Hideyuki Kawabata

High mobility group box 1 is upregulated after spinal cord injury and is associated with neuronal cell apoptosis.

Study Design. Cerebrocortical culture and rat spinal cord injury (SCI) model were used to examine the expression of high mobility group box 1 (HMGB1), TNF-&agr;, and Rage by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical examination. In addition, relationship between upregulation of HMGB1 and neural cells apoptosis was evaluated after SCI. Objective. To evaluate the upregulation of HMGB1, TNF-&agr;, and Rage after SCI. Summary of Background Data. It is known that the mode of delayed neuronal cell death after SCI is apoptosis. Apoptotic cell death is influenced by several injury-promoting factors which include pro-inflammatory cytokines. Inhibition of apoptosis promotes neurologic improvement following SCI. However, the factors which transmit inflammatory signaling following SCI have not yet been clarified in detail. HMGB1 was reported as an important mediator of inflammation. We examined the expression of HMGB1, TNF-&agr; and Rage following acute SCI. Methods. Expression of HMGB1, TNF-&agr; and Rage was examined by RT-PCR and immunohistochemical examination. Apoptotic cell death was evaluated by TUNEL methods. Results. HMGB1 was exported from nuclei to cytoplasm in active caspase-3 positive apoptotic cell in vitro. In addition, HMGB1, TNF-&agr;, and Rage was expressed in same cell after NMDA treatment. RT-PCR revealed that expression of HMGB1 and TNF-&agr; was upregulated following SCI. Immunohistochemical examination revealed that the numbers of HMGB1-, TNF-&agr;-, and Rage-positive cells were increased following SCI. The number of TUNEL-positive cells was significantly increased at 12 hours after injury, and was maximal at 72 hours after injury. However, HMGB1- and TNF-&agr;-positive cells were maximal in number 48 hours after injury, while Rage-positive cells were maximal in number at 24 hours after injury. These data suggest that HMGB1, TNF-&agr;, and Rage were upregulated following SCI but preceding the apoptotic cell death. Conclusion. Our findings suggest that HMGB1 play a role in the induction of apoptosis via inflammatory reaction.

Stress deprivation from the patellar tendon induces apoptosis of fibroblasts in vivo with activation of mitogen-activated protein kinases

The effect of stress deprivation on the tendon tissue has been an important focus in the field of biomechanics. However, less is known about the in vivo effect of stress deprivation on fibroblast apoptosis as of yet. This study was conducted to test a hypothesis that complete stress deprivation of the patellar tendon induces fibroblast apoptosis in vivo with activation of Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) within 24 h after treatment. A total of 35 mature rabbits were divided into stress-shielded (n=15), sham-operated (n=15), and control (n=5) groups. To completely shield the patellar tendon from stress, we used an established surgical method. Animals were sacrificed at 24 h, and 2, 4, 7, and 14 days after the treatment. Tendon specimens underwent TUNEL assay and immunohistological examinations of active caspase-3, JNK, and p38. Both the number and the ratio of TUNEL-positive and caspase-3-positive cells were significantly greater (p<0.0001) in the stress-shielded group than in the sham group at 24 h, 2, 4, and 7 days. Concerning JNK and p38, both the number and the ratio were significantly greater (p<0.0001) in the stress-shielded group than in the sham group at 24 h, 2, and 4 days. This study demonstrated that complete stress deprivation induces fibroblast apoptosis in vivo with activation of JNK and p38 within 24 h. This fact suggested that the fibroblast apoptosis caused by stress deprivation is induced via the mitogen-activated protein kinase signaling pathway.

Clinical Outcome of Arthroscopic Partial Resection of Hip Acetabular Labrum Tear: A Case Report

51歳男性．1年程前より，誘因なく右股関節痛が出現し，平成18年10月当科紹介受診．股関節内外旋での疼痛認めるも，単純レントゲンにて明らかな異常を認めなかった．腰椎を含め，他部位に異常を認めず，臨床所見より股関節唇損傷を疑い，MRI，CT arthrographyを行った．その結果，いずれにおいても関節唇の一部に関節唇損傷を疑う所見を認めた．また，関節内局麻注入にて一時的な症状改善を認め，症状，画像を総合的に判断し，最終的に関節唇損傷と診断し，関節鏡を行った．鏡視にて前外側の関節唇損傷を認め，鏡視下関節唇切除術を行った．術後早期より，歩行時の疼痛などの症状の改善を認め，経過良好である．股関節唇損傷は症状やCT arthrography，MRI，関節内局麻注入などで診断されることが多いが，画像上明らかな異常所見がない例も少なくない．原因が明らかでない股関節痛が持続する症例では，関節唇損傷も考慮に入れて，関節鏡を用いた．診断治療を行うことは有効な方法であると考える．

Clinical Findings of Chiari Pelvic Osteotomy with Arthroscopic Debridement for Osteoarthritis of Hip

（目的）キアリ骨盤骨切り術施行時と内固定材料抜釘時に股関節鏡を行い，鏡視所見と治療成績について検討した．（対象と方法）2001年以降のキアリ症例44例47股中，鏡視を行い得た10例10股（全例女性）を対象とした．手術時平均年齢は43歳で，抜釘術までの期間：平均1年1ケ月，病期分類は進行期3例，末期7例であった．評価はJOAスコアと種田分類を用いた．（結果と考察）JOAスコアは48点から74点に改善していた．種田分類では多くの症例で変化なかった．疼痛などの臨床所見はよく改善されていたが，関節鏡所見の変化は乏しく，臨床成績との関連性は明らかではなかった．またキアリ変法に関節内処置を併用することが，どれほど臨床成績の向上に貢献しているかも不明であるため，今後長期にわたる経過観察が必要であると思われる．