Treating Chronic Inflammation

Chronic inflammation is not compatible with optimal health. Related to diabetes, cardiovascular disease and stroke, as well as some cancers, it has been characterized as the plague of postindustrial societies — and that certainly applies to ours. While the genesis of chronic inflammation is multifactorial, it includes a sedentary lifestyle, stress, obesity, and lack of cardiovascular fitness. Recent emphasis has been placed on the use of C-reactive protein (CRP) as a marker for inflammation. Production of CRP is related to stimulation of the interleukin group of inflammatory proteins, particularly IL-6. Measured with a simple blood test, CRP levels have been used as a marker for rheumatoid arthritis for years, and now the emphasis has shifted to other chronic diseases.

Based on CRP testing, the American Heart Association suggests that patients with values of 1 mg per liter or less are at low risk for cardiovascular events, while those with 3 mg per liter are at high risk. The U.S. Centers for Disease Control and Prevention recommends comparing tests taken two weeks apart.

Attempts have been made to reduce overproduction of CRP, chiefly through lifestyle changes. The clinical goals are improved diet, increased physical activity, reduced stress, and reduction in weight and blood pressure (where indicated). As with any behavioral change, these attempts have met with mixed results, depending on the cooperation of the individuals involved. In general, when participants meet these goals, improvements in CRP levels are seen.

INFORMATION AND COMMUNICATION ARE KEY WAYS TO ADDRESS THIS PROBLEM

Researchers have examined interleukin blockers as a means of reducing the expression of these inflammatory cytokines — and a number of drugs have shown the potential to block, reduce or interrupt their effect. Studies using these medications have demonstrated a reduction in CRP and other inflammatory markers. Unfortunately, the subjects who received these medications often had more opportunistic infections than individuals in the placebo groups.

Some attempts have been made to link chronic periodontal infections to CRP levels — but with mixed results. At present, it is safe to say that chronic periodontitis is related to cardiovascular disease, diabetes mellitus, obesity, metabolic syndrome and rheumatoid arthritis. Therefore, it is in patients’ best interests to reduce periodontal inflammation.

Information and communication are key ways to address this problem. Patients should be aware that chronic inflammatory diseases, including periodontal conditions, are relevant to their overall health. They should also know that CRP levels can easily be monitored through testing, and the various ways CRP levels can be controlled or reduced. In addition to patient education, oral health professionals should monitor periodontal and peri-implant spaces for inflammation. Bleeding on probing, increased probing depths and negative radiographic changes are indications of chronic inflammatory issues, and clinicians should work to address inflammation. For while the future may bring more reliable drugs to control CRP levels, until then, behavioral change remains our patients’ best hope.

Thomas G. Wilson Jr., DDS
Editor in Chief
twilson@belmontpublications.com


From Decisions in Dentistry. January 2018;4(1):6.

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