y, et al. The associations between major dietary patterns and risk of periodontitis. J Clin Periodontol. 2021;48:2–14.
15. Polak D, Shapira L. An update on the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J Clin Periodontol. 2018;45:150-166.
16. Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J Clin Periodontol. 2013;40 Suppl 14:S113-134.
17. Kudiyirickal MG, Pappachan JM. Periodontitis: An often-neglected complication of diabetes. World J Diabetes. 2024;15:318-325.
18. American Dental Association. Nutrition and Oral Health. Available at ada.org/resources/ada-library/oral-health-topics/nutrition-and-oral-health. Accessed February 18, 2026.
19. Wang ML, Minyé HM, Egan KA, Heaton B. Community-based sugar-sweetened beverage intervention associated with short-term improvements in self-rated oral health. Community Dent Oral Epidemiol. 2021;49:533-540.
20. Pan W, Feng J. The impact of low dietary inflammatory index diet on clinical parameters in patients with chronic kidney disease: a retrospective comparative study. J Inflamm Res. 2023;16:4943-4954.
21. Marx W, Veronese N, Kelly JT, et al. The dietary inflammatory index and human health: an umbrella review of meta-analyses of observational studies. Adv Nutr. 2021;12:1334–1348.

From Decisions in Dentistry. February/March 2026;12(1):32-35.

Despite substantial evidence to support early, conservative management, temporomandibular joint disorders (TMDs or TMJDs) remain one of the most common reasons for referral to dental/medical specialists in the United States.¹ TMDs comprise a subset of orofacial pain conditions affecting the masticatory muscles and/or temporomandibular joints.

Dental school education often focuses on screening and referral as management for TMDs. This approach relies on geographic and financial access to a provider offering TMD treatment. As their community’s primary dental provider, general dentists are frequently left with few practical options to help patients with TMD. This is exacerbated by the potential for TMDs to worsen if not properly managed during the initial presentation.

Much of the confusion over the diagnosis and management of TMDs comes from the prevalence of comorbidities and difficulty in distinguishing TMJ dysfunction and associated musculature from other complex orofacial pain conditions. Common screening questions focus on pain in/around the TMJ area, type and location of headaches, abnormal or limited jaw function as noted with difficulty eating, limited opening, getting stuck open or closed, popping/clicking/grating sounds, history of injury to face/head or neck, and time of symptom onset.² Patients are also asked about changes in their bite or face shape. Oral health professionals should include comprehensive screening questionnaires for TMDs and known comorbidities as part of their regular dental intake exams before initiating treatment (Table 1).

Any affirmative response on the patient questionnaire warrants further discussion, followed by clinical examination. The initial assessment should include panoramic radiographic examination; evaluation of TMJ function through measurement of maximum comfortable opening; palpation of TMJs during opening; listening to TMJs using a stethoscope (especially for grating sounds characteristic of bony degradation); and evaluation of face shape, interarch relationships, and symmetry both at rest and during mandibular function.

Acute Patient

Muscle-related disorders, including myalgias and myofascial pain, are commonly seen in general practice settings.^5,6 Patients often present with recently developed symptoms, as longer-standing TMD tends to progress to joint-related problems due to structural changes. The primary symptoms of muscle-related disorders are pain in masseteric and temporalis muscles and perceived limitation of function.

Referred pain in other muscles of the masticatory system and the area of the TMJs may also be noted. The location of pain can be confirmed by palpation, especially for the masseter and temporalis.⁶ Patients commonly report the onset of these symptoms following some triggering event, such as a long dental appointment or psychological stress associated with parafunctional habits.

Daytime and/or nighttime clenching and bruxism are also correlated. Limited opening may be noted by the patient or measured clinically to be less than 40 mm from incisal edge to incisal edge. Variation in the degree of pain experienced throughout the day frequently depends on activities and level of psychological stress. Patients often express a sensation of fullness in the ears and occasionally report tinnitus. Deviation upon opening can occur with asymmetric muscle spasm, necessitating re-evaluation of the medical history for a systemic etiology. Patients who clench and brux may report a change in the shape of their face due to hypertrophy of masticatory muscles. Clinicians may observe signs of wear and damage to the dentition.

