Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoking has long been suspected to be associated with a variety of oral conditions including periodontal diseases. Experimental evidence accumulated over the last 2 decades has indicated that cigarette smoking is probably a true risk factor for periodontitis. This environmental exposure has been associated with 2- to 3-fold increases in the odds of developing clinically detectable periodontitis. Smokers have both increased prevalence and more severe extent of periodontal disease, as well as higher prevalence of tooth loss and edentulism, compared to non-smokers. The greater severity of periodontal destruction may be partly accounted for by the reported increases in the rate of periodontal disease progression. The noxious effect of smoking has been shown to be dose dependent and to be particularly marked in younger individuals; in these subjects, up to 51% of the observed risk of periodontitis was associated with smoking. Much of the literature has also indicated that smokers affected with periodontitis respond less favorably to both non-surgical, surgical, and regenerative periodontal treatments. The success rate of dental implants has also been shown to be compromised in smokers. Furthermore, longterm studies have pointed out that smoking was associated with recurrence of periodontitis during periodontal maintenance; the effect appeared to be dose dependent, with heavy smokers (> 10 cigarettes/day) presenting with higher levels of disease progression. The indication that previous smokers have lower levels of risk for periodontitis compared to current smokers is considered to be the strongest available evidence that smoking cessation will result in improved periodontal health and that smoking cessation counseling should be an integral part of periodontal therapy and prevention. So far, however, no randomized controlled clinical trial establishing the effect of smoking cessation and/or reduction on the periodontal outcomes has been reported. Given the present state of uncertainty about the periodontal benefits, but in light of the established general health gains for the patient that could be derived from a smoking cessation program, practitioners are incorporating smoking cessation counseling as an integral part of periodontal therapy. Furthermore, smoking status represents a key parameter to assess the periodontal risk of an individual subject and therefore to make evidence-based clinical decisions.
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PMID:Cigarette smoking and periodontal diseases: etiology and management of disease. 972 93

There has been increasing interest in the interrelationship between systemic osteoporosis, oral bone loss, tooth loss, and risk factors for these conditions. Because the severity of alveolar bone loss increases with age, it has long been hypothesized that it may, in part, be related to systemic conditions that also predispose the patient to osteoporosis/osteopenia. The purpose of this paper is to review the risk factors for osteoporosis and periodontitis, as well as the evidence that loss of oral bone mineral may be related to systemic osteopenia. There is also evidence that therapies designed to influence systemic bone mineral density, such as hormone replacement and bisphosphonate therapy, may be associated with less tooth loss and a slower loss of alveolar bone, respectively.
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PMID:Osteoporosis: a possible modifying factor in oral bone loss. 972 15

Periodontitis is a chronic inflammation of the supporting structures of the dentition which constitutes one of the most common causes of adult tooth loss. While certain microorganisms have been associated with the onset of the disease process, the exact pathogenetic mechanisms underlying periodontal destruction are still poorly understood. We have tested the hypothesis that gingival fibroblasts from diseased sites contribute to pathogenesis by possessing a secretory phenotype characterized by an exuberant secretion of inflammatory mediators and cytokines. Of the cytokines and mediators tested, fibroblast IL-1beta and prostaglandin E2 (PGE2) secretion was not different between health and disease. However, we have shown that fibroblasts from periodontal lesions produce in vitro greater amounts of IL-6 and IL-8 constitutively than healthy controls. When fibroblasts were stimulated with a panel of endogenous or exogenous response modifiers, the magnitude of cytokine and mediator stimulation above constitutive levels did not differ between health and disease. A strong positive correlation was identified between IL-6 or IL-8 constitutive secretion levels in vitro and the in situ expression of these cytokines within the connective tissues from where these cells originated, indicating that the in vitro phenotype mirrors their in vivo function. Furthermore, we present evidence which indicates that increased cytokine secretion by fibroblasts in disease is due to an elevated proportion of subpopulations with higher cytokine secretory capacity. Finally, we demonstrated that cultures from diseased sites are composed of cells with higher levels of constitutive CD40 expression, which may contribute to the increased IL-6 and IL-8 secretory phenotype.
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PMID:Increased presence of interleukin-6 (IL-6) and IL-8 secreting fibroblast subpopulations in adult periodontitis. 973 73

Numerous epidemiological studies have shown that caries is the main reason for tooth loss. More recent epidemiological data seem to show an increasing trend of tooth loss due to periodontal reasons rather than caries. In considering the issue of periodontal disease and tooth loss the following observations were made. The presence of initial attachment loss, bone height and the habit of smoking significantly increase the risk of tooth mortality. There is a strong correlation between smoking, the severity of periodontal disease and tooth mortality. Cross-sectional population surveys of tooth loss reported lower anterior teeth to be the most frequently extracted due to periodontal reasons, followed by upper anteriors and upper second molars. However, in long term maintenance studies, molars were lost most frequently. Periodontal reasons for tooth loss were mainly mobility followed by furcation involvement. Periodontal surgery did not significantly enhance tooth retention in high risk groups. Ethnic differences observed were not significant and would need further investigations to address variables such as cultural differences, health habits, diet and socio-economic status. In conclusion, periodontal tooth mortality was found to be associated with the loss of periodontal attachment and risk groups with advanced periodontitis contributing to major tooth loss in a minority of the population.
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PMID:Periodontal disease and tooth loss. 977 3

