• Maxillofacial Plastic and Reconstructive Surgery
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• v.30 no.3
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• pp.292-295
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• 2008

Temporomandibular joint cysts usually occur between the second and fourth decade of life. There is a female predominance to male of approximately 3 to 1. The patients complain of swelling, pain and sometimes decreased mouth opening. Synovial cysts of the temporomandibular joint seem to develop by an increase of intraarticular pressure due to trauma or inflammation which causes capsular herniation. However, if inflammatory synovial cysts develop by an increase of synovial fluid into inflammation tissue in the capsule without capsular herniation, a differential diagnosis should include synovial chondromatosis and synovitis. This is a case report of a synovial cyst developed in a capsule of the temporomandibular joint.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2001.11a
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• pp.14-20
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• 2001

Rheumatoid arthritis (RA) is one of the most typical rheumatic diseases, and is characterized by chronic inflammation, cartilage destruction and joint deformity ［1,2］. During this process, profound hypertrophic changes of the synovium with infiltration of immune cells, increased vascularity, and hyperplasia result in the formation of a synovial pannus that invades cartilage and bone ［3］. In early stages of RA, the synovial membrane begins to invade the cartilage. In established RA, the synovial membrane becomes transformed into inflammatory tissue, the pannus (Fig. 1). The cell types that occupy cartilage-pannus junctions include synovial macrophages, fibroblasts, mast cells, polymorphonuclear lymphocytes (PMNs), and displaced, probably differentiated condrocytes ［4-6］. Recent studies of rheumatoid synovial tissue have demonstrated localized accumulations of mast cells and evidence of their activation/degranulation［7］.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.43 no.5
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• pp.336-342
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• 2017

Synovial chondromatosis is a rare benign lesion originating from the synovial membrane. It presents as adhesive or non-adhesive intra-articular cartilaginous loose bodies. Although the causes of synovial chondromatosis have not been fully elucidated, inflammation, external injury, or excessive use of joints have been suggested as possible causes. Synovial chondromatosis has been reported to occur most frequently at large joints that bear weights, with a rare occurrence at the temporomandibular joint (TMJ). When synovial chondromatosis develops at TMJ, clinical symptoms, including pain, joint sounds, and mouth opening may common. Moreover, synovial chondromatosis rarely spreads to the mandibular condyle, glenoid cavity, or articular eminence of TMJ. The goal of this study was to discuss the methods of surgery and other possible considerations by reviewing cases of patients who underwent surgery for synovial chondromatosis that extended to the temporal bone.

• Natural Product Sciences
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• v.13 no.4
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• pp.289-294
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• 2007

Ethanolic extract (50% v/v) and alkaloid fraction of Tylophora indica leaves were examined for lysosomal enzyme inhibitory activity in adjuvant-induced arthritic rats. The alkaloid fraction showed statistically significant inhibition of arthritic lesions (p < 0.05) from day 18, (p < 0.025) from day 20 and (p < 0.001) from day 21 onwards in the adjuvant-induced arthritis, which was comparable to the response of standard drug Indomethacin. The ethanolic extract was less significant than the alkaloidal fraction in inhibition of arthritis. Alkaloid fraction showed significant (p < 0.001) inhibitory effect on the lysosomal enzyme activities in adjuvantinduced arthritic rats. It also significantly prevented decrease in collagen levels and synovial damage observed during arthritis and also inhibited increase in urinary excretion levels of collagen degradation products like hydroxyproline, hexosamine, hexuronic acid, etc. Both ethanolic extract as well as the alkaloid fraction, however, did not show any significant activity in normal nonarthritic rats. The ethanolic extract and the alkaloid fraction may thus be able to inhibit the progress of inflammation and inhibit the destructive activity of lysosomal enzymes on structural macromolecules like collagen etc. in the synovial capsule in joints during arthritic states. They may thus prevent synovial damage observed during arthritis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.4
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• pp.871-877
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• 2008