Importance of Diagnostic Loading

The value of mechanically loading the TMJs is immeasurable. We believe that true TMDs involving the masticatory muscles and/or TMJs cannot be clearly differentiated from other orofacial pain conditions without this diagnostic tool. Various methods have been described using some means to position the mandibular condyles in centric relation (bimanual manipulation, chin point guidance, anterior jig, etc) and modestly load the TMJs with force to reproduce the patient’s symptoms.^7-9

If performed effectively and with care, both muscle- and TMJ-related pain can be easily identified, providing the clinician with a specific direction for treatment. James Metz, DDS, of Columbus, Ohio, and the late Bill McHorris, DDS of Memphis, Tennessee, developed a protocol using a leaf gauge to load the TMJs.^10-12 This method has proven reliable in identifying whether conservative occlusal splint therapy may be helpful.

To use the leaf gauge, the patient is instructed to bite on a select number of leaves (20 to 25 leaves is often a good starting point) with anterior teeth, then protrude the mandible, followed by retrusion (Figure 1). The leaf gauge must be positioned at the maxillary midline. The mandible is then held in centric relation position with a mild-to-moderate squeezing force on the leaf gauge. This causes bilateral contraction of lateral pterygoid and temporalis muscles (Figure 2). The lateral pterygoids are involved with normal and abnormal movement of the condylar-disc complex. The patient must not squeeze with full force but should be squeezing tightly enough so that the leaf gauge does not slide out if gently tugged on. The patient then holds this position for 7 to 10 minutes, unless acute pain develops. During this time, the clinician must periodically check that posterior teeth do not begin to contact as the condyle seats further into the fossa. If tooth contact does develop, additional leaves are added, and the process is repeated. If a patient develops pain, the clinician should palpate muscles and joints to locate the pain and establish severity. If/when the patient develops acute pain, the leaf gauge may be removed, and the patient is asked to report when the pain dissipates.

Patients with a TMJ problem will develop acute pain almost instantly when loaded on the leaf gauge. For these individuals, the TMJ loading test will reveal pain that tends to linger after removing the leaf gauge. This pain may be quite severe, so patients should be warned at the outset of the need to diagnostically reproduce their symptoms.

Patients with muscle problems typically feel pain come on slowly over several minutes. For these patients, the pain will usually dissipate over a few minutes upon removal of the leaf gauge. It is not uncommon for these patients to also have reported some mild TMJ clicking/popping caused by extended partial contraction of the superior head of the lateral pterygoid muscle and slight dislocation of the disc, resulting in the condyle clicking past the edge of the discal tissue.¹¹ If managed early, these patients may return to normal function and experience resolution of the clicking/popping. However, if left untreated, long-term damage to connective tissues results in more severe issues.

Related Symptoms

Patients presenting with TMD symptoms following physical trauma (such as a car accident), with clinical evidence of a joint problem, or with systemic medical conditions known to involve the TMJ (eg, rheumatoid arthritis or osteoarthritis) may warrant referral to an orofacial pain specialist or oral surgeon (Table 2). Other medical specialties may also need to be engaged. Clinical evidence of a chronic joint problem can include grating sounds, or crepitus, upon evaluation of TMJ with a stethoscope and evidence of condyle degradation on panoramic radiograph (eg, “beaking” and radiographically visible disruption of corticated bone on condyle). Patients with long-term degeneration of some component of the TMJ do not always present with pain or clinically evident limitation of function. For symptomatic individuals, load testing will quickly produce severe and lingering pain.

Role of the Airway

The airway potentially plays a significant role in the development and progression of TMDs. Research indicates a frequent co-occurrence of sleep-disordered breathing (including sleep apnea and bruxism) and TMDs.^13,14 Therefore, screening for obstructive sleep apnea (OSA) risk factors, such as those identified with the STOP-BANG questionnaire, should be included in every TMD evaluation.

Patients with positive risk factors should be referred to a sleep physician for further evaluation. Importantly, upper airway resistance syndrome (UARS), a condition often undetected by traditional sleep studies, might manifest as TMD symptoms.¹⁵ Oral health professionals should consider the impact of OSA and UARS on TMD treatment, including splint design and treatment duration. For example, increasing the vertical dimension of occlusion or excessive bulk of an occlusal splint could negatively affect airway patency due to alterations in tongue and mandible position.¹⁶

Conversely, appropriately designed and titrated oral appliances can effectively manage both TMD and sleep-disordered breathing, improving overall health and quality of life.¹⁷ Ongoing research will likely yield further insights and recommendations regarding the interplay between TMD and airway health.

Clinical Management

For most patients with muscle-related TMD, a combination of palliative self-care, anti-inflammatory medications, and conservative occlusal splint therapy will be sufficient (Table 3).³ Palliative measures include rest, soft diet, and hot or cold compresses. Exercises involve opening and moving the lower jaw laterally while applying light resistance by hand. Caution is recommended with at-home exercises, as some patients will attempt to strain or open the jaw forcefully or beyond normal physiological limits, which can damage the TMJ over time. Opening excessively when yawning is discouraged; instructing patients to use their fist to limit the opening until they can train themselves not to open so wide is an option.

