2006
DOI: 10.1177/154405910608500709
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Increase in RANKL: OPG Ratio in Synovia of Patients with Temporomandibular Joint Disorder

Abstract: Although a recent study suggested the involvement of RANKL and osteoprotegerin (OPG) in the pathogenesis of bone-destructive disease, no study has focused on the RANKL:OPG ratio in the synovial fluid of patients with temporomandibular joint (TMJ) disorder. This communication reports on the concentrations of RANKL and OPG in synovial fluid from TMJ patients and healthy control individuals. In contrast to an unchanged concentration of RANKL, a strong decrease in the concentration of OPG was detected in the synov… Show more

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Cited by 34 publications
(25 citation statements)
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“…In addition, it has been shown previously that significant amounts of sRANKL (10.9 ± 2.2 pg/ml) are produced by OPG-knockout chondrocytes in vitro, indicating that sRANKL can indeed be produced by chondrocytes in the setting of an altered RANKL/OPG ratio [23]. In human osteoarthritis of the temporomandibular joint, sRANKL levels in the synovial fluid were not increased compared to normal [24]; however, supporting our findings sRANKL is increased in the serum of patients with primary knee OA [25]. Since elevated RANKL levels were mainly in the deep cartilage it might diffuse into the underlying bone and then into the local vasculature rather than through the layer of cartilage into the synovial fluid.…”
Section: Discussionmentioning
confidence: 92%
“…In addition, it has been shown previously that significant amounts of sRANKL (10.9 ± 2.2 pg/ml) are produced by OPG-knockout chondrocytes in vitro, indicating that sRANKL can indeed be produced by chondrocytes in the setting of an altered RANKL/OPG ratio [23]. In human osteoarthritis of the temporomandibular joint, sRANKL levels in the synovial fluid were not increased compared to normal [24]; however, supporting our findings sRANKL is increased in the serum of patients with primary knee OA [25]. Since elevated RANKL levels were mainly in the deep cartilage it might diffuse into the underlying bone and then into the local vasculature rather than through the layer of cartilage into the synovial fluid.…”
Section: Discussionmentioning
confidence: 92%
“…[6,8,10] Since OPG decrease ratios are not so high in the GCF of gingivitis patients in comparison with those in other rheumatoid and periodontal diseases, [6][7][8] this might explain why gingivitis is a relatively mild inflammative disease and not bonedestructive disease. Previous data taken together with our current findings suggest that inflammation has a common mechanism to induce an increase in the RANKL:OPG ratio in the body fluid.…”
Section: Discussionmentioning
confidence: 94%
“…EGF appears to contribute to inflammatory responses, as well as to other physiological and pathological processes. [5] Whereas a recent study also suggests the involvement of the receptor activator of NF-kB ligand (RANKL) and osteoprotegerin (OPG) in the pathogenesis of bone-destructive disease such as rheumatoid arthritis and periodontal disease, [6][7][8][9][10][11] no one has examined the level of RANKL and OPG in the body fluid of the patients with gingivitis except for one. [12] Several investigators have examined gingival crevicular fluid (GCF) for cellular immune-response indicators, as the levels of such indicators are considered to serve as possible markers of active periodontal disease, [13][14][15][16][17][18] but, thus far, no one has looked at the level of growth factors, especially EGF and TGF-a in gingivitis.…”
Section: Drop In Transforming Growth Factor-a and Osteoprotegerin Levmentioning
confidence: 97%
“…[8] In addition to the increase in the level of RANKL protein in the inflamed synovium of rheumatoid arthritis patients, [9] we demonstrated earlier that OPG concentrations in the synovial fluid were lower in patients with rheumatoid arthritis (as compared with patients with other forms of arthritis), which resulted in an increased local and systemic RANKL:OPG ratio. [10] We also demonstrated an elevation of RANKL and a decrease in OPG in gingival crevicular fluid of patients with periodontal disease [11,12] and in synovia of patients with tempomandibular joint disorder, [13] suggesting that RANKL and OPG are important factors involved in bone and joint destruction in humans, and that OPG has a protective role in bone-destructive diseases.…”
Section: Introductionmentioning
confidence: 91%