Osteoporotic Changes in the Periodontium Impair Alveolar Bone Healing.

atrophy osteogenesis osteoporosis periodontal ligament repair tooth extraction

Journal

Journal of dental research
ISSN: 1544-0591
Titre abrégé: J Dent Res
Pays: United States
ID NLM: 0354343

Informations de publication

Date de publication:
04 2019
Historique:
pubmed: 11 1 2019
medline: 30 1 2020
entrez: 11 1 2019
Statut: ppublish

Résumé

Osteoporosis is associated with decreased bone density and increased bone fragility, but how this disease affects alveolar bone healing is not clear. The objective of this study was to determine the extent to which osteoporosis affects the jaw skeleton and then to evaluate possible mechanisms whereby an osteoporotic phenotype might affect the rate of alveolar bone healing following tooth extraction. Using an ovariectomized mouse model coupled with micro-computed tomographic imaging, histologic, molecular, and cellular assays, we first demonstrated that the appendicular and jaw skeletons both develop osteoporotic phenotypes. Next, we demonstrated that osteoporotic mice exhibit atrophy of the periodontal ligament (PDL) and that this atrophy was accompanied by a reduction in the pool of osteoprogenitor cells in the PDL. The paucity of PDL-derived osteoprogenitor cells in osteoporotic mice was associated with significantly slower extraction socket healing. Collectively, these analyses demonstrate that the jaw skeleton is susceptible to the untoward effects of osteoporosis that manifest as thinner, more porous alveolar bone, PDL thinning, and slower bone repair. These findings have potential clinical significance for older osteopenic patients undergoing reconstructive procedures.

Identifiants

pubmed: 30626268
doi: 10.1177/0022034518818456
pmc: PMC6429667
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

450-458

Subventions

Organisme : NIDCR NIH HHS
ID : R01 DE024000
Pays : United States

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Auteurs

M Arioka (M)

1 Division of Plastic and Reconstructive Surgery, Department of Surgery, School of Medicine, Stanford University, Stanford, CA, USA.
2 Department of Clinical Pharmacology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.

X Zhang (X)

1 Division of Plastic and Reconstructive Surgery, Department of Surgery, School of Medicine, Stanford University, Stanford, CA, USA.
3 State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Z Li (Z)

1 Division of Plastic and Reconstructive Surgery, Department of Surgery, School of Medicine, Stanford University, Stanford, CA, USA.
4 Department of Orthopedics, Tianjin Medical University General Hospital, Tianjin, China.

U S Tulu (US)

1 Division of Plastic and Reconstructive Surgery, Department of Surgery, School of Medicine, Stanford University, Stanford, CA, USA.

Y Liu (Y)

1 Division of Plastic and Reconstructive Surgery, Department of Surgery, School of Medicine, Stanford University, Stanford, CA, USA.
3 State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

L Wang (L)

3 State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

X Yuan (X)

1 Division of Plastic and Reconstructive Surgery, Department of Surgery, School of Medicine, Stanford University, Stanford, CA, USA.

J A Helms (JA)

1 Division of Plastic and Reconstructive Surgery, Department of Surgery, School of Medicine, Stanford University, Stanford, CA, USA.

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