Heme oxygenase-1 (HO-1), an inducible heme-degrading enzyme, is expressed by macrophages and endothelial cells in response to various stresses and mediators of inflammation. HO-1 has been recently implicated in regulation of angiogenesis via expression of VEGF. The purpose of this study was to determine the effects of HO-1 modulation on the collagen-induced arthritis (CIA) model and on angiogenesis via up- regulation of VEGF expression in human synovial fibroblast. DBA/1J mice were treated with an inhibitor of HO-1, tin protoporphyrin IX (SnPP), or with an inducer of HO-1, cobalt protoporphyrin IX (CoPP), from day 1 to day 35 after CIA induction. The clinical evolution of disease was monitored visually. At the end of the experiment, histopathologic changes were examined on the joints. VEGF expression in paws were measured by immunohistochemical stain. mRNA expression of HO-1 and VEGF stimulated with various concentration of $TNF-{\alpha}$, CoPP accessed on human synovial fibroblast by RT-PCR. Effects of pretreatment with SnPP on mRNA expression of HO-1 and VEGF in the presence of CoPP and $TNF-{\alpha}$ in synovial fibroblast was accessed by Real-time RT-PCR. Administration of cobalt protoporphyrin IX significantly induced the inflammatory response, with increased arthritis index and expression of VEGF in the paws of the arthritis models. Treatment with SnPP significantly reduced the severity of CIA through inhibition of joint inflammation and cartilage destruction. The expression of VEGF were also significantly reduced by SnPP treatment in the paw. CoPPIX as inducer of HO-1, increased HO-1 and VEGF expression dose dependently in synovial fibroblast. In contrast, inhibition of HO-1 activity by SnPPIX abrogated CoPPIX-induced HO-1 and VEGF production in synovial fibroblast. Stimulation with $TNF-{\alpha}$ increased HO-1 and VEGF expression itself and showed additive effect on HO-1 and VEGF expression when it treated with CoPP. When SnPP was treated with CoPP and $TNF-{\alpha}$, it abrogated the CoPP induced HO-1 and VEGF expression and also abrogated $TNF-{\alpha}$ induced HO-1 and VEGF expression in synovial fibroblast. The effects of HO-1 induction in rheumatoid arthritis results in aggravation of arthritis via up-regulation of VEGF. I concluded that inhibition of the expression or activity of HO-1 could be a therapeutic target of rheumatoid arthritis.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.18 no.2
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• pp.308-315
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• 1996

Osteoarthritis is a noninflammatory degenerative disease affecting the articular surfaces and is accompanied by remodeling of the underlying bone. The sympotms of osteoarthritis of the temporomandibular joint are pain in the joint and muscles of mastication, limitation. Osteoarthritis is generally accepted that several factors can contribute to the trauma, aging process, internal derangement and MPDS. Radiographic features of the osteoarthritis are seen flattening of joint, sclerosis on flattened area and osteophyte or anterior lipping. In the past, osteoarthritis was considered to self-limiting disease. Currently, synovial chondromembrane is part of the process of osteoarthritis secondary to trauma. Synovial chondromatosis is an uncommon disease of cartilaginous transformation of synovial membrane with formation of loose bodies within the joint space. The pathogenesis is more an active metaplastic than a neoplastic process. The cause of synovial chondromatosis is unknown. Although trauma and inflammation have all been cited as possible factors in tis pathogenesis. The clinical sign and symptoms are unilateral swelling of the joint region, pain in the joint area and crepitus seem to be the most reliable signs and symptoms. Radiographic evidence of loose bodies may or may not be present. This is a case report of 66 year old female with synovial chondromatosis, that is advanced disease of the osteoarthrits. We treated patient with surgical excision of lose bodies, diskectomy and synovectomy. The defected articular fossa area was reconstructed with temporalis fascia flap. The result was satisfactory.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.2
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• pp.212-224
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• 2013

This study intends to clarify how Sayeok-tang(here in after reffered to SYT) affect C57BL/10 mice whose osteoarthritis was induced by papain. Osteoarthritis was induced by injecting papain in the knee joint of 3 groups(n=6) of mice. Normal group was non-treatment group and was not injected papain, whereas control mice were orally administered with $200{\mu}{\ell}$ of physiological saline. Positive comparison group was medicated with 100 mg/kg of Joins$^{(R)}$ mixed with $200{\mu}{\ell}$ of physiological saline. Experimental group was medicated with 400 mg/kg of SYT mixed with $200{\mu}{\ell}$ of physiological saline. Both Positive and experimental comparison groups were orally medicated once per day for 4 weeks. After the experiment, the functions of liver and kidney, inflammation cytokine values within serum, degree of revelation for inflammation cytokine genes, immune cells within blood, metabolism of arachidonic acid and amount of cartilage were measured and histopathological changes in the knee joint structures were observed. As results, SYT had no significant effect on the liver and kidney functions. Interleukin-$1{\beta}$(IL-$1{\beta}$), interleukin-6(IL-6), monocyte chemo attractant protein-1(MCP-1) and tumor necrosis factor-${\alpha}$(TNF-${\alpha}$) were significantly decreased. Inflammation cytokines in joints were all significantly decreased. Prostaglandin $E_2(PGE_2)$, thromboxane $B_2(TXB_2)$ were significantly decreased. Destruction of cartilage on micro computed tomography(CT)-arthrography was meaningfully decreased. In terms of histopathology, infiltration of inflammation, proliferation of synovial membrane, subsidence of cartilage and bone due to penetration of excessive formation of synovial cell and destruction of cartilage were small. Based on all results mentioned above, Sayeok-tang(SYT) is believed to be meaningful for suppressing the progress of osteoarthritis and its treatments because of its anti-inflammatory effects and alleviation of pain with histopathological effective efficacy.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.19 no.2
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• pp.191-199
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• 1997

