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Objective To review cellular mechanisms that have been proposed to mediate the indirect and direct effects of estrogen on articular cartilage, and to outline the remaining clinical questions that need to be clarified before utilizing the beneficial effects of estrogen for the prevention of osteoarthritis in early postmenopausal women. Design Summary of original research papers and reviews listed in Pubmed (1980-2007). Results Estrogen receptors have been identified in articular chondrocytes from various animals and humans. Molecular studies showed that estrogen can elicit genomic and rapid non-genomic effects on various cell types, including chondrocytes, and the latter effects are only inducible in females. In addition to direct effects, estrogen can also affect the homeostasis of articular cartilage by modulating the expression/production of different molecules such as various growth factors, inflammatory cytokines, matrix metalloproteinases, and reactive oxygen species. Moreover, in vivo observation argues for the notion that inhibition of subchondral bone turnover is also part of the mechanisms by which estrogen (and antiresorptive agents in general) can protect against joint degradation. Published studies undertaken at cellular, tissue, and in vivo levels illustrate that the effect of estrogen on cartilage may depend on the dose applied, the administration route, the time of initiation, and whether it is combined with a progestin. Conclusions The herein reviewed direct and indirect effects of estrogen on articular cartilage further corroborate the due consideration of estrogen therapy for maintaining not only bone but also cartilage health in postmenopausal women. Future studies in postmenopausal women are needed to clarify whether the efficacy of estrogen therapy can be further optimized by using other forms of estrogen, other progestins, or by initiating the therapy in the peri- or early postmenopausal period. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate changes in the circulating levels of the C-telopeptide of type II collagen (CTX-II) with relation to disease onset and structural damage of cartilage in a rodent model of collagen-induced arthritis (CIA), and to investigate immunolocalization of the CTX-II epitope in the articular cartilage of affected joints. METHODS: Seven-week-old female Lewis rats were immunized with type II collagen and monitored using blood sampling at weekly intervals. At study termination (day 23), the animals were killed, synovial fluid was collected, and the affected joints were scored macroscopically for disease severity and underwent immunohistochemical evaluation. RESULTS: At the time of disease onset (day 15), which was characterized by redness and swelling of the affected joints (mean +/- SD macroscopic severity score 9.1 +/- 1.6), there was a 355% increase in serum CTX-II levels. The early change in serum CTX-II from day 0 to day 15 showed a significant association with the severity of cartilage damage (r = 0.61, P < 0.01). Immunostaining revealed extensive presence of the CTX-II epitope in the damaged, uncalcified cartilage tissue. CONCLUSION: The elevation in serum CTX-II concomitant with the onset of disease and proportional to cartilage damage demonstrates that CTX-II is a sensitive diagnostic tool for monitoring joint disease in the rodent model of CIA. Furthermore, the immunohistochemical findings are consistent with the concept that the major source of serum CTX-II is the damaged articular cartilage. [ABSTRACT FROM AUTHOR]

Migraine is a subjective complaint and no laboratory test has until now been of value. The aim of the present study is to evaluate whether histamine inhalation may be used as a diagnostic test for migraine. In a double blind study design, 15 migra neurs and 15 control subjects scored headache intensity and characteristics before, during, and in the subsequent 12 h after inhalation of increasing doses of histamine (0, 2, 4, 8, 16, 32 and 64 mg/ml). During the histamine inhalations, headaches increased dose-dependently in both groups Eleven of the migraineurs and eight of the healthy controls experienced headaches after the inhalations These headaches fulfilled the IHS criteria for migraine without aura in six of the migraineurs, but in none of the control subjects. Using this as a test parameter, the specificity of the test was 1, but the sensitivity was only 0.4. Our results indicate that histamine inhalation is a specific but insensitive laboratory test for migraine. Migraineurs should be informed about the risk of a migraine attack being provoked before histamine inhalation in pulmonary laboratories. [ABSTRACT FROM AUTHOR]