Literature DB >> 3164372

The mechanism of pocket formation. A light microscopic study on undecalcified human material.

T Takata1, K Donath.   

Abstract

Two hundred eighteen human teeth with surrounding periodontal tissues in different stages of pathogenesis were studied under light microscopy using the "sawing and grinding" technique. This was done without decalcification and with special emphasis on the dentogingival junction area so as to study the mechanism of pocket formation. Thirty early, 133 established, and 214 advanced lesions were included. No initial lesion was seen. Pocket formation, provoked by microbacterial plaque, seemed to be initiated by the degenerative changes in the second or third cell layers from the innermost cells in the most coronal part of the junctional epithelium facing the microbial plaque. Consequently, an intraepithelial cleavage was formed followed by the degeneration and desquamation of the cells lining the split. This resulted in a deep crevice and gingival pocket formation in both early and established lesions. In advanced lesions, the deep pocket epithelium was exposed for such a long distance adjacent to the plaque and calculus, that the epithelium could be directly affected by toxic bacterial products and mechanical irritation of calculus. Finally, the epithelium became very thin and ulcerated, and a typical periodontal pocket was formed. The disruption of the epithelial barrier along with the concomitant penetration of bacteria and/or their toxic products were considered to be the most significant factors related to the conversion of an established lesion to an aggressive lesion.

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Year:  1988        PMID: 3164372     DOI: 10.1902/jop.1988.59.4.215

Source DB:  PubMed          Journal:  J Periodontol        ISSN: 0022-3492            Impact factor:   6.993


  8 in total

1.  Changes in Inflammatory and Bone Turnover Markers After Periodontal Disease Treatment in Patients With Diabetes.

Authors:  Kenneth E Izuora; Echezona E Ezeanolue; Michael F Neubauer; Civon L Gewelber; Gayle L Allenback; Guogen Shan; Guillermo E Umpierrez
Journal:  Am J Med Sci       Date:  2016-04-23       Impact factor: 2.378

2.  The optimization of ligature/bone defect-induced periodontitis model in rats.

Authors:  Jingyi Gao; Simin Cai; Zijie Wang; Dan Li; Minyi Ou; Xinlu Zhang; Zhihui Tian
Journal:  Odontology       Date:  2022-06-03       Impact factor: 2.885

3.  Host-bacteria crosstalk at the dentogingival junction.

Authors:  M T Pöllänen; M A Laine; R Ihalin; V-J Uitto
Journal:  Int J Dent       Date:  2012-07-26

4.  DENTAL LOSS AMONG AMBULATORY PATIENTS WITH DIABETES.

Authors:  Kenneth E Izuora; Echezona E Ezeanolue; Michael F Neubauer; Civon L Gewelber; Gayle L Allenback; Guillermo E Umpierrez
Journal:  J Clin Transl Endocrinol       Date:  2016-06

5.  Non-Inflammatory Destructive Periodontal Disease.

Authors:  Thaís Yumi Umeda Suzuki; Eunice Fumico Umeda Kina; Juliana Kina; Mônica Kina
Journal:  Open Dent J       Date:  2016-03-10

6.  Oral microbial extracellular DNA initiates periodontitis through gingival degradation by fibroblast-derived cathepsin K in mice.

Authors:  Takeru Kondo; Hiroko Okawa; Akishige Hokugo; Bhumika Shokeen; Oskar Sundberg; Yiying Zheng; Charles E McKenna; Renate Lux; Ichiro Nishimura
Journal:  Commun Biol       Date:  2022-09-14

7.  Presence of bacteria in dentinal tubules.

Authors:  José Ricardo Kina; Juliana Kina; Eunice Fumico Umeda Kina; Mônica Kina; Ana Maria Pires Soubhia
Journal:  J Appl Oral Sci       Date:  2008 May-Jun       Impact factor: 2.698

Review 8.  Regulation of defensive function on gingival epithelial cells can prevent periodontal disease.

Authors:  Tsuyoshi Fujita; Tetsuya Yoshimoto; Mikihito Kajiya; Kazuhisa Ouhara; Shinji Matsuda; Tasuku Takemura; Keiichi Akutagawa; Katsuhiro Takeda; Noriyoshi Mizuno; Hidemi Kurihara
Journal:  Jpn Dent Sci Rev       Date:  2017-12-15
  8 in total

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