Microbial dental plaque initiates periodontal disease but the form and severity of the disease is dependent on the environmental, genetic and host defenses to this challenge. Systemic disorders or variations and environmental exposures may modify the normal defenses and influence the resultant periodontal disease. A reduction in number or function of polymorphonuclear leukocytes results in increased severity of periodontal destruction. Many drugs such as phenytoin, nifedipine, and cyclosporine predispose to gingival overgrowth in conjunction with microbial plaque and host response characteristics and thus may modify pre-existing periodontitis. Changes in circulating hormone levels may result in an increased severity of plaque-induced gingival inflammation but not typically in any increased susceptibility to periodontal attachment or bone loss. Hormonal changes as seen during and after menopause have been associated with osteoporosis but there is a lack of studies linking menopause or an estrogen-deficient state to a higher susceptibility to periodontal disease. Immunosuppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune processes, such as HIV infection, may predispose the individual to periodontal destruction. It is difficult, however, to determine the precise causative agent in these conditions and it is particularly complex when immunosuppressive drugs are prescribed together with antibiotics for variable periods of time. The evidence for smoking having a deleterious influence on periodontal health is convincing. Nutritional deficiencies in animals have been shown to affect the periodontal tissues but epidemiologic data do not support the suggestion that such deficiencies play an important role in chronic periodontal disease. Gingival bleeding is the most consistent oral feature of vitamin C deficiency, or scurvy, but there is also some evidence to suggest that avitaminosis-C may aggravate established chronic periodontitis (143, 144). Stress and other psychosomatic conditions which may have direct anti-immune effects or indirect, behavior-mediated effects on the body's defenses may prove to be important in the etiology of periodontitis and necrotizing ulcerative gingivitis and periodontitis. The role or relative importance of these mechanisms has yet to be fully elucidated but the evidence that stress, neural factors, and depression can influence the immune system is increasing. Many genetic disorders have numerous host response modifications, which may render the individual susceptible to periodontal disease. Many genetic conditions influence the periodontium during childhood and the periodontal manifestations of the disease may resemble the early onset forms of periodontitis; the effects of such diseases may persist into adulthood. Although systemic diseases such as diabetes will aggravate all forms of periodontitis, chronic or adult periodontitis is the most prevalent and thus will be the most common form presenting with diabetes-induced modifications. Currently, numerous genetic polymorphisms relevant to inflammatory and immune processes have been suggested and are being investigated for their modifying effects on periodontal disease. The literature on how periodontitis is modified by systemic factors, with the exception of the link with diabetes, HIV infection, and smoking, is as yet sparse and clearly well controlled cross-sectional and longitudinal studies are needed to fully elucidate the relationship between environmental modifiers and genetic influences and periodontitis.
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