Mandibular trauma is developed due to traffic accident, fall down, industrial injury, and others. TMJ disorder is usually also developed after facial traumatic injury. Many authors suggested that disc displacement or tearing, acute synovitis, TMJ ankylosis, traumatic arthritis, or effusion are developed after facial trauma. It is still very controversible what is the best treatment of TMJ injury such as condylar fracture and meniscal injury. In TMJ injury, synovial inflammation is developed and pain mediators such as prostaglandin E2 or leukotriene B4 are released from the synovial membrane. This can be a cause of TMJ disorder. I present a variety of experimental study about the condylar fracture and meniscal injury and enzyme-immunoassay of synovial fluid after mandibular trauma that have been studied since 1992 and establish the treatment criteria of traumatic TMJ injury. I think that the treatment option of condylar fracture depends upon the surgeon's criteria exclusively. There are no significant differences between conservative and surgical treatment. If the aggressive functional physical therapy and long-term followup be performed, the favorable functional recovery of TMJ can be obtained. And I think that the initial surgical management of meniscus of TMJ is unnecessary in condylar fracture. And also arthrocentesis can be available to release the patient's subjective symptoms and improve the healing of injured TMJ.

• Molecules and Cells
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• v.19 no.2
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• pp.180-184
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• 2005

IL-17 is a major proinflammatory cytokine secreted by activated T-lymphocytes that accumulates in the inflamed joints of rheumatoid arthritis (RA) patients. Additional IL-17-related molecules and their receptors have been discovered and may also contribute to RA pathogenesis. We examined the expression of the prototypic IL-17 (IL-17A) and its homologs, IL-17B-F, by RT-PCR analyses of synovial fluid mononuclear cells (SFMCs) and peripheral blood mononuclear cells (PBMCs) from RA patients. We also tested for induction of the IL-17 receptor homologs upon stimulation of the fibroblast-like synoviocytes (FLSs) of RA patients with IL-17. The patients' SFMCs expressed IL-17C, E and F in addition to IL-17A. As in the case of IL-17, IL-15 appears to be the major inducer of these homologs in RA SFMCs. We detected transcripts of IL-17R, as well as those of IL-17RB, C and D, in the FLSs of RA patients. Whereas IL-17R expression increased upon in vitro stimulation with IL-17, expression of IL-17RB, C and D was unchanged. However the possibility of cross-interaction between other IL-17 homologs and receptor isoforms remains to be investigated. Our data suggest that these additional homologs should also be considered as targets for immune modulation in the treatment of RA joint inflammation.

• Advances in Traditional Medicine
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• v.5 no.4
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• pp.251-261
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• 2005

Rheumatoid arthritis (RA) is an autoimmune/inflammatory disorder with a complex genetic component. RA is characterized by chronic inflammation of the synovial membrane in the joint, which leads to the progressive destruction of articular cartilage, ligament and bone. Several cytokines such as tumor necrosis $factor-{\alpha}\;TNF-{\alpha}\;and\;interleukin-1{\beta}\;(IL-1{\beta})$ and interleukin-6 (IL-6) have been implicated in the pathological mechanisms of synovial tissue proliferation, joint destruction and programmed cell death in rheumatoid joint. Genome wide screening of subjects suffering from autoimmune diseases especially arthritis revealed linkage to inflammatory molecules like $TNF-{\alpha},\;IL-1{\beta}$ and IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-kappaB $(NF-{\kappa}B)$ and human leucocyte antigen/major histocompatibility complex (HLA/MHC) locus. The status of the pharmacological mechanism of herbal drugs in the light of genome wide screening results has been discussed to reinforce the therapeutic potential and the pharmacological basis of the herbal drugs.