• 한국정밀공학회:학술대회논문집
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• 한국정밀공학회 2010년도 추계학술대회 논문집
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• pp.653-654
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• 2010

• 대한기계학회논문집B
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• 제36권11호
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• pp.1081-1090
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• 2012

외상성 관절염 발생시 슬관절에서의 해면골 미세구조 변화 특성에 대한 연구는 부족한 실정이다. 따라서 본 연구에서는 생체 내 미세 단층 촬영을 통해, 소동물(SD rat; 10 마리)의 경골 골단 해면골 미세구조 변화패턴을 연속적으로 추적 관찰하여 정량적으로 분석하였다. 외상성 관절염 군(5 마리)에는 전방십자인대절제술을 실시하였고, 정상군(5 마리)에는 아무런 외과적 처치를 가하지 않았다. 외상성 관절염군은 정상군과 비교시 수술후 8 주까지 약 4-16%의 유의한 골 미세구조 차이를 나타내었다(P<0.05). 동일 기간 동안 골 밀집 정도 및 골 형성 정도는 5-15% 정도로 유의한 차이를 나타내었다(P<0.05). 본 연구는 외상성 관절염 발생에 의한 경골 골단 해면골의 골 미세구조 변화 특성 기준 정립 및 외상성 관절염의 이해와 치료에 도움이 될 것으로 기대된다.

• IMMUNE NETWORK
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• 제24권2호
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• pp.17.1-17.16
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• 2024

We have reported that anterior cruciate ligament (ACL) injury leads to the differential dysregulation of the complement system in the synovium as compared to meniscus tear (MT) and proposed this as a mechanism for a greater post-injury prevalence of post traumatic osteoarthritis (PTOA). To explore additional roles of complement proteins and regulators, we determined the presence of decay-accelerating factor (DAF), C5b, and membrane attack complexes (MACs, C5b-9) in discarded surgical synovial tissue (DSST) collected during arthroscopic ACL reconstructive surgery, MT-related meniscectomy, osteoarthritis (OA)-related knee replacement surgery and normal controls. Multiplexed immunohistochemistry was used to detect and quantify complement proteins. To explore the involvement of body mass index (BMI), after these 2 injuries, we examined correlations among DAF, C5b, MAC and BMI. Using these approaches, we found that synovial cells after ACL injury expressed a significantly lower level of DAF as compared to MT (p<0.049). In contrast, C5b staining synovial cells were significantly higher after ACL injury (p<0.0009) and in OA DSST (p<0.039) compared to MT. Interestingly, there were significantly positive correlations between DAF & C5b (r=0.75, p<0.018) and DAF & C5b (r=0.64 p<0.022) after ACL injury and MT, respectively. The data support that DAF, which should normally dampen C5b deposition due to its regulatory activities on C3/C5 convertases, does not appear to exhibit that function in inflamed synovia following either ACL injury or MT. Ineffective DAF regulation may be an additional mechanism by which relatively uncontrolled complement activation damages tissue in these injury states.

• 대한의생명과학회지
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• 제8권3호
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• pp.195-202
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• 2002

Osteoarthritis (OA), the most common form of arthritis, involves the destabilization of the normal balance between the degradation and the synthesis of articular cartilage and subchondral bone within a joint. As articular cartilage degrades over time, its smooth surface roughens and bone-against-bone contact ensues, producing the inflammation response symptomatic of this 'wear and tear' disease. Although a variety of genetic, developmental, metabolic, and traumatic factors may initiate the development of osteoarthritis, its symptoms (joint pain, stiffness, and curtailed function) typically evolve slowly, and patients experience periods of relative calm alternation with episodes of inflammation and pain. Rheumatoid arthritis (RA), an autoimmune disease of unknown etiology characterized by chronic synovitis and cartilage destruction, affect 1% of the total population. Cartilage is a specialized connective tissue in which the chondrocytes occupy only 5% of the volume. Cartilage is particularly rich in extracellular matrix, with matrix making up 90% of the dry weight of the tissue chondrocytes have cell processes that extend a short distance into the matrix, but do not touch other cells thus in cartilage, cell-matrix interactions are essential for the maintenance of the extracellular matrix. In this study, subtractive hybridization method was utilized to detect genes differentially expressed in chondrocytes treated with methylprednisolone. We have isolated 57 genes that expressed differentially in the chondreocytes by methylprednisolone. 13 clones of them were analyzed with sequencing and their homologies were searched. 8 cDNAS included KIAA 0368, upregulated during skeletal muscle growth 5 (usmg 5), ribosomal protein S 18 (RPS 18), skeletal muscle ryanodine receptor, radial spoke protein 3 (RSP 3), ribosomal protein QM, ribosomal protein L37a (RPL37A), cytochrome coxidase subunit VIII (COX8).