• The korean journal of orthodontics
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• v.38 no.3
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• pp.187-201
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• 2008

Objective: The aim of this study was to determine whether cortical punching stimulates the expression of matrix metalloproteinase-1, -8, and -13 in orthodontic tooth movement in rats. Methods: A total of 32 male sprague-dawley rats at 15 weeks old were divided into two groups of 16 rats each, to form the tooth movement with cortical punching (TMC) group and tooth movement only (TM) group. A total of 20 gm of orthodontic force was applied to rat incisors to cause experimental tooth movement. Cortical punching was performed on the palatal side near the central incisor with a 1.0 mm width microscrew in the TMC group. The duration of tooth movement was 1, 4, 7, and 14 days. Results: Measurements of the mRNA expression were selected as the means to determine the identification of expression of MMP-1, -8, and -13. In the TMC group, the expression of collagen type I was greater than that of the TM group from day 4 to day 14. Expression of TIMP-1 in the TM group was greater than that of the TMC group in the pressure side of PDL and alveolar bone cell at day 4. In the TMC group, TIMP-1 was expressed at the osteoclast, but not at the tooth surface of the TM group at day 14, Maximum induction of the mRNA of MMP-1 was observed on day 4 in the TMC group, but it was observed on day 7 in the TM group. MMP-8 mRNA of the TMC group was twice greater than that of the TM group at f days. In the TMC group, maximum induction of MMP-13 mRNA was observed on day 1. Conclusions: These findings suggested that cortical punching can stimulate remodeling of PDL and alveolar bone connective tissues during experimental orthodontic tooth movement in rats.

• Journal of Oral Medicine and Pain
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• v.31 no.2
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• pp.185-197
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• 2006

The aim of this study was to investigate the beneficial effect of a daily dose of 300 mg of ASU taken for more than 3 months on the subjects diagnosed as osteoarthritis of temporomandibular joint by RDC/TMD. Total 68 outpatients(15-54y) of female except menopause in Orofacial Pain Clinics of the Pusan National University Hospital were randomly assigned to either an ASU group(n=36) or a placebo group(n=32). The pain, noise and limited mouth opening(LOM) were evaluated by numerical analogue scale(NAS, range 0-10) and maximum comfortable opening(MCO) were measured by milimeter scale. The difference of simple uptake rate(SUR) on bone scan, hot spot(HS) on coronal SPECT, condylar bony changes on CT between the ASU and placebo groups were compared to investigate the objective effect. The obtained results were as follows. 1. Comparison of the NAS of pain, noise, LOM and MCO before treatment and 3, 6 and 9 months after treatment showed no significant difference between the ASU and placebo groups. 2. Comparison of the NAS of pain, noise, LOM and MCO before treatment and 3, 6 and 9 months after treatment showed no significant difference between the ASU and placebo groups without splint treatment, but showed more increased MCO in the ASU group than the placebo group with splint treatment at 6, 9 months after treatment. 3. Comparison of the NAS of pain before treatment and 3, 6 and 9 months after treatment that the NAS of pain at first visit divided into two groups(above or below 6) showed more decreased the NAS of pain in the ASU group than the placebo group that the NAS of pain at first visit was above 6. 4. Comparison of the NAS of pain, noise, LOM and MCO during 6 months period showed improvement of clinical symptoms within group, but no significant difference between subjects. 5. The simple uptake ratio(SUR) on bone scan and hot spot(HS) on coronal SPECT showed more increased SUR and HS in affected side than non-affected side of the ASU and placebo groups. 6. Comparing of condylar bony changes, osseous remodeling were observed highest, osteophyte lowest in the affected and non-affected side of the two groups. After treatment, comparison of condylar bony changes were observed more decreased erosive features in the ASU group than the placebo group.

• Journal of Oral Medicine and Pain
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• v.33 no.2
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• pp.195-204
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• 2008