Some providers may prescribe a short-term regimen of a low-dose skeletal muscle relaxer, such as cyclobenzaprine, though most of the time it is not necessary. Oral steroid use can be beneficial for some patients. However, providers should ensure familiarity with potential side effects and drug interactions and be prepared to manage any complications. For patients without medical contraindications, a regimen of nonsteroidal anti-inflammatory drugs is most helpful for managing both pain and inflammation.

A flat plane stabilization splint is the most frequently prescribed occlusal device for muscle-related TMD. This type of splint has a long track record for effectively managing symptoms when used correctly.^18,19 Adjusting and managing stabilization splints may be somewhat tedious, as repeated visits are necessary.

Alternatives for muscle-related TMDs include full or partial coverage anterior bite planes/plates.^20,21 These splints do not engage posterior tooth contacts, which may help minimize activation of masticatory muscles. Additionally, partial coverage anterior bite plates achieve deprogramming before restorative treatment (Figure 3).²² Some providers have raised concerns about unmonitored long-term use of occlusal splints, including stabilization splints and anterior bite plates.^23-25 Any occlusal appliance used to manage TMD will require follow-up after no more than 2 weeks and careful evaluation of risks/benefits before continuing long-term use. Occasionally, muscle-related TMD issues are associated with collapse or loss of posterior occlusal support, which may require complex oral rehabilitation. Additionally, younger patients with mixed dentition may present with muscle-related TMDs that are often self-limiting and successfully managed with palliative home measures. Occlusal splint therapy is usually not advised in growing and developing patients.

A variety of alternative treatment options have been promoted for muscle-related TMD, such as Botox or steroid injections, trigger point injections, dry needling, and laser therapy. Each has mixed results and its own set of risks and benefits.³ The provider should be appropriately trained and capable of managing undesirable outcomes for any adjunctive therapy prescribed.

If palliative measures, appropriate pharmaceutical use, and occlusal splint therapy do not result in some improvement after 2 weeks, or symptoms begin to worsen, use of the occlusal splint should cease and a specialist should be consulted.

Conclusion

While TMDs are a complex group of orofacial pain conditions, the primary dental provider must identify them early. Proper identification and prompt management of TMDs have significant repercussions on progression of the condition, any restorative dental treatment, and potential comorbid conditions. Through proper screening, including using the leaf gauge to mechanically load the TMJs, the general dentist should feel empowered to conservatively manage common muscle-related TMDs and confidently refer to a specialist when indicated.

