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11. |
Origins of cementum |
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Oral Diseases,
Volume 2,
Issue 1,
1996,
Page 63-69
L Hammarström,
I Alatli,
CD Fong,
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摘要:
There are diverging opinions about the role of Hertwig's epithelial root sheath in the formation of cementum. In the present review this role is discussed. There is increasing evidence that Hertwig's epithelial root sheath is actively involved in the formation of both acellular and cellular cementum. The development of acellular cementum seems to be associated with secretion of enamel‐related proteins by cells of the epithelial root sheath. Formation of the matrix for cellular cementum appears to be induced by exposure of the inner layer of the epithelial root sheath to the mesenchymal cells in the dental follicle. Experimental studies with I‐hydroxyethylidene‐I, I‐bisphosphonate (HEBP) indicate that the formation of acellular cementum must be preceded by mineralization of the mantle dentin. If the mineralization is inhibited by means of HEBP, there is precocious separation of the two layers of the epithelial root sheath after which matrix for a cellular type of cementum is
ISSN:1354-523X
DOI:10.1111/j.1601-0825.1996.tb00205.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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12. |
Collagenases and tissue inhibitors of metalloproteinases: a functional balance in tissue degradation |
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Oral Diseases,
Volume 2,
Issue 1,
1996,
Page 70-76
JJ Reynolds,
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摘要:
BACKGROUND: Members of the family of matrix metalloproteinases (MMPs; also called collagenases or matrixins) are key enzymes in matrix degradation. They function at neutral pH and can digest synergistically all the matrix macromolecules. Biochemical and clonal studies indicate that there are three major groups: the specific collagenases cleave interstitial collagens; the gelatinases degrade types IV, V, VII and XI collagens and act synergistically with collagenases by degrading denatured collagens (gelatins): and the stromelysins have broader specificity and can degrade basement membrane collagens as well as proteoglycans and matrix gly‐coproteins. Others not in these groups are matrilysin, metalloelastase and a recently cloned membrane‐bound metalloproteinase. MMPs are Zn2+‐ and Ca2+‐requiring endopeptidases and are secreted in a latent proform: activation involves the loss of a propeptide.Naturally occurring inhibitors, TlMPs (Tissue Inhibitors of MetalloProteinases), are important controlling factors in the actions of MMPs, and tissue destruction in disease processes often correlates with an imbalance of MMPs over TIMPs. The major inhibitor is TIMP‐I (or TIMP), a 30‐kDa glycoprotein that is synthesised by most cells. A second unglycosylated inhibitor, TIMP‐2, which is less abundant, has the interesting property of binding to the proform of gelatinase A and is involved in controlling its activation.BIOLOGICAL AND PSYCHOLOGICAL IMPLICATIONS: The expression of MMPs and TlMPs by cells is regulated by many cytokines (particularly interleukin‐I, IL‐I), growth factors and hormones, some of which are specific to cell type and others that are ubiquitous (eg transforming growth factor β, TGF‐β). Many of these factors are products of monocytes/macrophages and their production in inflammatory situations is therefore part of the chain of events leading to tissue degradation. From many recent studies it seems that tissue destruction, both physiological and pathological, is correlated with an imbalance of inhibitors over proteinases. We proposed that one way in which pathogenic organisms might mediate tissue degradation in periodontal diseases is through the ability of cell wall antigens to stimulate cytokine production by circulating mononuclear cells. These would then induce MMP synthesis by resident gingival cells (or by the mononuclear cells themselves), thereby initiating degradative events. We have identified MMPs in human gingival biopsy specimens by using specific poly‐clonal antibodies and indirect immunofluorescence. Their distributions are extremely variable, both in the connective tissue and the epithelium, but the results indicate that host cell production of MMPs may contribute to tissue degradation in periodontal disease. TIMP could also be found in some situations and cou
ISSN:1354-523X
DOI:10.1111/j.1601-0825.1996.tb00206.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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13. |
Keratinocyte integrins in wound healing and chronic inflammation of the human periodontiurn |
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Oral Diseases,
Volume 2,
Issue 1,
1996,
Page 77-86
H Larjava,
K Haapasalmi,
T Salo,
C Wiebe,
V‐J Uitto,
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摘要:
Periodontal epithelium plays a critical role in protection, destruction and repair of human periodontium. During optimal repair, epithelium migrates and covers the wound surface to prevent infection and damage of the vulnerable underlying connective tissue. During periodontal destruction, junctional epithelium undergoes transformation to pocket epithelium that has quite different characteristics from junctional epithelium. In the course of periodontal disease the epithelial attachment to the tooth surface is lost and the epithelium proliferates and extends pseudo‐rete ridges deep into the inflamed connective tissue. Both scenarios, repair and destruction, involve active epithelial migration either in the wound provisional matrix or in the inflamed connective tissue matrix, respectively. This review covers recent research data on cellular receptors, integrins, that mediate epithelial cell migration during wound healing and destruction of human periodontiur
ISSN:1354-523X
DOI:10.1111/j.1601-0825.1996.tb00207.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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14. |
Diagnostic strategies of periodontitis based on the molecular mechanisms of periodontal tissue destruction |
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Oral Diseases,
Volume 2,
Issue 1,
1996,
Page 87-95
H Okada,
S Murakami,
M Kitamura,
T Nozaki,
Y Kusumoto,
H Hirano,
H Shimauchi,
Y Shimabukuro,
T Saho,
