FasL is a catabolic factor in alveolar bone homeostasis

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F23%3A00568970" target="_blank" >RIV/67985904:_____/23:00568970 - isvavai.cz</a>

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/10.1111/jcpe.13750" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1111/jcpe.13750</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/jcpe.13750" target="_blank" >10.1111/jcpe.13750</a>

Jazyk výsledku

angličtina

Název v původním jazyce

FasL is a catabolic factor in alveolar bone homeostasis

Popis výsledku v původním jazyce

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 Fasl(gld) 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 Fasl(gld) 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 Fasl(gld) mice were found to have more periodontal bone than their WT littermates. Fasl(gld) 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.

Název v anglickém jazyce

FasL is a catabolic factor in alveolar bone homeostasis

Popis výsledku anglicky

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 Fasl(gld) 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 Fasl(gld) 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 Fasl(gld) mice were found to have more periodontal bone than their WT littermates. Fasl(gld) 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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/GF19-29667L" target="_blank" >GF19-29667L: FasL v osteogenezi, zdraví a nemoci parodontu</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Clinical Periodontology

ISSN

0303-6979

e-ISSN

1600-051X

Svazek periodika

50

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

396-405

Kód UT WoS článku

000890832000001

EID výsledku v databázi Scopus

2-s2.0-85142602948