References

1. Klasser GD, Abt E, Weyant RJ, Greene CS. Temporomandibular disorders: Current status of research, education, policies, and its impact on clinicians in the United States of America. Quintessence Int. 2023;54:328-334.
2. Schiffman E, Ohrbach R, Truelove E, et al. Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) for Clinical and Research Applications: recommendations of the International RDC/TMD Consortium Network and Orofacial Pain Special Interest Group. J Oral Facial Pain Headache. 2014;28:6-27.
3. Hoffmann RG, Kotchen JM, Kotchen TA, Cowley TA, Dasgupta M, Cowley AW Jr. Temporomandibular disorders and associated clinical comorbidities. Clin J Pain. 2011;27:268-274.
4. Thomas DC, Khan J, Manfredini D, Ailani J. Temporomandibular joint disorder comorbidities. Dent Clin North Am. 2023;67:379-392.
5. Ferrillo M, Ammendolia A, Paduano S, et al. Efficacy of rehabilitation on reducing pain in muscle-related temporomandibular disorders: A systematic review and meta-analysis of randomized controlled trials. J Back Musculoskelet Rehabil. 2022;35:921-936.
6. Dawson PE. Functional Occlusion from TMJ to Smile Design. St. Louis:Mosby Elsevier; 2007:86-89.
7. Lövgren A, Visscher CM, Alstergren P, Lobbezoo F, Häggman-Henrikson B, Wänman A. The outcome of a temporomandibular joint compression test for the diagnosis of arthralgia is confounded by concurrent myalgia. Clin Oral Invest. 2020;24(1):97-102.
8. de Wijer A, Lobbezoo-Scholte AM, Steenks MH, Bosman F. Reliability of clinical findings in temporomandibular disorders. J Orofac Pain. 1995;9:181-191.
9. Huffman Dental Products. How to Guide for Huffman Leaf Gauge. Available at: prestige-dental.co.uk/app/uploads/2023/04/Huffman-Leaf-Gauge-How-to-Guide.pdf. Accessed February 20, 2026.
10. McHorris WH. Non-surgical management of noisy joints. J Tenn Dent Assoc. 1986;66:31-35.
11. McHorris WH. Treatment of TMJ dysfunction. J Tenn Dent Assoc. 1980;60:21-23.
12. Kato T, Thie NMR, Huynh N, Miyawaki s, Lavigne GJ. Topical review: Sleep bruxism and the role of peripheral sensory influences. J Orofacial Pain. 2003;17:191-213.
13. Carra MC, Huynh N, Lavigne G. Sleep bruxism: A comprehensive overview for the dental clinician interested in sleep medicine. Dent Clin N Am. 2012;56:387-413.
14. Dubrovsky B, Raphael KG, Lavigne GJ, et al. Polysomnographic investigation of sleep and respiratory parameters in women with temporomandibular pain disorders. J Clin Sleep Med. 2014;10:195-201.
15. Gagnon Y, Mayer P, Morisson F, Rompré PH, Lavigne GJ. Aggravation of respiratory disturbances by the use of an occlusal splint in apneic patients: A pilot study. Int J Prosthodont. 2004;17:447-453.
16. Metz JE, Attarian HP, Harrison MC, et al. High-resolution pulse oximetry and titration of a mandibular advancement device for obstructive sleep apnea. Front Neurol. 2019;10:757.
17. Kuzmanovic Pficer J, Dodic S, Lazic V, Trajkovic G, Milic N, Milicic B. Occlusal stabilization splint for patients with temporomandibular disorders: Meta-analysis of short and long term effects. PLoS One. 2017;12:e0171296.
18. Capp N, Eder A. Occlusion and splint therapy. In: Tooth Wear. London: Springer International Publishing; 2022:135-152.
19. Fu AS, Mehta NR, Forgione AG, Al-Badawi EA, Zawawi KH. Maxillomandibular relationship in TMD patients before and after short-term flat plane bite plate therapy. Cranio. 2003;21:172-179.
20. Seiler A, Lukic N, Özcan M, et al. Temporomandibular joint space variation and masticatory muscle activation during clenching with full versus partial covering occlusal splints. Clin Oral Investig. 2024;28:584.
21. The Metz Center Lab Services. Available at: http://themetzcenter.com/lab_services.html. Accessed February 20, 2026.
22. Bereznicki T, Barry E, Wilson NHF. Unintended changes to the occlusion following the provision of night guards. Br Dent J. 2018;225:715-722.
23. Bereznicki T, Barry E, Wilson NHF. Unintended changes to the occlusion following the provision of night guards. Part two: management. Br Dent J. 2019;226:649-656.
24. Magdaleno F, Ginestal E. Side effects of stabilization occlusal splints: a report of three cases and literature review. Cranio. 2010;28:128-135.

From Decisions in Dentistry. February/March 2026;12(1):36-39.

Occlusal guards play a crucial role in treating myofascial pain, nocturnal bruxism, clenching, and occlusal-incisal attrition in both adults and children.^1,2 Capturing an accurate centric relation (CR) bite registration is critical for making and equilibrating an occlusal guard. A properly designed CR occlusal guard manages bite forces by loading the temporomandibular joints (TMJs) with all teeth contacting simultaneously.

A study of bite forces by Manns et al³ compared electromyographic (EMG) activity in patients exhibiting canine guidance with that in patients displaying group function. During working and nonworking excursions of the mandible, both the masseter and temporalis muscles work half as much in canine guidance as in group function. The decrease in muscle contractions among the elevator muscles resulted from the lack of posterior tooth contacts. A later EMG study by Manns et al⁴ concluded that elevator muscle contractions and joint health depend on posterior tooth contacts and canine guidance functioning to prevent posterior tooth contacts during excursive movements of the mandible.

These findings make a compelling case for designing canine guidance in occlusal guards for patients with myofascial pain. Canine guidance results in the temporalis and masseter muscles releasing their contractions (ie, becoming more relaxed) and the inability to exert the magnitude of harmful forces on teeth and restorations as when posterior interferences are present. The efficacy of therapy with an occlusal guard (ie, how effectively it relaxes the elevator muscles [masseter, temporalis, medial pterygoid, and superior belly of the lateral pterygoid]) depends on how accurately it is equilibrated and on the level of patient compliance.

Introduction of Leaf Gauges

In 1973, Long⁵ introduced leaf gauges to facilitate the separation of posterior teeth to locate CR. A popular brand of leaf gauges employs 50 flexible mylar strips, or leaves, that are riveted together so they can open like a fan (Figure 1). The leaves are approximately 0.1 mm thick, 13 mm wide, 60 mm long, and autoclavable.