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摘要:
OBJECTIVE: Periodontitis is a disease showing differences in disease progression between patients and between sites within a patient. Routine clinical examinations today are not useful enough to distinguish susceptible patients and active lesions from resistant patients and chronic lesions. Diagnostic markers should be pathogenic and inflammatory factors participating in periodontal tissue destruction. These are both local and systemic factors.MATERIALS AND METHODS: First of all, pathogenic factors and proinflammatory cytokines or mediators in gingival crevicular fluid (GCF) were examined and the difference was found between active and inactive periodontitis lesions distinguished by attachment loss. Active lesions were detected by discriminant‐function analysis of these examinations, although the sensitivity of differential diagnosis was low. Then, we established a novel needle biopsy for understanding the pathophysiological conditions elicited in active and chronic inflammatory processes of periodontal tissue destruction. A variety of cytokines and mediators were detected in biopsied specimens by reversed transcription polymerase chain reactions (RT‐PCR). Cytokine profiles were varied in inflamed periodontal biopsies. As IFNy mRNA expression was enhanced in inflamed gingiva, antigen‐presenting‐cell (APC) functions of human gingival fibro‐blasts (HGF) were examined.RESULTS: Despite the phenotypical resemb!ance of IFNγ‐treated HGF to so‐called APC, HLA‐DR positive HGF could not induce proliferation but suppressed proliferation of alloreactive peripheral blood T cells (PBT). However, HLA‐DR positive HGF stimulated the prolifer‐ative responses of PBT which had been primed with allo‐APC. Regulatory immune responses by IFNγ were different in T cell conditions.CONCLUSIONS Various kinds of cytokines participated in periodontal inflammation, and every cytokine is multifunctional. Complex and compound inflammatory processes can be clarified by examining cytokine networks and the precise effects of each cytokine on each of the cell types comprising periodontal tissue. It is, therefore, necessary for establishing diagnostic strategies to integrate pathogenic and inflammatory factors in periodo
ISSN:1354-523X
DOI:10.1111/j.1601-0825.1996.tb00208.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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15. |
Cellular immunity and hypersensitivity as components of periodontal destruction |
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Oral Diseases,
Volume 2,
Issue 1,
1996,
Page 96-101
GJ Seymour,
E Gemmell,
M KjeIdsen,
K Yamazaki,
T Nakajima,
K Hara,
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摘要:
BACKGROUND: Cellular immunity has been implicated in periodontal destruction for over 25 years. Studies in the 1970s used lymphocyte transformation and lympho‐kine assays to establish a role for cell‐mediated mechanisms in periodontal disease. lmmunohistological studies subsequently showed that the formation of gingivitis followed a similar pattern to the formation of a delayed type hypersensitivity reaction. Further functional studies suggested that a T cell/macrophage immunoregulatory imbalance may exist locally in the periodontitis lesion and that this imbalance may be antigen specific. RECENT EVIDENCE: More recently, T cell subsets have been dichotomised on the basis of their cytokine profiles. In general, Thl cells produce IL‐2 and IFN‐gamma while Th2 cells produce IL‐4, IL‐5 and IL‐6. The major function of Th l cells is to mediate delayed type hypersensitivity. In contrast the major function of Th2 cells is to provide B cell help.HYPOTHESIS: A model for periodontal disease has now been developed based on this functional dichotomy which provides a framework for the study of cytokine profiles in periodontal disease. Early studies in this context have demonstrated a higher proportion of IL‐4 producing cells in periodontitis tissues suggesting a role for Th2 cells in the progressive lesion. Clonal studies have shown that the selection of a particular cytokine profile is not antigen dependent and that differences may be due to the host susceptibility although this remains to be determined.CONCLUSION: These emerging data clearly establish a role for cell‐mediated mechanisms in the control of periodontal destruction and raise the possibility that in the future cytokine therapy for the treatment of periodontal disease in susceptible subjects may becom
ISSN:1354-523X
DOI:10.1111/j.1601-0825.1996.tb00209.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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16. |
The use of micromachined surfaces to investigate the cell behavioural factors essential to osseointegration |
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Oral Diseases,
Volume 2,
Issue 1,
1996,
Page 102-115
J Qu,
B Chehroudi,
DM Brunette,
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摘要:
OBJECTIVE: Although currently available implants can be used to achieve osseointegration under well‐defined conditions, a greater understanding of cell behaviour is required to improve the designs and embark on actual tissue engineering.MATERIALS AND METHODS: We employed micromachined substrata to investigate some of the main behavioural responses of osteoblasts from rat fetal calvaria to surface topography. In particular, confocal laser scanning microscopy (CLSM), differential interference contrast microscopy, time‐lapse cinemicrography, immunofluo‐rescence, digital radiography and image analysis were used to investigate cell adhesion, cell shape and cytoske‐leton distribution, tissue organization, cell differentiation, and microenvironment.RESULTS AND CONCLUSIONS A grooved surface permitted the attachment of more cells than a smooth one. Cell shape and cytoskeleton were strikingly influenced as early as 20 min after cell attachment, when the cytoskeleton begins to align with the topography. Some grooved surfaces appeared to promote osteogenesis in vitro as assessed by the production of bone‐like nodules. Moreover, these nodules align with the topographyin vitro, and preliminary results indicate that bone‐like tissue also aligns with grooves when such surfaces are implan
ISSN:1354-523X
DOI:10.1111/j.1601-0825.1996.tb00210.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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