Periodontal disease is a significant cause of tooth loss in humans and is one of the most prevalent diseases associated with bone loss. Following bacterial colonization, the gingiva becomes inflamed and, in some cases, progresses to destruction of alveolar bone. To investigate the temporal movement of inflammatory cells toward alveolar bone and the role of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in this process, studies were carried out in a Macaca fascicularis primate model of experimental periodontitis. IL-1 and TNF activity was inhibited by local application of soluble receptors to IL-1 and TNF by injection into interdental papillae. The results indicate that following induction of experimental periodontitis, the front of inflammatory cells progresses toward alveolar bone and is associated with osteoclast formation. These processes are inhibited by blockers to IL-1 and TNF. These studies suggest that the conversion from gingivitis to periodontitis is directly associated with the movement of an inflammatory infiltrate toward alveolar bone, and that this activity is at least partially dependent upon IL-1 and/ or TNF.
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PMID:Interleukin-1 and tumor necrosis factor antagonists inhibit the progression of inflammatory cell infiltration toward alveolar bone in experimental periodontitis. 992 73

The purpose of this paper is two-fold: (1) to review the evidence that osteoporosis and post-menopausal estrogen deficiency are associated with progressive alveolar bone loss and an elevated risk of tooth loss; and (2) to propose the use of tetracyclines, specifically low-dose doxycycline (LDD) (and, perhaps in the future, the chemically modified tetracyclines), to mitigate alveolar bone loss in post-menopausal osteoporotic/osteopenic women. Design concepts for a randomized clinical trial to study the effects of LDD on progressive alveolar bone loss in this patient population are reviewed. Since osteoporosis affects over 20 million people in the United States, progressive alveolar bone loss in this patient group represents a potentially significant public health problem unique from common adult periodontitis. Stopping progressive alveolar bone loss is essential to prevent both tooth loss and micro-architectural deterioration of alveolar bone.
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PMID:Potential application of low-dose doxycycline to treat periodontitis in post-menopausal women. 997 43

Periodontitis is a chronic inflammatory disease which gradually destroys the supporting tissues of the teeth, leading to tooth loss in adults. The lesions are characterized by a persistence of inflammatory cells in gingival and periodontal connective tissues. To understand what mechanisms are involved in the establishment of chronic lesions, we hypothesized that infiltrating lymphocytes might be resistant to apoptosis. However, both Bcl-2 and Bcl-xL were weakly detected in lymphocytes from the lesions, compared with those from peripheral blood, suggesting that these cells are susceptible to apoptosis. Nevertheless, very few apoptotic cells were observed in tissue sections from the lesions. Lymphocytes from the lesions expressed mRNA encoding Fas, whereas Fas-ligand mRNA was very weakly expressed in lymphocytes from the lesions and in periodontal tissues. Since the results indicated that lymphocytes in the lesions might be susceptible to Fas-mediated apoptosis but lack the death signal, we next investigated if these lymphocytes actually undergo apoptosis by the addition of anti-Fas antibodies in vitro. Fas-positive lymphocytes from the lesions underwent apoptosis by these antibodies, but Fas-negative lymphocytes and Fas-positive peripheral lymphocytes did not undergo apoptosis by these antibodies. These results indicate that lymphocytes in the lesions are susceptible to activation-induced cell death and are induced to die by apoptosis after the addition of exogenous Fas ligand.
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PMID:In vitro induction of activation-induced cell death in lymphocytes from chronic periodontal lesions by exogenous Fas ligand. 1002 94

Loss of all natural permanent teeth (edentulism) substantially reduces quality of life, self-image, and daily functioning. Although loss of teeth results from oral diseases such as dental caries and periodontitis, it also reflects patient and dentist attitudes, availability and accessibility of dental care, and the prevailing standard of care. One of the national health objectives for 2000 is to reduce to no more than 20% the proportion of persons aged > or =65 years who have lost all their natural teeth (objective 13.4). Edentulism has been declining in the United States since the 1950s, but few state-specific data are available on adult tooth loss. To estimate the prevalence of edentulism among persons aged > or =65 years, CDC analyzed data from the 46 states that participated in the oral health module of the 1995-1997 Behavioral Risk Factor Surveillance System (BRFSS). This report summarizes the findings from this analysis, which indicate a large state-specific variation in edentulism and that many states have not yet achieved the national health objective for preventing total tooth loss.
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PMID:Total tooth loss among persons aged > or =65 years--selected states, 1995-1997. 1009 21

Older adults present special problems for the dentist trying to establish or reestablish esthetics. Periodontal diseases are of concern for this population since tooth loss from these widespread problems increases with age. In general, this loss occurs because of increased exposure time to pathogenic bacteria, not some change inherent in the body brought on by the aging process. The profession has begun to place more emphasis on systemic risk factors and their role in modifying periodontal inflammation. The current thinking is that bacteria are necessary to initiate and sustain periodontal diseases, but the clinical manifestation is dictated to a significant extent by systemic factors. Smoking, diabetes, and being positive for the interleukin-1 genotype predispose the patient to developing more severe disease. For those older adults who lose teeth, dental implants have emerged as reliable replacements, and concerns about placing these devices in patients who have lost teeth as a result of periodontitis appear to be largely unfounded.
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PMID:Periodontal diseases and dental implants in older adults. 1032 Nov 96

Leukocyte adhesion deficiency is a rare inherited defect of phagocytic function resulting from a lack of leukocyte cell surface expression of beta2 integrin molecules (CD11 and CD18) that are essential for leukocyte adhesion to endothelial cells and chemotaxis. A small number of patients with leukocyte adhesion deficiency-1 have a milder defect, with residual expression of CD18. These patients tend to survive beyond infancy; they manifest progressive severe periodontitis, alveolar bone loss, periodontal pocket formation, and partial or total premature loss of the primary and permanent dentitions. We report on a 13-year-old boy with moderate leukocyte adhesion deficiency-1 and severe prepubertal periodontitis. This case illustrates the need for the dentist to work closely with the pediatrician in the prevention of premature tooth loss and control of oral infection in these patients.
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PMID:Leukocyte adhesion deficiency in a child with severe oral involvement. 1039 59


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