I hope this article is illuminating on this most important of dental subjects.
The effects of early gingivitis, as dental professionals are aware, are reversible with adequate oral hygiene, although a gingival infection may persist for months or years, yet never progress to periodontitis.
Numerous attempts have been made to pinpoint which microorganisms in the supragingival plaque are the culprits in gingivitis.
Gingival inflammation may be influenced by steroid hormones, occurring as puberty gingivitis, pregnancy gingivitis, and gingivitis associated with birth control medication or steroid therapy.
Certain prescription drugs can also lead to gingival overgrowth and inflammation —these include the antiepileptic drug phenytoin (Dilantin); cyclosporine, an immunosuppressive therapy for transplant patients; and various calcium channel blockers used in heart disease.
A form of gingivitis common fifty years ago, but relatively rare today, is acute necrotizing ulcerative gingivitis, also known as Vincent’s infection or trench mouth.
People under extreme stress have an increased susceptibility to this condition, and an association between smoking and this type of gingivitis is well recognized and was demonstrated as early as 1946; it has also been seen in HIV-positive patients.
Adult periodontitis often begins in adolescence but is usually not clinically significant until the mid-30s; prevalence and severity increase do not accelerate with age.
Most researchers agree periodontitis results from a mixed infection but a particular group of gram-negative bacteria are key to the process.
The bacteria most frequently cited are Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus, Treponema denticola, and Actinobacillus actinomycetemcomitans.
Neutrophils (a type of white blood cell) and antibodies are the major immune defences against bacterial attack. The neutrophil/antibody axis is critical for full protection against periodontal diseases.
One of the strongest behavioural associations is with tobacco use. The risk of alveolar bone loss for heavy smokers is seven times greater than for those who have not smoked.
Cigarette smoking also may impair the normal host response in neutralizing infection. Smokers have decreased levels of salivary and serum immunoglobulins as well as depressed numbers of helper T cells.
Smoking also alters the cells that engulf and dispose of bacteria—neutrophils and other phagocytes—affecting their ability to clear pathogens.
Epidemiologic studies have found such additional factors as increasing age, infrequent dental visits, low education level, low income, co-morbidities, and inclusion in certain racial or ethnic populations are associated with increased prevalence of periodontitis.
Sex is another factor, with males tending to higher levels of periodontal diseases. Female hormones, though, may play a similar protective role as they do in protecting against osteoporosis.
More clinical attachment loss and edentulousness have been reported in osteoporotic than in nonosteoporotic women.
Studies have shown oestrogen replacement therapy in postmenopausal women not only gives protection against osteoporosis, but also results in fewer teeth lost to periodontal disease.
I hope this article serve to strengthen the translation of proven disease prevention approaches into health care practice, and personal lifestyle behaviours.
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