Osteoarthritis is caused by joint degeneration, a process that includes progressive loss of articular cartilage accompanied by attempted repair of articular cartilage, remodeling and sclerosis of subchondral bone, and osteophyte formation. The most common causative factor that either causes or contributes to osteoarthritis is overloading of the articular structures of the joint. The diagnosis of temporomandibular joint(TMJ) osteoarthritis is based on the patient's history and clinical findings such as limited mandibular opening, crepitation and tenderness to palpation on TMJ. The diagnosis is usually confirmed by TMJ radiographs, which will reveal evidence of structural changes in the subarticular bone of the condyle or fossa. Plain radiography techniques such as panoramic, transcranial, transpharyngeal views can be used in most dental offices for evaluation of the TMJs. However, plain radiographs are often limited due to overlapping and distortion of anatomical structures. The aim of this study was to compare the clinical examination and panoramic view with computed tomography for diagnosis of temporomandibular degenerative joint disease, and to compare the findings of condylar bony changes through panoramic radiography with that of computed tomography, hence, to confirm the limitations of clinical and panoramic radiography, and the validity of the computed tomography for diagnosis of temporomandibular degenerative joint disease. The pathophysiology of the TMJ osteoarthritis remains poorly understood, and current treatments are based more on speculation than science, and symptomatic treatments often fail to provide satisfactory pain relief. For diagnosis of TMJ osteoarthritis, clinical examination and radiographic examination for confirmation of the bony changes are essential, and computed tomography are clearly superior to plain radiographs for their limitations.

• The korean journal of orthodontics
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• v.36 no.4
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• pp.242-250
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• 2006

Objective: Periodontal ligament fibroblasts have an ectomesenchymal origin and are thought to play a crucial role for not only homeostasis of periodontal tissues but also bone remodeling, wound healing and regeneration of tissues. Recently, it has been reported that UNC-50 is not expressed in gingival fibroblasts but in PDL fibroblasts. The purpose of this study was to examine the expression of UNC-50 and osteocalcin in the periodontium after application of intermittent force. Methods: Twelve rats had 40 grams of mesially-directed force applied at the upper molar for 1 hour/day. Four rats were sacrificed at 1, 3 and 5 days. Immunohistochemical localization of UNC-50 and osteocalcin antibody was carried out. The results showed apposition of new cellular cementum and a slight increase in periodontal space at the tension side. Results: Strong UNC-50 expression was observed in the differentiating cementoblasts close to PDL fibroblasts in the tension side whereas it was barely expressed at the compression side. Expression was strong at day 3, and decreased at day 5. Osteocalcin immunoreactivity expression was strong in differentiating cementoblasts at the tension side. Conclusion: It can be suggested that UNC-50 is related to the differentiation of cementoblasts, and may be responsible for the molecular event in PDL cells under mechanical stress.

• The korean journal of orthodontics
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• v.33 no.3 s.98
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• pp.169-183
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• 2003

Tooth movement by orthodontic force effects great tissue changes within the periodontium, especially by shifting the blood flow in the pressure side and resulting in a hypoxic state of low oxygen tension. The aim of this study is to elucidate the possible mechanism of apoptosis in response to hypoxia in MC3T3El osteoblasts, the main cells in bone remodeling during orthodontic tooth movement. MC3T3El osteoblasts under hypoxic conditions ($2\%$ orygen) resulted in apoptosis in a time-dependent manner as estimated by DNA fragmentation assay and nuclear morphology stained with fluorescent dye, Hoechst 33258. Pretreatment with Z-VAD-FMK, a pancaspase inhibitor, or Z-DEVD-CHO, a specific caspase-3 inhibitor, completely suppressed the DNA ladder in response to hypoxia. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase-1 activity (YVADase) was detected. To confirm what caspases are involved in apoptosis, Western blot analysis was performed using anti-caspase-3 or -6 antibodies. The 10-kDa protein, corresponding to the active products of caspase-3, and the 10-kDa protein of the active protein of caspase-6 were generated in hypoxia-challenged cells in which the processing of the full length form of caspase-3 and -6 was evident. While a time course similar to this caspase-3 and -6 activation was evident, hypoxic stress caused the cleavage of lamin A, which was typical of caspase-6 activity. In addition, the stress elicited the release of cytochrome c into the cytosol during apoptosis. Furthermore, we observed that pre-treatment with SB203580, a selective p38 mitogen activated protein kinase inhibitor, attenuated the hypoxia-induced apoptosis. The addition of SB203S80 suppressed caspase-3 and -6-like protease activity by hypoxia up to $50\%$. In contrast, PD98059 had no effect on the hypoxia-induced apoptosis. To confirm the involvement of MAP kinase, JNK/SAPK, ERK, or p38 kinase assay was performed. Although p38 MAPK was activated in response to hypoxic treatment, the other MAPK -JNK/SAPK or ERK- was either only modestly activated or not at all. These results suggest that p38 MAPK is involved in hypoxia-induced apoptosis in MC3T3El osteoblasts.