Interaction between periodontal disease and systemic secondary amyloidosis: from inflammation to amyloidosis.

BACKGROUND

It has become increasingly clear in recent years that periodontal disease can cause a dramatic increase in the levels of markers of systemic inflammation, and that periodontal treatment can result in reduction in the levels of these markers. We have previously shown that the prevalence of moderate to severe periodontitis was significantly higher in patients with familial Mediterranean fever (FMF) with amyloidosis than in patients with FMF without amyloidosis. Thus, the aim of this study is to investigate if chronic periodontitis is associated with secondary amyloidosis in the Black Sea region of Turkey.

METHODS

A total of 112 patients with biopsy-proven secondary amyloidosis (59 patients with FMF, 40 patients who were either chronically infected or had malignant disease, 13 patients with periodontitis) and 22 healthy subjects, were included in this study. Periodontal health and disease were evaluated using gingival index (GI), papillary bleeding index (PBI), plaque index (PI), and periodontal disease index (PDI). The concentrations of serum acute phase reactants (APRs) were measured at baseline and at 4 to 6 weeks after completion of the non-surgical periodontal therapy.

RESULTS

The prevalence of moderate to severe periodontitis was 47.5% in patients with FMF, 72.5% in patients who were either chronically infected or had malignant disease, and 84.6% in patients with periodontitis. Serum levels of APRs in patients with amyloidosis were reduced significantly after non-surgical periodontal therapy (P <0.01).

CONCLUSIONS

Periodontitis can increase the levels of APRs and potentiate the development of amyloidosis either by themselves or association with traditional factors, such as FMF and other chronic inflammatory diseases. Thus, preventing or treating periodontitis might prevent or at least alleviate the progression of amyloidosis. Periodontal evaluation should be performed as part of a medical assessment and considered as an etiologic factor for secondary amyloidosis.