title: Morphological and cellular examinations of experimentally induced malocclusion in mice mandibular condyle.
abstract: Occlusal alignment is known clinically to have a widespread influence on the stomatognathic system, including the temporomandibular joint and masticatory muscles. However, while occlusion is still an important determinant of most dental treatments, the exact effect of occlusal alignment is unclear because of a lack of conclusive scientific evidence. In this study, a malocclusion model system is used to examine the cellular and histologic alterations in the contralateral condyle of mice after a malocclusion was induced by a build-up of resin on the left maxillary molars. A significant decrease in the thickness of the condylar cartilage was found in the 1-week experimental group, together with increased apoptosis and decreased proliferation in the condylar head, which included cartilage and subchondral bone. Additionally, the number of TRAP-positive osteoclasts and MPO- and F4/80-positive inflammatory cells in the subchondral bone were significantly higher in the 1-week experimental group. Unbalanced malocclusion caused increased bone remodeling, as evidenced by increased osteoclastic activity and inflammatory responses (macrophages and neutrophils, respectively). However, these alterations in the 1-week experimental group were subsequently attenuated and restored almost to the baseline at 3 weeks after the induction of the malocclusion.
authors: Department of Oral Medicine, School of Dentistry, Kyungpook National University, Daegu, South Korea.
authors: Jae-Kwang
authors: JK
authors: Jung
authors: Wern-Joo
authors: WJ
authors: Sohn
authors: Youngkyun
authors: Y
authors: Lee
authors: Yong Chul
authors: YC
authors: Bae
authors: Jae-Kap
authors: JK
authors: Choi
authors: Jae-Young
authors: JY
authors: Kim
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D021621:Imaging, Three-Dimensional; D020287:In Situ Nick-End Labeling; D007527:Isoenzymes / Q000378:metabolism; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008310:Malocclusion / Q000139:chemically induced* / Q000473:pathology*; D008335:Mandibular Condyle / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009195:Peroxidase / Q000378:metabolism; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D007527:Isoenzymes; D019394:Ki-67 Antigen; D009195:Peroxidase; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase