Periodontitis Essay

Periodontitis is a chronic infectious disease, triggered by the host immune response to an array of periodontal biofilm-associated microorganisms, which ultimately leads to the inflammation of the tissues supporting the teeth.
The initial host response to bacterial infection is a local inflammatory reaction that activates the innate immune system. An imbalance between biofilms and immune system results in over expression of an array of pro-inflammatory cytokines, propagation of inflammation through the gingival tissues and subsequent destruction of alveolar bone. Thus, the inflammatory process results in destruction of connective tissue and alveolar bone – Hallmark of periodontal disease.
Diagnosis of periodontal disease has been primarily based upon clinical and radiographic measures of periodontal tissue destruction. These parameters provide a measure of past destruction and are of limited use in early diagnosis (Frodge et al, 2008)1. Biomarkers of disease play an important role in life
Osteopontin (OPN) is a non-collagenous, calcium binding, glycosylated phosphoprotein produced by osteoblasts (Rodan, 1994)3. Osteopontin level reflects active lesions of aggravated periodontal disease accompanied by alveolar bone resorption. The concomitant increase of osteopontin in plasma is caused by spillage or overflow of osteopontin from the diseased periodontal tissues or produced by circulating activated macrophages. The level of osteopontin before and after treatment can be used to assess the severity of periodontal disease.
Treatment of periodontal disease includes both non-surgical and surgical therapy. Non-surgical therapy remains the corner stone of periodontal treatment. It includes scaling and root planing under local anaesthesia to provide patient comfort and to control the disease progression. Systemic therapy may be employed as an adjunct to local measures and for control of systemic