Abstract:The distribution of bone loss in 156 patients, 12-32 years old, with juvenile periodontitis was analyzed according to age, sex, and teeth affected. The criteria for bone loss were: vertical or horizontal bone loss involving more than one-third of the root as judged by radiographs. Three age groups were established: 12-18, 19-25, and 26-32 years old. Three types of bone loss localization were defined: I. First molars and/or incisors. II. First molars, incisors and some additional teeth (total less than 14 teeth… Show more
“…Autosomal recessive (AR) and X-linked dominant (XD) transmission with partial penetrance are two hypotheses currently favored in the dental literature [Fourel, 1972;Jorgenson et al, 1975;Melnick et al, 1976;SaxCn, 1980b;SaxCn and Nevanlinna, 1984;Vandesteen et al, 19841. It is perhaps not surprising that no clear consensus as to the genetic mechanism has emerged, in view of (1) variation in expression and age of onset of the trait; (2) it's low population prevalence, and sex specific incidence; (3) the inherent difficulties involved in formally rejecting either hypothesis by analysis of sibships data; and (4) the difficulties involved in obtaining multigenerational data and adequate sample sizes.…”
Two rare types of familial periodontitis, a localized form usually diagnosed in late adolescence, and a more generalized form with a latter mean age of diagnosis, have been analyzed with respect to genetic models currently favored in the dental literature. These include autosomal recessive and X-linked dominant (partial penetrance) inheritance. Since there is variation in severity, extent, age of onset, altered sex ratio of affected individuals, and a low population prevalence, it is not surprising that genetic mechanisms heretofore have not been revealed. We have compared the likelihoods of 33 kindreds ascertained through affected probands under the above genetic models. Our findings include (1) several families in which both forms of early onset periodontitis co-occur, making it unlikely that the clinical varieties of the disease have unrelated genetic causes; (2) the autosomal recessive model is far more likely than the X-linked dominant model. The superiority of the recessive hypothesis arises from the fact that there are only a few instances of affected individuals having affected parents and because the skewed sex ratio is shown to be incompatible with X-linked inheritance. These conclusions are largely insensitive to the assumptions of the analysis. We conclude that the X-linked dominant hypothesis is inadequate, and while the autosomal recessive model is by no means proven, it is clearly favored.
“…Autosomal recessive (AR) and X-linked dominant (XD) transmission with partial penetrance are two hypotheses currently favored in the dental literature [Fourel, 1972;Jorgenson et al, 1975;Melnick et al, 1976;SaxCn, 1980b;SaxCn and Nevanlinna, 1984;Vandesteen et al, 19841. It is perhaps not surprising that no clear consensus as to the genetic mechanism has emerged, in view of (1) variation in expression and age of onset of the trait; (2) it's low population prevalence, and sex specific incidence; (3) the inherent difficulties involved in formally rejecting either hypothesis by analysis of sibships data; and (4) the difficulties involved in obtaining multigenerational data and adequate sample sizes.…”
Two rare types of familial periodontitis, a localized form usually diagnosed in late adolescence, and a more generalized form with a latter mean age of diagnosis, have been analyzed with respect to genetic models currently favored in the dental literature. These include autosomal recessive and X-linked dominant (partial penetrance) inheritance. Since there is variation in severity, extent, age of onset, altered sex ratio of affected individuals, and a low population prevalence, it is not surprising that genetic mechanisms heretofore have not been revealed. We have compared the likelihoods of 33 kindreds ascertained through affected probands under the above genetic models. Our findings include (1) several families in which both forms of early onset periodontitis co-occur, making it unlikely that the clinical varieties of the disease have unrelated genetic causes; (2) the autosomal recessive model is far more likely than the X-linked dominant model. The superiority of the recessive hypothesis arises from the fact that there are only a few instances of affected individuals having affected parents and because the skewed sex ratio is shown to be incompatible with X-linked inheritance. These conclusions are largely insensitive to the assumptions of the analysis. We conclude that the X-linked dominant hypothesis is inadequate, and while the autosomal recessive model is by no means proven, it is clearly favored.
“…Bacterial products can exert a direct effect or can act indirectly by inducing inflammatory changes. In localised juvenile periodontitis (LJP) there is marked tissue destruction, especially bone resorption, but minimal inflammation (Baer, 1971;Hsrmand and Frandsen, 1979), and the direct cytotoxic effects of bacterial products appear to play an important role. Such effects on the fibroblasts of the periodontium result in a decrease in cell numbers and a net loss of collagen (Page and Schroeder, 1976).…”
Summary. Cytotoxic effects of bacteria found in dental plaque are usually attributed to lipopolysaccharides (LPS) or ill-defined toxins. Many bacteria implicated in periodontal disease produce surface exopolymers (capsules) recently shown to stimulate bone resorption. Capsular material and LPS extracted from Actinobacillus (Haemophilus) actinomycetemcomitans were purified and examined for their effects on cultures of human gingival fibroblasts. DNA and collagen synthesis were significantly inhibited by capsular material (0.1-50 pglml). LPS caused only modest inhibition of DNA synthesis at 10 and 50 pg/ml, and had no effect on collagen synthesis. Release of lactate dehydrogenase from fibroblasts was not increased by LPS nor by capsular material, showing that the inhibitory effects were not due to cell death. Capsular material, but not LPS, caused a pronounced increase in cell size; a doubling of the nuclear area occurred within 72 h exposure. These results indicate that the capsule of A . actinomycetemcomitans may play an active role in the tissue destruction characterising inflammatory periodontal disease.
“…However, there are patients who experienced disease progression until tooth loss occurs despite a non-adequate conventional treatment has been done. 3,20,21 Table 2 also illustrates a systemic disease, smoking, hormonal changes in women, and the consumption of certain drugs. It is important to note when determining diagnosis, prognosis, and selection of appropriate therapy.…”
Aggressive Periodontitis is one of periodontal disease that generally affects individuals less than 30 years old, with a rapid attachment loss and alveolar bone destruction. Special features of the disease are affected incisors and first molars with symmetrical bilateral destruction. The purpose of this study was to determine the prevalence and characteristics of Aggressive Periodontitis at Student Clinics, Faculty of Dentistry Padjadjaran University on May to July 2010. Based on accidentally sampling, 415 new patients at Dental and Oral Hospital, Faculty of Dentistry Padjadjaran University and Dental and Oral Polyclinic at RSUP dr. Hasan Sadikin Bandung were participated in this study. Each subject filled out the questionnaire and did clinical examination. Patients with attachment loss â„ 4 mm were reffered for radiographic and microbiologic examination to support the diagnosis. The results showed that there were 13 patients who has the diagnostic criteria of Aggressive Periodontitis. Nine patients were diagnosed as Localized Aggressive Periodontitis, and 4 patients as Generalized Aggresive Periodontitis. It is concluded that the prevalence of Aggressive Periodontitis was 3.13%, and indicated low prevalence. Characteristics of Localized Aggressive Periodontitis patients were female in 20-29 age range, whereas characteristics of Generalized Aggressive Periodontitis patients were male in 30-39 age range.
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