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FasL is a catabolic factor in alveolar bone homeostasis

KA. Apaza Alccayhuaman, P. Heimel, JS. Lee, S. Tangl, U. Kuchler, J. Marchesan, L. Panahipour, S. Lettner, E. Matalová, R. Gruber

. 2023 ; 50 (3) : 396-405. [pub] 20221125

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc23004040

AIM: Fas ligand (FasL) belongs to the tumour necrosis factor superfamily regulating bone turnover, inflammation, and apoptosis. The appendicular and axial skeleton phenotype of mature Faslgld mice has been reported. The impact of FasL on the alveolar bone providing support for the teeth at mature stages under healthy and induced inflammatory conditions remains unknown. MATERIALS AND METHODS: We performed a phenotypical analysis of mice carrying the homozygous Faslgld mutation and wild-type (WT) mice (C57BL/6) under healthy conditions and upon ligature-induced periodontitis. After 12 days, micro-computed tomography analysis revealed the distance between the cement enamel junction and the alveolar bone crest. Additional structural parameters, such as the bone volume fraction (BV/TV) and the periodontal ligament space volume, were measured. Histological analyses were performed to visualize the catabolic changes at the defect site. RESULTS: Healthy Faslgld mice were found to have more periodontal bone than their WT littermates. Faslgld had no significant effect on inflammatory osteolysis compared to WT controls with ligatures. Histology revealed eroded surfaces at the root and in the inter-proximal bone in both strains. CONCLUSIONS: Our findings suggest that FasL is a catabolic factor in alveolar bone homeostasis but it does not affect the inflammatory osteolysis.

Citace poskytuje Crossref.org

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$a Apaza Alccayhuaman, Karol Alí $u Department of Oral Biology, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria $u Karl Donath Laboratory for Hard Tissue and Biomaterial Research, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria $1 https://orcid.org/0000000345655222
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$a AIM: Fas ligand (FasL) belongs to the tumour necrosis factor superfamily regulating bone turnover, inflammation, and apoptosis. The appendicular and axial skeleton phenotype of mature Faslgld mice has been reported. The impact of FasL on the alveolar bone providing support for the teeth at mature stages under healthy and induced inflammatory conditions remains unknown. MATERIALS AND METHODS: We performed a phenotypical analysis of mice carrying the homozygous Faslgld mutation and wild-type (WT) mice (C57BL/6) under healthy conditions and upon ligature-induced periodontitis. After 12 days, micro-computed tomography analysis revealed the distance between the cement enamel junction and the alveolar bone crest. Additional structural parameters, such as the bone volume fraction (BV/TV) and the periodontal ligament space volume, were measured. Histological analyses were performed to visualize the catabolic changes at the defect site. RESULTS: Healthy Faslgld mice were found to have more periodontal bone than their WT littermates. Faslgld had no significant effect on inflammatory osteolysis compared to WT controls with ligatures. Histology revealed eroded surfaces at the root and in the inter-proximal bone in both strains. CONCLUSIONS: Our findings suggest that FasL is a catabolic factor in alveolar bone homeostasis but it does not affect the inflammatory osteolysis.
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$a Heimel, Patrick $u Karl Donath Laboratory for Hard Tissue and Biomaterial Research, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria $u Department for Bioimaging, Ludwig Boltzmann Institute for Traumatology, The Research Center in Cooperation With AUVA, Vienna, Austria $u Austrian Cluster for Tissue Regeneration, Vienna, Austria
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$a Lee, Jung Seok $u Department of Oral Biology, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria $u Department of Periodontology, Research Institute for Periodontal Regeneration, College of Dentistry, Yonsei University, Seoul, Republic of Korea $1 https://orcid.org/0000000312765978
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$a Tangl, Stefan $u Karl Donath Laboratory for Hard Tissue and Biomaterial Research, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria $u Austrian Cluster for Tissue Regeneration, Vienna, Austria
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$a Kuchler, Ulrike $u Department of Oral Surgery, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria
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$a Marchesan, Julie $u Division of Comprehensive Oral Health, Adams School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
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$a Panahipour, Layla $u Department of Oral Biology, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria
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$a Lettner, Stefan $u Karl Donath Laboratory for Hard Tissue and Biomaterial Research, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria $u Austrian Cluster for Tissue Regeneration, Vienna, Austria
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$a Matalová, Eva $u Laboratory of Odontogenesis and Osteogenesis, Institute of Animal Physiology and Genetics, Czech Academy of Sciences, Brno, Czech Republic
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$a Gruber, Reinhard $u Department of Oral Biology, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria $u Austrian Cluster for Tissue Regeneration, Vienna, Austria $u Department of Periodontology, School of Dental Medicine, University of Bern, Bern, Switzerland $1 https://orcid.org/0000000154009009
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