A leaf gauge is an occlusal stop; it is placed in the anterior section of the mouth, between the maxillary central incisors, to eliminate posterior deflective occlusal interferences to CR. The patient is then directed to attempt to occlude on the posterior teeth. With the leaf gauge properly placed at the midline, between the central incisors,the posterior teeth are separated while maintaining the tripodization of the mandible (ie, the narrow anterior stop forms a tripod effect between the anterior teeth and the two condyles in their respective positions in the glenoid fossae). When this condition exists, the mandible is said to be “tripodized.” Maintaining this separation for 5 to 15 minutes will allow patients’ elevator and lateral pterygoid muscles to deprogram from their existing deflective occlusal contacts.⁶ Subsequently, these muscles adapt to their new environment by changing their contraction activity and changing the position of the mandible.

Technique for Using the Leaf Gauge

Following are the appropriate steps to using the leaf gauge to digitally record CR and equilibrate a maxillary occlusal guard.

1. After both dental arches have been digitally scanned, use a leaf gauge to create an interocclusal CR record at a vertical dimension (VD) that provides sufficient space between posterior teeth for the thickness of an occlusal guard. Enough leaf gauges should be used to allow 2 to 3 mm of clearance between the first molars. Incisal openings of 3 and 4 mm are approximately equivalent to first molar openings of 2 and 3 mm, respectively.)
2. Position the patient in the dental chair with the head tipped back approximately 30° to 45°. Place the leaf gauges in the mouth and ask the patient if any posterior teeth are contacting. Use shim stock to check this. To ensure that the condyles are not deflected away from the condylar braced position in the fossae, ask the patient to first protrude and then retrude the mandible, and then bite on the leaves with a “half-hard” bite (ie, a bite force that is the same as that exerted when he/she is swallowing). Again, use shim stock to check for unwanted posterior tooth contacts.

If tooth contacts are detected, then add additional leaves until the patient no longer feels any posterior contacts. As the elevator muscles deprogram (relax), the mandible changes position, and new posterior tooth contacts could become evident when checking with shim stock. This occurs as the relaxed muscles seat the condyles in their CR positions in the fossae, bringing the teeth closer together.

Simultaneously, new posterior contacts could become evident when checking with shim stock. After 30 seconds, if the patient feels a posterior tooth contact because of the relaxation of the elevator muscles, add leaves, one at a time, until the patient can bite for 2 to 5 minutes without sensing any posterior contact. During that time, instruct the patient to hold the leaf gauge in the retruded position with a half-hard bite.

Repeated checks with shim shock are required to make sure no posterior tooth contact occurs. The patient must not exert excessive biting force on the leaf gauge, as this can cause the condyles to move inferiorly and posteriorly. This could also occur if the mandible is not maintained in its midmost position as the patient occludes on the leaf gauge. The time needed to accomplish this procedure will vary depending on the degree of muscle tension and the psychological state and cooperativeness of the patient.

The position of the condyles while the posterior teeth no longer touch is considered a braced or seated CR position that is made possible when the muscles are no longer influenced by their deflective malocclusion. Protrusion of the mandible, along with the simultaneous distraction of the condyles from the fossae, may be avoided with this technique because contraction of the lateral pterygoid muscles is diminished as the patient bites firmly on the leaf gauge.^7,8

3. The leaf gauge should be left in the mouth for at least 5 minutes to allow the muscles to deprogram. As new posterior contacts could become evident when checking with shim stock, the required vertical distance between the first molars decreases. At that point, add enough leaves to reestablish the 2- to 3-mm clearance requirement for an occlusal guard. Then check again with shim stock.

If mild tenderness or tension is noted in the TMJ area while the patient is biting on the leaf gauge — secondary to muscle strain — then ask the patient to protrude and retrude the jaw and then bite. When no tenderness or tension is recognized, the condyles are likely in the correct CR position for therapy with an occlusal guard, and an interocclusal bite registration could be recorded.

4. Scan both dental arches. Then, with the leaf gauge in place and providing an interocclusal distance of approximately 3 mm between the first molars, scan the right and left buccal sides (ie, the buccal bite) of the posterior teeth (Figure 2).

