PubMed · 9540526
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D D Epstein. 1994. Why overdentures?. https://pubmed.ncbi.nlm.nih.gov/9540526/
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Endochondral bone formation includes a cascade of cellular events such as proliferation, maturation, hypertrophic conversion and calcification of chondrocytes and the cartilage replacement by bone. During these processes, hypertrophic conversion and calcification of chondrocytes (the late-phase differentiation) is a crucial process of chondrogenic differentiation. Indian hedgehog (Ihh), a secreted protein expressed in early hypertrophic chondrocytes, is thought to be involved in regulation of hypertrophic conversion via a feedback loop through the perichondrium. In the present study, we showed by Northern analysis and in situ hybridization that Smoothened (Smo), a key component in hedgehog signal transduction, was expressed in chondrocytes in both adult mice and mouse embryos at 16 days post-coitum in vivo, suggesting that Ihh directly acts on chondrocytes. We previously reported that Ihh, Patched and Smo were all expressed in differentiated ATDC5 cells. Exogenously administered mouse recombinant N-terminal protein of Ihh (mrIhh-N) upregulated the gene expression of type X collagen, a phenotypic marker of hypertrophic chondrocytes, as well as osteoprotegerin ligand (OPGL), a potent stimulator of osteoclastogenesis and osteoclast activity, while it did not modulate the expression of Ihh itself, bone morphogenetic protein (BMP)-4, BMP-6, transforming growth factor (TGF)-beta1 and TGF-beta2 in differentiated ATDC5 cells. Moreover, when added to the osteoclast cultures, mrIhh-N markedly stimulated the formation of resorption pits on dentine slices. Our data support the hypothesis that Ihh stimulated the late-phase chondrogenic differentiation in differentiated ATDC5 cells and upregulated the gene expression of OPGL in these cells.
Exudative macrophages are the most prevalent inflammatory cells during the entire pathogenetic process in experimentally induced rat periapical lesions. To clarify the significance of macrophages in the pathogenesis of periapical lesions, the way in which the phenotype of ED1 (a general marker for mononuclear phagocytes)-positive cells is modulated in actively expanding lesions was investigated, by immunoperoxidase staining with a panel of antibodies that recognize several activation-associated molecules on macrophages. Periapical lesions were induced experimentally by exposing the pulp in the lower first molars of Wistar rats. Active lesion expansion with morphological diversification of ED1-positive cells occurred between 14 and 28 days after the injury. Double immunoperoxidase staining revealed that ED1-positive cells coexpressing class II molecules of the major histocompatibility complex (MHC) molecules, inducible nitric oxide synthase (iNOS) and/or CD11a increased during the period of active lesion expansion. Increases of endothelial cells expressing intracellular adhesion molecule-1 and CD25 (interleukin-2 receptor)-expressing lymphocytes were also seen during the same period. Moreover, there existed two particular subpopulations of ED1 + cells in the established lesion at 28 days: (1) ED1++/class II MHC - /iNOS+ cells, located around the periapical abscess, and (2) ED1+/class II MHC+/ iNOS- cells with slender or dendritic morphology, distributed predominantly in the outer portion of the lesion where T lymphocytes were abundant. The first cell type could be a macrophage with potent phagocytic and antimicrobial actions, and the second might possess sufficient antigen-presenting capacity to cause the activation of T lymphocytes. It was concluded that macrophages, when activated, may participate in triggering lesion expansion. Functionally distinct subpopulations of macrophages may occupy different sites within the lesion where they can most effectively exert their specific functions.
Periapical bone destruction earlier was shown to be mediated primarily by interleukin (IL)-1alpha in a rat model. The production and action of IL-1alpha is in turn potentially modulated by a network of cytokines, which are produced by infiltrating T-helper type 1 (Th1) and type 2 (Th2) lymphocytes, and resident connective tissue cells within the lesion. This study was designed to examine the kinetics of expression of 10 cytokines in experimentally induced murine periapical lesions, including bone-resorptive [IL-1alpha, tumour necrosis factor alpha (TNFalpha), IL-6, IL-11], Th1-type [IL-2, IL-12, interferon-gamma (IFNgamma)] and Th2-type (IL-4, IL-6, IL-10, IL-13) mediators. Cytokine mRNA expression was assessed qualitatively by reverse transcription-polymerase chain reaction, and cytokine proteins quantified by enzyme-linked immunosorbent assay. IL-1alpha and TNFalpha protein and mRNA were highly expressed, beginning on day 7, and increased to day 28. IL-6 increased to day 14 and then declined, whereas the expression of IL-11 was not modulated by pulp exposure. Most of the Th1-type cytokines, including IL-2, IL-12, and IFNgamma, showed an increase in mRNA and/or protein expression in periapical lesions after pulpal exposure; the expression of Th2-type cytokines was similarly increased, but had declined at the latest time-point (day 28), suggesting possible inhibition by Th1-type mediators. Significant correlations were observed between levels of IL-1alpha and Th1-derived pro-inflammatory mediators IL-2, IL-12, TNFalpha, and IFNgamma. There was a lack of correlation between IL-1alpha and Th2-type anti-inflammatory mediators, including IL-4, -6, and -10. These results indicate that a cytokine network is activated in the periapex in response to bacterial infection, and that Th1-modulated pro-inflammatory pathways may predominate during periapical bone destruction.