AI Article Synopsis

  • * The research highlights how SPOCK-1, an important protein, contributes to gum thickening by promoting changes in gum cell behavior while also examining its role alongside inflammation and cyclosporin-A (CsA) in enhancing DIGO in mouse models.
  • * Findings indicate that Spock1-Tg mice, which overexpress SPOCK-1, experienced greater gingival overgrowth and bone loss when treated with CsA, suggesting that increased collagen production and inflammation play a significant part in the development of DIGO in this context.

Article Abstract

Drug-induced gingival overgrowth (DIGO), induced by certain immunosuppressive drugs, antihypertensive agents, and antiepileptic drugs, may contribute to the formation of deeper periodontal pockets and intractableness in periodontitis. To date, multiple factors such as enhanced matrix production, inflammation, and reduced matrix degradation might be involved in the pathogenesis of DIGO. We have previously reported that SPOCK-1, a heparan sulfate proteoglycan, could affect gingival thickening by promoting epithelial-to-mesenchymal transition (EMT) in gingival keratinocytes. However, few studies have investigated whether a combination of these factors enhances the DIGO phenotype in animal models. Therefore, we investigated whether SPOCK-1, periodontal inflammation, and cyclosporin-A (CsA) could cooperatively promote gingival overgrowth. We first confirmed that Spock-1 overexpressing (Spock1-Tg) mice showed significantly thicker gingiva and greater alveolar bone loss than WT mice in response to ligature-induced experimental periodontitis. DIGO was induced by the combination of CsA administration and experimental periodontitis was significantly enhanced in Spock1-Tg mice compared to that in WT mice. Ligature-induced alveolar bone loss in CsA-treated Spock1-Tg mice was also significantly greater than that in CsA-treated WT mice, while being accompanied by an increase in and levels and a reduction in matrix metalloprotease expression. Lastly, SPOCK-1 promoted RANKL-induced osteoclast differentiation in both human peripheral blood mononuclear cells and murine macrophages, while peritoneal macrophages from Spock1-Tg mice showed less TNFα and IL-1β secretion than WT mice in response to lipopolysaccharide. These results suggest that EMT, periodontal inflammation, and subsequent enhanced collagen production and reduced proteinase production contribute to CsA-induced DIGO pathogenesis.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10753830PMC
http://dx.doi.org/10.3389/fphys.2023.1298813DOI Listing

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Article Synopsis
  • * The research highlights how SPOCK-1, an important protein, contributes to gum thickening by promoting changes in gum cell behavior while also examining its role alongside inflammation and cyclosporin-A (CsA) in enhancing DIGO in mouse models.
  • * Findings indicate that Spock1-Tg mice, which overexpress SPOCK-1, experienced greater gingival overgrowth and bone loss when treated with CsA, suggesting that increased collagen production and inflammation play a significant part in the development of DIGO in this context.
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SPOCK1 induces adipose tissue maturation: New insights into the function of SPOCK1 in metabolism.

Biochem Biophys Res Commun

December 2020

Section of Periodontology, Kyushu University Faculty of Dental Science, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. Electronic address:

SPOCK1 is a calcium-binding matricellular proteoglycan that has been extensively studied in several cancer cells. Previously, we generated a mouse line overexpressing SPOCK1 (Spock1-Tg mouse) and showed that SPOCK1 might play an important role in drug-induced gingival overgrowth, indicating that it possesses physiological functions in non-cancer diseases as well. Although SPOCK1 was reported to be secreted from human adipocytes, its role in adipocyte physiology has not been addressed yet.

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