At this point, the scans are ready to go to the dental laboratory for the fabrication of an occlusal guard. The prescription should instruct the laboratory to incorporate the following design features in the guard:

• All functional cusp tips should contact the guard evenly and simultaneously in CR.
• The acrylic prominences built into the guard in the canine areas should be angulated approximately 30° to 45° to the occlusal plane to allow the mandibular canines to disclude posterior teeth during laterotrusive movements.
• The canines and as many incisors as possible should contact during protrusive movement for incisal guidance.
• Only the mandibular canines should contact during canine-guided movements.
• The occlusal guard should not move during CR closure or any eccentric jaw movement.⁹

5. When the guard is delivered and fits properly without rocking, the leaf gauge is inserted between the maxillary incisors. Add enough leaves to eliminate any posterior contact between the guard and the mandibular teeth. Follow the instructions described in step 2 to allow the muscles to deprogram. If the posterior teeth contact the guard, then increase the number of leaves to separate the teeth. Verify this with shim stock. To relax the muscles, permit the patient to bite on the gauge for 5 minutes.
6. To bring the guard into equilibrium, gradually decrease the number of leaves until the first point of contact on the guard can be detected with shim stock. Mark the contact with the blue side of thin articulating ribbon. Remove the guard and lightly adjust the contact with a football-shaped stainless steel laboratory bur until additional blue CR contacts appear on the guard. Do not create deep concavities in the guard when adjusting the contacts. To ensure continued muscle deprogramming while adjusting the guard outside the patient’s mouth, place the leaf gauge in the mouth to prevent the teeth from contacting.
7. Reinsert the appliance and assess additional contacts on the guard by subtracting one leaf at a time. Use the same procedure outlined in step 6. The muscles should be reprogrammed, also known as “intervening deprogramming,”throughout the process of adjusting the guard by providing additional 1-minute periods of deprogramming after every subtraction of two to three leaves. This enables the patient to be maintained more accurately in the CR position.⁶
8. At an opening of approximately two leaves, continue subtracting leaves and assess with shim stock until all opposing mandibular functional (buccal) cusp tips contact simultaneously and evenly on the guard in CR. Adjust the anterior ramp of the guard to ensure there is immediate comfortable anterior disocclusion of the posterior teeth during protrusive, working, and nonworking excursions of the mandible.¹⁰

The only laterotrusive contacts that should be present are those of canines contacting evenly during canine-guided movements (Figure 3). No additional adjustments of the guard are needed when one or two leaves will separate the mandibular posterior teeth from the guard when the mandible is in CR.

9. Areas on the guard where contacts were adjusted should not be polished as this could result in the loss of CR contacts. The minor roughness produced by the fluted laboratory carbide bur will not harm opposing enamel; we have never encountered a patient who became uncomfortable because of the slight roughness generated by adjustments with a bur.
10. Follow-up care is recommended in 1 to 3 weeks when the patient fails to demonstrate any of the occlusal contacts on the guard mentioned in step 8. If a minor adjustment is needed, it may be completed using the method outlined above.

Discussion

Soft occlusal guards have been prescribed for various reasons; however, they are not recommended for patients with myofascial pain because they tend to increase masseter muscle activity during maximum clenching.¹¹ A properly equilibrated hard occlusal guard decreases EMG activity in both masseter and temporalis muscles.¹²

The interocclusal bite registration record is the most important record obtained in restorative dentistry, and neuromuscular relaxation is a vital part of a physiologically sound interocclusal bite registration recording protocol. The CR system described here is free from all posterior tooth contacts or interferences. A leaf gauge between the anterior teeth helps the patient retrude the mandible while recommended biting forces of closure relax the elevator and lateral pterygoid muscles to permit the condyle-disk assembly to remain against the posterior slope of the articular eminence, and to maintain the desired minimal vertical opening.

Thin, flexible leaf gauges result in minimal incisal opening, and they readily conform to the concave palatal surfaces of maxillary incisors. When the mandibular incisors exert force against the steep guidance created by the gauge above the occlusal plane, the mandible rotates the condyles into the anterior-superior part of the articular fossae.

Use of a leaf gauge allows the patient to position the mandible without help from the dentist; it helps to overcome operator error that occurs when the dentist must manipulate the patient’s mandible to guide it to CR, which is the greatest difficulty encountered when attempting to equilibrate a patient’s occlusion. When coupled with bilateral mandibular manipulation, as advocated by Dawson,¹³ leaf gauges are especially helpful in obtaining a CR bite registration and transferring it when mounting a patient’s cast or scan on an actual or virtual articulator, respectively.

At our university, under the supervision of prosthodontic faculty members, preclinical (D2) students practice bilateral mandibular manipulation on each other and learn how to use leaf gauges to obtain accurate CR interocclusal bite registrations to mount casts in their articulators.

