Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chronic Periodontitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1976

Bone morphology and bone loss in periodontal disease.

A clinical study of the distribution of different types of bone defects in chronic periodontitis was carried out on 30 patients. An analysis of 176 defects suggests that their distribution reflects the original morphology of the alveolar bone. The role of function as a determinant of that morphology is examined. While there appears to be a relationship between functional stress and the phylogenesis of the bone, there is no direct relationship between function and ontogenesis. A study of growth remodelling of the mandible in several animals indicates that the pattern of activity is dictated by a drive to achieve a mature form which is the expression of the genetic endowment. Normal function and normal muscle stress are part of the environment in which complete growth can take place, but they do not appear to play a more active role in determining the form of growth; abnormal function does not allow normal growth to take place. The relationship between functional stress and the morphology and activity of the mature bone is not clear. Osteoporosis of age, as measured by the metacarpal index in 101 patients with chronic periodontitis, did not appear to be significantly related to the bone loss score. However, in 54 females patients, aged 35-45 years, a significant correlation was found between the metacarpal index and a "rapidity of bone loss" score.

Adult↗
PubMed1977

[The pathomorphology of chronic apical periodontitis].

The clinical, roentgenological and histopathological diagnoses of thirty apical processes are compared. The paper also discusses certain histopathological characteristics. As a result of these investigations, a proposal is made to modify the classification of chronic apical processes.

Chronic Disease↗
PubMed1975

Osseous coagulum: a histologic evaluation.

Chronic periodontitis can be successfully simulated in primates by the method employed in this study. Osseous defects can be created with a marked degree of similarity to one another and subsequently rendered into chronic lesions for healing-repair studies. The chronic periodontal ossious defects corrected by the osseous coagulum technique and by curettage in the rhesus monkey in this study were repaired by the regeneration of the architecture of the lost tissue. The use of the osseous coagulum in two- and three-walled periodontal osseous defects led to a more rapid osteogenesis in such defects as compared to correction by curettage alone. This rapid filling of the osseous defects may serve to inhibit the apical migration of the epithelial attachment during the early stages of repair, and thereby inhibit a subsequent recurrence of the defect. Clinically and histologically, no readily apparent distinction could be made in the healing process between the two- and three-walled lesions.

Alveolar Process↗
PubMed1976

Pathogenesis of inflammatory periodontal disease. A summary of current work.

Chronic periodontitis, a common disease of microbial origin, is the major cause of tooth loss in adult humans. The disease serves as a convenient experimental model for analysis of many aspects of chronic inflammation. A consideration of currently available data has permitted the formulation of a new concept of the pathogenesis of this disease. The gingival tissues respond within 2 to 4 days to a beginning accumlation of microbial plaque with a classic acute exudative vasculitis which we have termed the initial lesion. This response, which includes loss of perivascular collagen, is comparable to that elicited in most other tissues subjected to acute injury and may be a consequence of the elaboration and release of chemotactic and antigenic substances by microbial plaque. Within 4 to 10 days, the early lesion develops. It is characterized by a dense infiltrate of lymphocytes and other mononuclear cells, pathologic alteration of fibroblasts, and continuing loss of the connective tissue substance. The structural features of the early lesion are consistent with those expected in some form of cellular hypersensitivity, and a mechanism of this kind may be important in the pathogenesis. The early lesion is followed by the established lesion which develops within 2 to 3 weeks and is distinguished by a predominance of plasma cells in the absence of significant bone loss. The established lesion, which is extremely widespread in humans and in animals, may remain stable for years or decades, or it may become converted into a progressive destructive lesion. Factors causing this conversion are not understood. In the advanced lesion, plasma cells continue to predominate although loss of the alveolar bone and periodontal ligament, and disruption of the tissue architecture with fibrosis are also important characteristics. The initial, early, and established lesions are sequential stages in gingivitis and they, rather than the advanced lesion which is manifest clinically as periodontitis, make up the major portion of inflammatory gingival and periodontal disease in humans.

Adolescent↗
PubMed1979

[Characterization of Mycoplasma salivarium in periodontal diseases].

Research for oral mycoplasms has been conducted on individuals affected with periodontal disease. In 66 out of 100 samplings taken from lesions distinctive or gingivitis, it has been possible to identify Mycoplasma salivarium, by means of specific culture medium and serological reactions. A good correlation has been established between the oral hygiene index and the presence of Mycoplasma salivarium. 80% of the samplings taken from the periodontal pockets of patients affected with chronic periodontitis have revealed the presence of Mycoplasma salivarium. There is a close connection between the stage of the infection and the depth of the pockets. The deeper periodontal tissues of 63 out of the same 100 subjects bear evidence of Mycoplasma salivarium, which, besides the processes already described in relation to bacteria, would come to imply a direct action of mycoplasms on the cell metabolism.

Adult↗