Necrotizing Periodontal Diseases: Epidemiology, Clinical Features, and Etiopathogenesis

Necrotizing periodontal diseases (NPDs) are a group of clinical conditions characterized by necrosis of the gingival, periodontal, and/or oral mucosa. They include necrotizing gingivitis (NG), necrotizing periodontitis (NP), necrotizing stomatitis (NS), and noma. This study reviewed the epidemiology, etiology, and pathogenesis of these diseases. NPDs are characterized by distinct clinical features, including pain, inflammation, tissue necrosis, and unprovoked gingival bleeding, and can lead to rapid destruction of the soft and hard tissues of the periodontium and/or oral mucosa. A meta-analysis conducted in this study estimates the overall prevalence of NG was 0.04%, and is highest for Latin America (0.08%) and Asia (0.07%), among HIV-positive individuals (0.07%), and drug addicts (0.08%). The prevalence of NPD lesions is higher in young than in older age groups, particularly those with severe malnutrition. NPDs are opportunistic infections caused by the oral biofilm, in the presence of other etiological and predisposing factors. Although these causes are somewhat different from the etiological factors of periodontitis, the distinction is not well defined. Pre-existing gingival inflammation and/or periodontitis and a mixed infection are necessary causes but are not sufficient for the development of NPDs. These etiological factors, together with one or more other predisposing factors, including immunosuppression, severe psychological stress, severe malnutrition, heavy smoking, heavy alcohol consumption, uncontrolled diabetes, and HIV infection, significantly increase the risk of the development of NPDs. We propose a model that describes the causal pathway of NPDs whereby an opportunistic infection in predisposed individuals leads to microbial invasion of the gingival tissues and the development of local inflammation and tissue necrosis, which can be followed by destruction of the soft and hard oral tissues. NPDs are phenotypically distinct from conventional forms of periodontitis. However, it is unclear whether these diseases are also pathophysiologically different, as there is insufficient understanding of the underlying biological mechanisms that lead to their development.