Experimental model of tooth movement by orthodontic force in mice and its application to tumor necrosis factor receptor-deficient mice

Abstract

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.

TNF-α Aggravates the Progression of Orthodontically-induced Inflammatory Root Resorption in the Presence of RANKL

“…This is consistent with reports from Yoshimatsu et al 15) and from In the agreement with these results, previous reports described elevated levels of TNF-α and RANKL in compression side following mechanical loading [18][19][20][21] . Given that the TNF-α and RANKL participate in osteoclastogenesis by upregulating osteoclast activity.…”

“…Experimental tooth movement was induced using the method reported by Yoshimatsu et al 15) with a Nickel-Titanium (Ni-Ti)…”

CCAAT/enhancer binding protein β-deficiency enhances type 1 diabetic bone phenotype by increasing marrow adiposity and bone resorption

“…Tartrateresistant acid phosphatase (TRAP5) was amplified using 5=-AAT GCC TCG ACC TGG GA-3= and 5=-CGT AGT CCT CCT TGG CTG CT-3= (63). Cathepsin K was amplified using 5=-GCA GAG GTG TGT ACT ATG-3= and 5=-GCA GGC GTT GTT CTT ATT-3= (67). Amplicons were compared with a 100 bp DNA ladder (Invitrogen, Carlsbad, CA) on a 2% agarose gel to verify RT-PCR results and to verify the absence of C/EBP␤ in the knockout animals.…”

Effect of Macrophage Colony-Stimulating Factor Receptor c-Fms Antibody on Lipopolysaccharide-Induced Pathological Osteoclastogenesis and Bone Resorption

“…However, the relationship between orthodontic movement and TNF-α is not fully understood as yet. Blocking M-CSF with an anti-c-Fms antibody was shown to inhibit osteoclast formation and tooth movement [39]. These results suggest that control of M-CSF could regulate osteoclast formation and subsequent orthodontic tooth movement.…”

“…During one study, the anti-c-Fms antibody was locally injected adjacent to the first molar every other day during the experimental period. The anti-c-Fms antibody was found to inhibit odontoclastogenesis and root resorption during orthodontic tooth movement [39].…”