If conventional bite registration materials (eg, polyvinyl siloxane, polyether, acrylic resin, or wax) are used to capture a CR bite registration to mount casts, polyvinyl siloxane is the most accurate, as it produces the least vertical error (24 µm), followed by polyether (30 µm), acrylic resin (57 µm), and wax (74 µm).¹⁴ No occlusal adjustment procedures should be attempted before the dentist has properly mounted casts on an articulator.

Leaf gauges could be used in occlusal therapy to periodically relieve painful spasms of the lateral pterygoid muscles, thereby eliminating the need for occlusal guards or the use of drugs to reduce muscle contractions.⁷ All occlusal discrepancies must be eliminated before any extensive restorative dental treatment. Any muscle strain caused by the leaf gauge may not result in a repeatable CR braced position of the condyles because of damage existing in the muscles, ligaments, or osseous structures.¹⁵

The leaf gauge system is pleasant for the patient, accurate, inexpensive, and adaptable to most occlusal schemes. Leaf gauges, however, may be contraindicated for patients with Class II, Division II malocclusion, as the condyles might be displaced downward and posteriorly when an inclined plane, such as a leaf gauge, is inserted between the maxillary incisors.¹³   A leaf gauge might also be ineffective in severe Class III malocclusions, where it might be necessary to use a very thick gauge.⁸  When a large discrepancy in the CR-to-maximum intercuspal position (ie, a large CR-maximum intercuspal position  shift of more than 2.5 mm of incisal separation) is discovered by using the leaf gauge, it might not be possible to eliminate the discrepancy without orthodontic or surgical intervention.

References

1. Solberg WK, Clark GT, Rugh JD. Nocturnal electromyographic evaluation of bruxism patients undergoing short term splint therapy. J Oral Rehabil. 1975;2:215-223.
2. Hachmann A, Martins EA, Araujo FB, et al. Efficacy of the nocturnal bite plate in the control of bruxism for 3 to 5 year old children. J Clin Pediatr Dent. 1999;24:9-15.
3. Manns A, Chan C, Miralles R. Influence of group function and canine guidance on electromyographic activity of elevator muscles. J Prosthet Dent. 1987;57:494-501.
4. Manns A, Miralles R, Valdivia J, et al. Influence of variation in anteroposterior occlusal contacts on electromyographic activity. J Prosthet Dent. 1989;61:617-623.
5. Long JH Jr. Locating centric relation with a leaf gauge. J Prosthet Dent. 1973;29:608-610.
6. Fleigel, III JD, Sutton AJ. Reliable and repeatable centric relation adjustment of the maxillary occlusal device. J Prosthodont. 2013;22:233-236.
7. Carroll WJ, Woelfel JB, Huffman RW. Simple application of anterior jig or leaf gauge in routine clinical practice. J Prosthet Dent. 1988;59:611-617.
8. Woelfel JB. New device for accurately recording centric relation. J Prosthet Dent. 1986;56:716-727.
9. Antonelli J, Hottel TL, Siegel SC, et al. The occlusal guard: a simplified technique for fabrication and equilibration. Gen Dent. 2013;61:49-54.
10. Antonelli JR. Selectively equilibrating the hard occlusal guard. Today’s FDA. 2019;31:92-95.
11. Cruz-Reyes RA, Martínez-Aragón I, Guerrero-Arias RE, García-Zura DA, González-Sánchez LE. Influence of occlusal stabilization splints and soft occlusal splints on the electromyographic pattern, in basal state and at the end of six weeks treatment in patients with bruxism. Acta Odontol Latinoam. 2011;24:66-74
12. Al-Quran FAM, Lyons MF. The immediate effect of hard and soft splints on the EMG activity of the masseter and temporalis muscles. J Oral Rehabil. 1999;26:559-563.
13. Dawson PE. Functional occlusion from tmj to smile design. In: Recording Centric Relation. 3rd ed. St. Louis: Elsevier Inc; 2007:92-101.
14. Kattadiyil MT, Alzaid AA, Campbell SD. What materials and reproducible techniques may be used in recording centric relation? best evidence consensus statement. J Prosthodont. 2021;30:34-42.
15. Olsen LF, Shaw AF. Use of leaf gauge in occlusal diagnosis and therapy. Quintess Int. 1984;7:611-621.

From Decisions in Dentistry. February/March 2026;12(1):40-45.

