Down Syndrome and Periodontal Disease

Abstract

Periodontal diseases are inflammatory diseases of the supporting structures of the teeth (Cochran, 2008; Kornman, 2008). They are initiated by periodontopathic bacteria and result in progressive destruction and loss of the periodontium (Cochran, 2008; Kornman, 2008). Progression of periodontal disease eventually leads to tooth loss (Chambrone, et al., 2010). Periodontal diseases are multifactorial with complex pathogenesis (Cochran, 2008; Kornman, 2008). Plaque bacteria trigger a host inflammatory response in the gingival tissues (Kornman, 2008). Neutrophils migrate from within the gingival tissues towards the gingival crevice and build a barrier wall against the bacteria (Kornman, 2008). Within the gingival connective tissue, the gingival macrophages and fibroblasts produce inflammatory cytokines (e.g. interleukin-1 and tumor necrosis factoralpha) that activate collagenases and other degrading enzymes (Kornman, 2008). These enzymes when released and activated destroy the gingival collagen. Lymphocytes are recruited to the gingival lesion to initiate an adaptive immune response and help with containing the infection (Kornman, 2008). With persistence of the microbial infection, the inflammatory changes in the gingival tissues expand apically and reach the alveolar bone (Cochran, 2008). Inflammatory mediators such as interleukin-1, interleukin-6, tumor necrosis factor alpha and prostaglandins induce osteoclasogenesis (Cochran, 2008). Increased inflammatory activity disrupts the normal balance of bone formation/resorption and results in alveolar bone loss (Cochran, 2008). Periodontal disease is a serious and morbid oral condition among Down-syndrome (DS) affected individuals (Morgan, 2007). Gingivitis and periodontitis start early in life and their severity increases with age (Reuland-Bosma, et al., 1988). Periodontal disease advances rapidly in DS individuals and is characterized by severe gingival inflammation, loss of periodontal attachment and radiographic alveolar bone loss (Agholme, et al., 1999; Saxen, et al., 1977). Heavy amounts of plaque and calculus are often present (Morgan, 2007). Periodontal disease is an important cause of tooth loss among DS individuals (Reuland-Bosma, et al., 2001). The exact reason (or reasons) for this increased susceptibility to periodontitis is (are) not known. Understanding the pathogenesis of periodontitis in DS individuals would greatly help with the management and control of the destructive process associated with the disease and help DS affected individuals retain their teeth hopefully throughout their lifetime. Previously researchers have investigated factors usually associated with periodontitis such as subgingival plaque microbial composition, immune and inflammatory responses individually in DS affected individuals. The individual factors investigated were never collectively evaluated together to provide an overall understanding of the pathogenesis of periodontitis in