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Calculus’ Role in Periodontal Inflammation

Until the 1960s, calculus was considered a primary etiologic factor in periodontal disease. The writings of Waerhaug and others emphasized the complete removal of supragingival and subgingival deposits as an important tenant of treatment.

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Until the 1960s, calculus was considered a primary etiologic factor in periodontal disease. The writings of Waerhaug and others emphasized the complete removal of supragingival and subgingival deposits as an important tenant of treatment. However, this view changed following publications by Loe and others that demonstrated the relationship between biofilm and gingivitis. Page and Schroeder later elucidated the role of this bacterial mass in the etiology of periodontitis. Since then, numerous papers have confirmed biofilm’s relationship with periodontal inflammation. 

During this time, emphasis diminished on calculus as an etiologic factor — yet this viewpoint has changed once again, as many have come to view calculus as a key inflammatory moderator. It is also seen as playing a role in ongoing periodontal disease, and as a reason behind the inadequate response to therapy seen in some patients. These accretions covered with biofilm have been shown to be associated with inflammation of the pocket wall to a much greater degree than that seen with biofilm alone. This argues for calculus removal. Unfortunately, this is no easy task.

MANY HAVE COME TO VIEW CALCULUS AS A KEY INFLAMMATORY MODERATOR

Although periodontitis is responsible for the majority of tooth loss in adults, if properly treated it can be halted or reversed. To ensure positive outcomes, patients must understand their role in treating periodontal disease. This requires adequate oral hygiene and adherence to suggested maintenance intervals. The dental team is responsible for patient education and effective treatment. The first step in most cases (stages I to IV) is closed subgingival scaling and root planing.Unfortunately, this is one of the most difficult procedures in dentistry and routinely fails to remove all subgingival calculus and biofilm. This is especially true for the deeper pockets seen in stage III and IV cases. 

The failure to completely remove calculus is a major reason for reinfection and subsequent tooth loss. Clinical signs of inflammation in a patient with good personal hygiene at reevaluation are an indication that root-borne deposits are still present. Stage III and IV cases require advanced treatment; for these patients, the therapist must understand that simply repeating closed scaling and root planing will not suffice. Such advanced care can be delivered by primary care providers with specialty-level skills or by periodontists. 

Patients with stage III or IV periodontitis are best treated with procedures that allow optimal visualization and removal of root-borne accretions. It has been demonstrated that adequate removal of subgingival calculus improves with the ability to see the deposits. In most cases, this requires a flap procedure — often with devices to improve visualization, including the dental endoscope and videoscope.

Compared to closed procedures alone, the use of these advanced techniques and tools has been shown to produce more successful outcomes in stage III and IV periodontitis cases. Although most stage I and II cases respond well to closed scaling and root planing, the majority of stage III and IV cases do not. This is not a condemnation of the clinical skills of the operator who used closed scaling and root planing, but merely an observation of the difficulty of achieving the desired therapeutic outcomes in advanced cases.

Thomas G. Wilson Jr., DDS
Editor in Chief
[email protected]

From Decisions in Dentistry. September 2021;7(9)4.

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