We evaluated the anti-osteoarthritic effects of deer bone extract on articular cartilage damage by using micro-computed tomography (micro-CT) in monosodium iodoacetate (MIA)-induced osteoarthritis (OA) in rats. Male Wistar rats (6 weeks of age) were randomly divided into 5 groups (10 rats/group): sham control (SC; PBS injection+PBS 1 mL treatment); negative control (NC; MIA injection+PBS 1 mL treatment); positive control (PC; MIA injection+250 mg/kg glucosamine sulfate/chondroitin sulfate mixture treatment); low dose (LDB; MIA injection+250 mg/kg deer bone extract treatment); and high dose (HDB; MIA injection+500 mg/kg deer bone extract treatment). After 50 days of treatment, we observed that the administration of deer bone extract protected against bone destruction and reduced the number of erosion lacunae. When deer bone extract was administered, the trabecular thickness distribution (Tb.Th) (LDB: 75.9 μm, HDB: 80.7 μm vs. NC: 48.0 μm) and the trabecular bone volume fraction ratio (BV/TV) (LDB: 43.8%, HDB: 48.2% vs. NC: 39.1%) were significantly restored. Additionally, the trabecular separation (Tb.Sp) increase caused by MIA was decreased significantly with the administration of deer bone extract (LDB: 73.4 μm, HDB: 81.2 μm vs. NC: 112.0 μm). We concluded that the oral administration of deer bone extract effectively relieved the morphological changes induced by MIA injection in an animal model.

Studies to elucidate the pathophysiology of osteoarthrosis have been hampered by the lack of a rapid, reproducible animal model that mimics the histopathology and symptoms associated with the disease. The aim of this study is to evaluate the radiological, histological and histomorphometrical findings of four different concentrations of sodium iodoacetate (MIA) to create osteoarthrosis by using an arthrocentesis technique on rabbit temporomandibular joint (TMJ). 12 New Zealand white male rabbits received an injection of MIA (50 μl dose of 1.5, 2, 2.5, 3mg/ml concentrations) to a single joint of each group by arthrocentesis. Computed tomography (CT) images were obtained pre- and post-injections at 2, 4 and 6 weeks. Early osteoarthritic changes in the rabbit TMJ were found histologically at 4 weeks and with a 3mg/ml concentration of MIA. The mean subchondral bone volume depended on the concentration of MIA and was 62±2.6%, 63±4.1%, 42±3.6% and 38±3.8%, respectively. A minor abnormality was found on CT in six joints at the 4-week follow up. MIA injection and arthrocentesis offer a rapid and minimally invasive method of reproducing histologically osteoarthrotic lesions in the rabbit TMJ.

Although there are several reports on pain behavioral tests in rat models of knee osteoarthritis (OA), most of them focus on the paw. The aim of this study was to investigate pain-related behaviors on the affected knee joint, the primary source of nociception, in animals with mono-iodoacetate-induced OA, using the knee-bend (which provides information on movement pain) and pin-prick tests, and to evaluate nociception elicited by walking using the CatWalk test. The von Frey and Randall-Selitto tests applied to the paw allowed us to compare our study results with previous studies. A further aim was to compare the behavioral nociceptive responses of the most used doses of mono-iodoacetate, 2 and 3 mg. Knee-bend score of OA animals was higher than those of control animals throughout the study (P < .05). At every time point, the ipsilateral hind-paw load of OA rats, as measured by the CatWalk test, was lower than that of control rats (P < .05), and paw withdraw threshold to von Frey filaments was also decreased (P < .01). No changes were observed in pin-prick and Randall-Selitto tests. Results obtained with the 2 doses of mono-iodoacetate were similar. The knee-bend and CatWalk tests are effective for evaluating movement-related nociception, a hallmark of clinical OA, which was present throughout the experimental period.
CONCLUSIONS: Behavioral characterization of models of OA pain is important and useful for use in future studies to test pharmacological treatments. Furthermore, it is important to find methods that correlate better with the human symptoms of OA.

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BACKGROUND: In the isolated liver of fed rats, a 10 mM ethanol perfusion rapidly induced a rapid 25% decrease in the total ATP content, the new steady state resulting from both synthesis and consumption. The in situ rate of mitochondrial ATP synthesis without activation of the respiration was increased by 27%, implying an increased energy demand. An attempt to identify the ethanol-induced ATP-consuming pathways was performed using 31P and 13C Nuclear Magnetic Resonance.
RESULTS: Ethanol (i) transiently increased sn-glycerol-3-phosphate formation whereas glycogenolysis was continuously maintained; (ii) decreased the glycolytic ATP supply and (iii) diminished the intracellular pH in a dose-dependent manner in a slight extend. Although the cytosolic oxidation of ethanol largely generated H+ (and NADH), intracellular pHi was maintained by (i) the large and passive excretion of cellular acetic acid arising from ethanol oxidation (evidenced by exogenous acetate administration), without energetic cost or (ii) proton extrusion via the Na+-HCO3- symport (implying the indirect activation of the Na+-K+-ATPase pump and thus an energy use), demonstrated during the addition of their specific inhibitors SITS and ouabaïn, respectively.
CONCLUSIONS: Various cellular mechanisms diminish the cytosolic concentration of H+ and NADH produced by ethanol oxidation, such as (i) the large but transient contribution of the dihydroxyacetone phosphate/sn-glycerol-3-phosphate shuttle between cytosol and mitochondria, mainly implicated in the redox state and (ii) the major participation of acetic acid in passive proton extrusion out of the cell. These processes are not ATP-consuming and the latter is a cellular way to save some energy. Their starting in conjunction with the increase in mitochondrial ATP synthesis in ethanol-perfused whole liver was however insufficient to alleviate either the inhibition of glycolytic ATP synthesis and/or the implication of Na+-HCO3- symport and Na+-K+-ATPase in the pHi homeostasis, energy-consuming carriers.

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