• Gold, the Global Fear Gauge: Up 65% in 2025, YTD 2026: Up 16%
• Delinquency Rates on Consumer Debt: 4.8%, highest since 2017
• 90+ Day Delinquency on Credit Card Debt: 12.7%, highest since 2011
• Retail Sales in 2025: Flat with 2024, inflation adjusted
• Michigan Consumer Sentiment Index: Jan 2026, lowest level in 10 years
• American Dental Association Survey of Dentist Confidence: Declined 34.3% in 2025
• New Job Creation in 2025: 180,000 jobs, worst since 2003

Your practice is one of your largest investments and, as of today, the economy is not yet officially in a dip. Should you consider monetizing a part of your practice value today while you are still growing?

If collections in your practice decline in 2026, you become ineligible for a high-value IDSO partnership until you deliver at least two quarters of growth. IDSOs are the highest value monetization strategy for practices with at least $1.5+ million in collections. There will be no interest in your practice if it is shrinking. Conversely, if you are growing at double-digit rates, your value will increase.

In a traditional doctor-to-doctor transition, values are often about 70% of collections. In an IDSO partnership, values often exceed 200% of collections, and for some Large Practice Sales clients, over 300% of collections. Practice values in an IDSO partnership are based on profitability and growth rate.

In a traditional transition, the retiring doctor will stay for a short period of time. In an IDSO partnership, the highest values are achieved for doctors with a 5 year or longer horizon to continue leading their practice. Timing your IDSO partnership is critical for value. If dentists choose their IDSO partner wisely, they will have FULL autonomy and continue to make both the clinical and business decisions in their practice.

But choosing an IDSO partner wisely is becoming more difficult. There are more than 1,000 IDSOs in the US, some over 35 years old and a few with 800+ practice partners each. However, LPS considers only about 100 of them qualified to bid on clients. More IDSOs are under stress than ever before. Fortunately, several of the IDSOs have recently completed recapitalizations in which doctors experienced 500+% increases in the value of retained ownership in 5 years or less.

All dentists should honestly assess their growth risk for 2026 and become educated on the record values in an IDSO partnership today. The IDSOs are growing rapidly. You will ultimately partner with one, or compete with many. Their size gives them leverage on both costs and reimbursement rates that you cannot compete with over time. The Boy Scout motto says it all, “Be prepared”!

Contact

Large practice sales
largepracticesales.com
844-976-5322

From Decisions in Dentistry. February/March 2026;12(1):27.

The speed of change in patient discovery is staggering. Google’s search interface alone has evolved more in the past 18 months than in the previous decade combined. According to HubSpot’s 2024 report, 61% of all online interactions begin with an AI-assisted recommendation. Patients are discovering providers through AI-driven summaries, map packs, and automated recommendation engines. Your next new patient may not see your website first.

While still important, a website is only one piece of a much larger visibility ecosystem. Patients evaluate your practice across multiple channels and each of these compares data about your practice. Even one inconsistent address or outdated service description can lower your visibility. Search engines and AI models use this collective data to determine which practices to surface first and which to overlook.

First impressions no longer happen at the front desk. They occur long before a prospective patient clicks your website. High-quality photos, accurate hours, consistent branding, and a steady flow of positive reviews all signal trustworthiness. Patients don’t want to guess whether a practice is credible — they want proof. AI systems are increasingly designed to recognize these credibility signals as well. A 2024 BrightLocal survey found that 76% of consumers have used Google reviews to select a healthcare provider, and 68% said inconsistent information made them distrust a business.

Many dental practices still rely on outdated marketing tactics, such as “set-it-and-forget-it’ search engine optimization, limited review generation, mismatched local listings, or minimal engagement on emerging channels. The result is predictable: competitors who embrace modern visibility strategies dominate local rankings.

Here are practical, high-impact steps dental teams can implement immediately:

1. Audit your digital footprint. Search your practice name on Google, Apple Maps, Bing, and popular AI search tools to confirm consistent information across all listings.
2. Post consistently. Even one Google Business Profile post per week reinforces relevance and activity.
3. Encourage reviews. Ask satisfied patients to share authentic experiences, including mentions of your city or specific services.
4. Build topical content. Create Q&A-style articles that answer common patient questions in natural language, including the types of queries people speak aloud or type into AI tools.
5. Optimize for local intent. Use city-specific landing pages and schema markup to help search engines and AI systems understand your geographic relevance.

The dental marketing landscape isn’t changing — it has already changed. Patients discover, compare, and make decisions faster than ever. Practices that adapt to AI-driven discovery, voice search, and multiplatform visibility will thrive. Those that don’t risk being overlooked, even if they provide exceptional care.

At DDS MediaPro, we help dental teams stay visible, credible, and competitive in today’s digital environment, from audits to activation. Reach out today: ddsmediapro.com; 866-239-1576.

From Decisions in Dentistry. February/March 2026;12(1):46.