As part of my continuing dedication to discussing and expanding the conversation on oral health, today I’m talking about when oral health goes wrong, starting with gum disease, periodontisis and the bacterias and habits which generate these problems.
The effects of early gingivitis are reversible with adequate oral hygiene. 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.
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 that periodontitis results from a mixed infection but that 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 also 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 additional factors such 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.
Refractory periodontitis, while not a specific form of disease, refers to cases in which patients continue to exhibit progressive disease at multiple sites despite aggressive mechanical therapy and/or administration of antibiotics.
If you have any questions, comments, or concerns on this subject or others, feel free to get in touch. Leave a comment here or find me on social media: