Literature DB >> 21235331

Salivary interleukin-1β levels in patients with chronic periodontitis before and after periodontal phase I therapy and healthy controls: a case-control study.

Rachna Kaushik1, Ramreddy K Yeltiwar, Kumar Pushpanshu.   

Abstract

BACKGROUND: The role of interleukin (IL)-1β in periodontal disease pathogenesis is well researched. This study aimed to assess and compare the salivary IL-1β levels in patients with chronic periodontitis before and after periodontal phase I therapy and periodontally healthy controls. Further, relationships between IL-1β levels and various clinical parameters were explored.
METHODS: Twenty-eight patients with moderate-to-severe generalized chronic periodontitis and 24 age-, race-, and ethnicity-matched controls participated in this study. Saliva samples were obtained from all patients. The clinical parameters recorded were clinical attachment loss (AL), probing depth, bleeding on probing, periodontal index, and gingival index. Clinical evaluation and sample collection were repeated 1 month after periodontal phase I therapy in patients with periodontitis. IL-1β levels were assessed using enzyme-linked immunosorbent assay.
RESULTS: Mean IL-1β levels in patients with periodontitis at baseline (1,312.75 pg/mL) were significantly higher (P <0.0001; eight-fold) than in controls (161.51 pg/mL). Although treatment in patients with periodontitis resulted in significant reduction in IL-1β levels (mean: 674.34 pg/mL; P = 0.001), they remained significantly higher (P <0.0001; four-fold) than control levels. There were significant correlations between IL-1β levels and all clinical parameters (P <0.01) except percentage sites with clinical AL >2 mm (P >0.05).
CONCLUSIONS: The data indicate that IL-1β levels are raised in the saliva of patients with chronic periodontitis, which are reduced after phase I therapy, suggesting a close association between salivary IL-1β and periodontitis. Additional longitudinal studies are needed to validate salivary IL-1β as a marker for periodontal disease.

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Year:  2011        PMID: 21235331     DOI: 10.1902/jop.2011.100472

Source DB:  PubMed          Journal:  J Periodontol        ISSN: 0022-3492            Impact factor:   6.993


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