Background: Low back pain is a common complaint which is always found in old age due to degeneration process. Degeneration process of spine, especially in the lumbar region is called lumbar osteoarthritis (OA). Various factors are thought to be the cause of lumbar OA, including primarily due to hormonal changes of estrogen and increase of age and body mass index in postmenopausal women. Methods: The purpose of this study is to determine the role of hormonal changes pathogenesis in lumbar osteoarthritis in postmenopausal women and its correlation with age and body mass index. Cross sectional analytic method had been conducted to determine the role of age, body mass index and estrogen for lumbar OA in postmenopausal women. The study was conducted in Sanglah General Hospital from October 2015 until March 2016 by anthropometric measures and blood samples. Results: From 196 samples showed that the estrogen deficiency in postmenopausal women have a correlation with the symptomatic lumbar OA (r=0.252, p = 0.000). While age and the body mass index in postmenopausal women has a correlation with symptomatic lumbar OA (r = 0.150 and 0.198, p = 0.000 and 0.013). Conclusions:The aging process, body mass index and estrogen deficiency correlated with the symptomatic OA lumbar in post-menopausal women. Suyasa IK et al. Int J Res Med Sci. 2016 May;4(5):1325-1328 International 4-6 These three components are familiar with the three joint complex interplay in lumbar osteoarthritis. There are 3 clinical signs and stages of the degeneration of spinal biomechanics i.e. disc dysfunctions, instability and stability. Keywords7 Spinal degeneration include disc degeneration (DD), facet joint osteoarthritis (OA Facet joint), changes in components of muscle and ligament degeneration. [5][6][7] Hormonal changes that occur during menopause will affect the occurrence of osteoarthritis. In postmenopausal women, the use of HRT (Hormone Replacement Therapy) lowered radiological progression. Estrogen stimulates proteoglycan changes in cartilage, either directly or indirectly through cytokines. 8,9 Estrogen directly affects the tissue by estrogen receptors on human articular chondrocytes and indirectly by secondary messenger.10 Estrogen affects the levels of cytokines in vitro and in vivo. Identification over two estrogen receptors ERα and ERβ on chondrocyte prove that cartilage is sensitive to estrogen.11 Several in vivo and in vitro studies also showed that chondrocytes respond to estrogen and affect its metabolism. 11,12 METHODSThe study was conducted from October 2015 until March 2016 at the Sanglah General Hospital Denpasar Bali. The aim of this study is to prove the correlation of age, body mass index and hormonal changes with symptomatic lumbar osteoarthritis in postmenopausal women.This study is a cross sectional analytic design with the sample are post-menopausal women population with consecutive sampling method.One hundred and ninety six post-menopausal women from the population were taken the anthropometry measure i.e. body weight...

Osteoarthritis (OA) arises from imbalance of cartilage metabolism between the synthesis and degradation of type II collagen by the chondrocyte. Collagen type II degradation is characterized by increase in the biomarker of Ctelopeptide fragment of type II collagen (CTX-II), while the anabolic process of cartilage is characterized by an increase in the biosynthesis of procollagen amino terminal N-propeptide type IIA (PIIANP). Platelet derived growth factor (PDGF) with Hyaluronic Acid (HA) as a potent growth factor can be used to stimulate the higher formation of chondrocyte and PIIANP levels and lower CTX-II levels in mouse knee osteoarthritis model.

Background: Hypothyroidism is a common side effect found in patients with multidrug-resistant tuberculosis taking ethionamide. The mechanism of ethionamide-induced hypothyroidism is potentially caused by the structure of ethionamide compounds chemically similar to thioamide, such as propylthiouracil (C7H8N2S), which inhibits thyroid hormone synthesis. However, hypothyroidism is caused not only by a lack of production but also by signaling alteration. Thyroid hormone action is mediated by thyroid hormone receptors (TRs), members of the nuclear receptor superfamily that regulate their target genes. Unfortunately, there are limited studies on the potential interaction of ethionamide with TRs. Objective: In the present study, we want to elaborate on the potential interaction of ethionamide with TRs which might alter the thyroid hormone genomic regulation. Methods: Molecular docking studies were used to evaluate the potential interaction between ethionamide with TRα and TRβ. Results: The molecular docking results on TRα showed more than one hydrogen bond-steric interaction formed from the ethionamide-amino acid residue interaction. Ethionamide-TRβ interaction showed more than one steric interaction, but the hydrogen bonds are not visualized. The docking score between ethionamide and TRα is −7.373 kcal/ mol and higher than its interaction with TRβ. Conclusion: These findings indicate that ethionamide can interact with TRα and TRβ. However, the ethionamide-TRα interaction is stronger than ethionamide-TRβ interaction. Our study reports a novel mechanism of action of ethionamide-induced hypothyroidism.

HighlightsThe giant cell tumor is a benign, primary skeletal neoplasm with variable biologic aggressiveness.A coexistence with hereditary multiple exostosis with expression of EXT-1 is very rare.BCL-2 gene is expressed only in malignant transformation of the giant cell tumor.The correlation between giant cell tumor and hereditary multiple exostosis is still not clearly determined.The case revealed giant cell tumor in hereditary multiple exostosis with positive EXT-1 without BCL-2 expression.