Experimental model of tooth movement by orthodontic force in mice and its application to tumor necrosis factor receptor-deficient mice.
Orthodontic tooth movement is achieved by mechanical loading; however, the biological mechanism involved in this process is not clearly understood owing to the lack of a suitable experimental model. In the present study, we established an orthodontic tooth movement model in mice using a Ni-Ti closed coil spring that was inserted between the upper incisors and the upper first molar. Histological examination demonstrated that the orthodontic force moved the first upper molar mesially without necrosis of the periodontium during tooth movement. The number of TRAP-positive osteoclasts on the pressure side significantly increased in a time-dependent manner. Quantitative real time-based reverse transcription-polymerase chain reaction analysis demonstrated increased levels of mRNA for cathepsin K. Immunohistochemical staining revealed the expression of tumor necrosis factor-alpha (TNFalpha) in periodontium on the pressure side of the first molar during orthodontic tooth movement. When this tooth movement system was applied to TNF type 1 receptor-deficient mice and TNF type 2 receptor-deficient mice, tooth movement observed in TNF type 2 receptor-deficient mice was smaller than that in the wild-type mice and TNF type 1 receptor-deficient mice. The number of TRAP-positive osteoclasts on the pressure side was significantly small in TNF type 2 receptor-deficient mice compared with that in TNF type 1 receptor-deficient mice on day 6 after application of the appliance. The present study indicates that TNFalpha signaling plays some important roles in orthodontic tooth movement.
Yoshimatsu
Masako
M
Division of Oral Pathology and Bone Metabolism, Department of Developmental and Reconstructive Medicine, Nagasaki University, Graduate School of Biomedical Sciences, Nagasaki, Japan.
Shibata
Yasuaki
Y
Kitaura
Hideki
H
Chang
Xin
X
Moriishi
Takeshi
T
Hashimoto
Fumio
F
Yoshida
Noriaki
N
Yamaguchi
Akira
A
D000135:Acid Phosphatase; D000818:Animals; D001696:Biomechanical Phenomena; D016723:Bone Remodeling; D056657:Cathepsin K; D002403:Cathepsins / Q000096:biosynthesis* / Q000235:genetics; D007527:Isoenzymes; D051379:Mice; D018345:Mice, Knockout; D023421:Models, Animal; D010010:Osteoclasts / Q000166:cytology / Q000378:metabolism; D010519:Periodontium / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000172:deficiency; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000172:deficiency; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071681:Tartrate-Resistant Acid Phosphatase; D014070:Tooth / Q000166:cytology; D014087:Tooth Movement Techniques; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D007527:Isoenzymes; D012333:RNA, Messenger; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase; D002403:Cathepsins; D056657:Cathepsin K; C534132:Ctsk protein, mouse