Occlusal stimuli influence on the expression of IGF-1 and the IGF-1 receptor in the rat periodontal ligament
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Termsuknirandorn, Saewadee
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Tokyo Med & Dent Univ, Grad Sch, Div Oral Hlth Sci, Dept Orofacial Dev & Funct,Bunkyo Ku, Tokyo 1138549, JapanTokyo Med & Dent Univ, Grad Sch, Div Oral Hlth Sci, Dept Orofacial Dev & Funct,Bunkyo Ku, Tokyo 1138549, Japan
Termsuknirandorn, Saewadee
[1
]
Hosomichi, Jun
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Tokyo Med & Dent Univ, Grad Sch, Div Oral Hlth Sci, Dept Orofacial Dev & Funct,Bunkyo Ku, Tokyo 1138549, JapanTokyo Med & Dent Univ, Grad Sch, Div Oral Hlth Sci, Dept Orofacial Dev & Funct,Bunkyo Ku, Tokyo 1138549, Japan
Hosomichi, Jun
[1
]
Soma, Kunimichi
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Tokyo Med & Dent Univ, Grad Sch, Div Oral Hlth Sci, Dept Orofacial Dev & Funct,Bunkyo Ku, Tokyo 1138549, JapanTokyo Med & Dent Univ, Grad Sch, Div Oral Hlth Sci, Dept Orofacial Dev & Funct,Bunkyo Ku, Tokyo 1138549, Japan
Soma, Kunimichi
[1
]
机构:
[1] Tokyo Med & Dent Univ, Grad Sch, Div Oral Hlth Sci, Dept Orofacial Dev & Funct,Bunkyo Ku, Tokyo 1138549, Japan
Objective: To test the hypothesis that hypofunction/recovered occlusal function has no effect on the changes in insulin-like growth factor-1 (IGF-1) and IGF-1 receptor expressions and cell proliferation of periodontal ligament (PDL) cells. Materials and Methods: To produce occlusal hypofunction, the appliances were attached to the rats' maxillary and mandibular incisors. Subsequently, occlusal contact of the molar area was thoroughly recovered by removal of the appliances. Results: In periodontal sections, localization of IGF-1, the IGF-1 receptor, and proliferating cell nuclear antigen (PCNA) immunoreactive cells was significantly more expressed in the control group compared with the hypofunctional group (P <.01). In addition, after the recovery of the occlusion, IGF-1, IGF-1 receptor, and PCNA were detected significantly much more than in the hypofunction group (P <.01). Conclusion: The hypothesis was rejected. This study suggests that occlusal stimuli induce cell proliferation of PDL cells by increasing IGF-1 and IGF-1 receptor expression.