Dental and periodontal phenotype in sclerostin knockout mice.
Sclerostin is a Wnt signalling antagonist that controls bone metabolism. Sclerostin is expressed by osteocytes and cementocytes; however, its role in the formation of dental structures remains unclear. Here, we analysed the mandibles of sclerostin knockout mice to determine the influence of sclerostin on dental structures and dimensions using histomorphometry and micro-computed tomography (μCT) imaging. μCT and histomorphometric analyses were performed on the first lower molar and its surrounding structures in mice lacking a functional sclerostin gene and in wild-type controls. μCT on six animals in each group revealed that the dimension of the basal bone as well as the coronal and apical part of alveolar part increased in the sclerostin knockout mice. No significant differences were observed for the tooth and pulp chamber volume. Descriptive histomorphometric analyses of four wild-type and three sclerostin knockout mice demonstrated an increased width of the cementum and a concomitant moderate decrease in the periodontal space width. Taken together, these results suggest that the lack of sclerostin mainly alters the bone and cementum phenotypes rather than producing abnormalities in tooth structures such as dentin.
1] Department of Oral Surgery, Medical University of Vienna, Vienna, Austria [2] Austrian Cluster for Tissue Regeneration, Vienna, Austria [3] Department of Oral Surgery and Stomatology, School of Dental Medicine, University of Berne, Berne, Switzerland.
Ulrike
U
Kuchler
1] Department of Oral Surgery, Medical University of Vienna, Vienna, Austria [2] Austrian Cluster for Tissue Regeneration, Vienna, Austria [3] Karl Donath Laboratory for Hard Tissue and Biomaterial Research, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria.
Uwe Y
UY
Schwarze
1] Department of Oral Surgery, Medical University of Vienna, Vienna, Austria [2] Austrian Cluster for Tissue Regeneration, Vienna, Austria [3] Karl Donath Laboratory for Hard Tissue and Biomaterial Research, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria.
Toni
T
Dobsak
1] Department of Oral Surgery, Medical University of Vienna, Vienna, Austria [2] Austrian Cluster for Tissue Regeneration, Vienna, Austria [3] Karl Donath Laboratory for Hard Tissue and Biomaterial Research, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria [4] Ludwig Boltzmann Institute for Experimental and Clinical Traumatology in AUVA Research Center, Vienna, Austria.
Patrick
P
Heimel
1] Department of Oral Surgery and Stomatology, School of Dental Medicine, University of Berne, Berne, Switzerland [2] Robert K. Schenk Laboratory of Oral Histology, School of Dental Medicine, University of Berne, Berne, Switzerland.
Dieter D
DD
Bosshardt
Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Basel, Switzerland.
Michaela
M
Kneissel
1] Department of Oral Surgery, Medical University of Vienna, Vienna, Austria [2] Austrian Cluster for Tissue Regeneration, Vienna, Austria [3] Laboratory of Oral Cell Biology, School of Dental Medicine, University of Berne, Berne, Switzerland.
Reinhard
R
Gruber
D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D005260:Female; D006023:Glycoproteins / Q000235:genetics*; D036341:Intercellular Signaling Peptides and Proteins; D051379:Mice; D018345:Mice, Knockout; D010519:Periodontium / Q000378:metabolism*; D010641:Phenotype; D014070:Tooth / Q000378:metabolism*
D048868:Adaptor Proteins, Signal Transducing; D006023:Glycoproteins; D036341:Intercellular Signaling Peptides and Proteins; C486030:Sost protein, mouse