Pressuring of Acupoints as a Complement to the Diagnosis of Stifle Diseases in Horses.

Diseases of the stifle joint remain a challenge for veterinarians. The objective of this study was to achieve a valuable acupuncture suggestive diagnosis to be considered for stifle joint diseases in horses. Thirty-nine nonlame horses involved in different activities were assessed. Acupuncture was independently performed by two evaluators. Reactions of the animal when pressurizing the point suggestive of stifle disease (PSSD), Bladder-20 and/or Bladder-21, were considered as the inclusion criteria for inclusion in the stifle group (SG, n = 31), and the animals with no reactions were assigned to the control group (n = 8). Radiographic and ultrasonographic examinations were performed and evaluated by two independent professionals blinded to the group allocation. Thermographic examination of the PSSD and stifles was also performed, after acclimatization. The ultrasound scores and radiographic findings were higher in the SG than in the control group. Thermography evidenced increased temperature in the PSSD and stifles in the SG. The minimum acupuncture diagnostic criteria for stifle joint disease had a sensitivity of 87.5% and a specificity of 57.0%, and the addition of the acupoints Gallbladder-dorsal tuber coxae, Gallbladder-27, and Spleen-13 to the minimum diagnostic criteria improved sensitivity and specificity. In conclusion, assessing the reaction at the demonstrated acupoints can facilitate a diagnosis of a potential stifle lesion.

Dietary fatty acid content regulates wound repair and the pathogenesis of osteoarthritis following joint injury.

OBJECTIVE: The mechanisms linking obesity and osteoarthritis (OA) are not fully understood and have been generally attributed to increased weight, rather than metabolic or inflammatory factors. Here, we examined the influence of fatty acids, adipokines, and body weight on OA following joint injury in an obese mouse model. METHODS: Mice were fed high-fat diets rich in various fatty acids (FA) including saturated FAs (SFAs), ω-6 polyunsaturated FAs (PUFAs), and ω-3 PUFAs. OA was induced by destabilising the medial meniscus. Wound healing was evaluated using an ear punch. OA, synovitis and wound healing were determined histologically, while bone changes were measured using microCT. Activity levels and serum cytokines were measured at various time-points. Multivariate models were performed to elucidate the associations of dietary, metabolic and mechanical factors with OA and wound healing. RESULTS: Using weight-matched mice and multivariate models, we found that OA was significantly associated with dietary fatty acid content and serum adipokine levels, but not with body weight. Furthermore, spontaneous activity of the mice was independent of OA development. Small amounts of ω-3 PUFAs (8% by kcal) in a high-fat diet were sufficient to mitigate injury-induced OA, decreasing leptin and resistin levels. ω-3 PUFAs significantly enhanced wound repair, SFAs or ω-6 PUFAs independently increased OA severity, heterotopic ossification and scar tissue formation. CONCLUSIONS: Our results indicate that with obesity, dietary FA content regulates wound healing and OA severity following joint injury, independent of body weight, supporting the need for further studies of dietary FA supplements as a potential therapeutic approach for OA.

Inactivation of xanthine oxidoreductase is associated with increased joint swelling and nitrotyrosine formation in acute antigen-induced arthritis.

OBJECTIVE: Arthritis is associated with increased articular formation of nitrotyrosine, which may contribute to injury. Nitrotyrosine is formed by nitration of tyrosine by reactive nitrogen species such as peroxynitrite, the formation of which may be enhanced by xanthine oxidoreductase (XOR), since it can generate nitric oxide from nitrite/nitrate, and superoxide during xanthine metabolism. We hypothesized that inactivation of XOR would protect against antigen-induced arthritis (AIA) and decrease nitrotyrosine formation. METHODS: AIA was induced with methylated bovine serum albumin (mBSA) in three groups of Wistar rats: animals fed on (1) tungsten-enriched chow (0.7 g/kg) (TG), which inactivates XOR, (2) standard chow (SG), and (3) rats treated with allopurinol (50 mg/kg/day; p.o.) (AG). Nitrotyrosine in patella-synovium was quantified by mass spectrometry three weeks after intra-articular (i.a.) antigen injection. RESULTS: Treatment with tungsten, but not allopurinol, suppressed plasma and articular XOR activity at < or = 0.9% of normal levels. XOR inactivation was associated with increased knee swelling 24-48 hrs post i.a. mBSA, compared with controls (mean increase +/- SEM of knee diameter from baseline of 3.3 +/- 0.5, 2.0 +/- 0.3 and 1.9 +/- 0.2 mm in TG, SG and AG (n = 14 each group), respectively; p < 0.05, TG vs SG, ANOVA). Mean ratio of articular nitrotyrosine-tyrosine (+/- SEM) was increased in the XOR-inactivated group, compared with controls: 12.3 +/- 0.7, 9.6 +/- 0.8 and 10.4 +/- 0.5 pg/microg in TG, SG and AG, respectively; p < 0.05, TG vs SG. CONCLUSION: Contrary to expectation, XOR inactivation was associated with increased joint swelling and articular tyrosine nitration in acute AIA, suggesting a novel, protective role for XOR in inflammatory arthritis.

Fascia lata autograft for treatment of congenital cranial cruciate ligament deficiency in a llama.

An 11.4-kg female llama that had been born without assistance while its dam was under observation at the veterinary teaching hospital was observed to ambulate abnormally on its right hind limb. A cranial drawer sign could be elicited in the right stifle. Cranial displacement of the tibia relative to the femur and dysplasia of the proximal end of the tibia were seen on radiographs. When the cria was 10 days old, the joint was stabilized with a fascia lata autograft. At the time of surgery, a segment of thin, loose tissue was found where the cranial cruciate ligament would have been. Three years after surgery, the llama gave birth to a normal cria and was 60 days pregnant with a second cria. To our knowledge, congenital cranial cruciate ligament deficiency with tibial dysplasia has not been reported in llamas. The heritability of these defects is unknown.