Nutritional Support for the Post-op Joint Sx Patient
World Small Animal Veterinary Association World Congress Proceedings, 2015
R. Palmer1, DVM, MS, DACVS; C. Villaverde2, BVSc, PhD, DACVN, DECVCN
1Professor - Orthopaedics, Sports Medicine & Rehabilitation, Veterinary Teaching Hospital, Colorado State University, Fort Collins, CO, USA; 2Adjunct Professor - Animal Nutrition, Universitat AutÁnoma de Barcelona, Spain

"Caribou"

4-year-old, m/n, Yorkshire Terrier, 4.3 kg, BCS = 6–7/9

History

Grade 5/5 lame on L thoracic limb after falling from couch

Past Pertinent History

Unsuccessful repair of R humeral condyle fracture at 9 months of age has resulted in non-painful, grade 5/5 lameness on R thoracic limb.

Exam

Non-ambulatory. Sits up; avoids weight-bearing on either thoracic limb; painful crepitus in left elbow upon passive range of motion.

Radiographs

Fracture of left humeral condyle. Malunion of right humeral condyle fracture.

Surgery

Anatomic reduction and stabilization of intra-articular fracture of left elbow.

Postoperative Nutritional Goals

Life-long protection of joint health is especially important since the patient has no function in the contralateral thoracic limb.

Weight loss to BCS 4–5/9. Initial target weight = 3.5 kg.

Promotion of Joint Health

The healthy joint is a highly metabolic organ comprised of cartilage, bone, synovium, neural and supportive muscle tissues whose function is critical to mobility and life quality. In post-traumatic joints, the metabolic balance may shift toward catabolism driven by cytokine cascades and inflammatory mediators. It is logical that nutritional support for the postoperative joint surgery patient should be directed at promoting anabolic functions while mitigating the catabolic processes.

For life-long promotion of joint health, we will consider dietary supplementation with nutraceuticals including glucosamine, chondroitin sulfate, and avocado-soybean unsaponifiables. Omega-3 fatty acids can be provided within a specific therapeutic diet, or in some instances via supplementation.

Avocado Soybean Unsaponifiables (ASU)

Prospective, randomized, double-blinded, placebo-controlled parallel-group studies have shown that ASU significantly reduced pain, functional impairment and NSAID reliance in humans suffering from OA in the knees and hips.1,2 Activated chondrocytes incubated with ASU showed reduced TNF-α, IL-1β, COX-2 and iNOS expression to levels similar to that of normal non-activated chondrocytes.3 The suppression of COX-2 and iNOS expression was paralleled by a significant reduction in PGE2 and nitrite. ASU also reduced TNF-α and IL-1β expression in activated monocyte/macrophage-like cells. These findings demonstrate the anti-inflammatory activity of ASU on both chondrocytes and synovial membrane macrophage prototypic cells and provide a scientific explanation for the pain-reducing and anti-inflammatory effects of ASU observed in OA patients.3

In a canine study, healthy young adult dogs were divided into 3 groups: (1) control, (2) 300 mg ASU orally every 3 days, and (3) 300 mg ASU orally once daily.4 Knee joint fluid was analyzed prior to supplementation and then each month to measure the levels of two isoforms of transforming growth factor β (TGF-β1 and TGF-β2). ASU, in both dosages, caused an increase in both TGF-β isoforms as compared to the control group. This study provides in vivo evidence for pro-anabolic effects of ASU since TGF-β is a stimulator of extracellular matrix production (type II collagen, proteoglycan) in chondrocytes.4 Further evidence of canine in vivo efficacy of ASU was provided in an ACL transection study in which the ASU-supplemented group showed reduced development of early OA cartilage and subchondral bone lesions (macroscopic and microscopic lesion severity, subchondral bone loss) as compared to placebo-treated controls.5 The therapeutic effect appeared to be mediated through inhibition of iNOS and MMP-13. A systematic review of human clinical trials was conducted.6

Out of 2,026 studies, 53 randomized human clinical trials (RCTs) met the inclusion criteria. Evidence of efficacy for OA treatment was classified for each nutritional compound (glucosamine and chondroitin sulfate were excluded) as good, moderate or limited. Good evidence was found for ASU, moderate evidence for methylsulfonylmethane (MSM) and SKI306X (a plant extract mixture), and limited evidence for Duhuo Jisheng Wan, cetyl myristoleate, lipids from green-lipped mussels and Harpagophytum procumbens extracts.6

ASU, Chondroitin Sulfate (CS), Glucosamine (Glu) Combinations

A recent study evaluated the effect of ASU, CS and ASU + CS combination upon proinflammatory cytokine (IL-1β, TNF-α) expression and PGE2 production from synovial lining surrogate cells.7 The ASU + CS combination inhibited IL-1β and TNF-α expression and PGE2 production better than either agent alone.7 Another study showed that canine chondrocytes propagated in microcarrier spinner culture retained their cartilage phenotype as evidenced by type II collagen production.8 When activated by IL-1β, these cells showed ~ 70% increased PGE2 production. Pre-incubation with ASU + CS + Glu combination decreased PGE2 production ~ 60% below that of non-activated control cells. This study provides evidence of a potent anti-inflammatory effect.8 A similar effect was noted in activated feline chondrocytes when ASU + CS + Glu pretreated cells were compared to positive (untreated activated cells) and negative (non-activated cells) controls.9 Recently, a study was conducted to evaluate the anti-inflammatory effect of ASU + epigallocatechin gallate (EGCG) on activated equine chondrocyte cell culture.10 EGCG is a major antioxidant component of green tea. Chondrocyte activation caused upregulated gene expression of COX-2 and increased PGE2 production and NF-κB nuclear translocation. Individually, ASU and EGCG marginally inhibited COX-2 expression and PGE2 production in activated chondrocytes. In contrast, ASU + EGCG combination reduced COX-2 expression close to that of non-activated control levels, significantly inhibited PGE2 production and NF-κB translocation. NF-κB is an essential transcription factor for COX-2 induction. Inhibition of the NF-κB pathway is known to attenuate COX-2 expression. This study demonstrates that the anti-inflammatory activity of ASU and EGCG is potentiated when used in combination.10

Collectively, a large body of in vitro evidence supports the conclusion that ASU + CS + Glu inhibits the expression and production of proinflammatory mediators in multiple species (canine, feline, equine and human) and in multiple joint cell lines (chondrocytes and synovial lining cells). Millis et al. evaluated 8 hound dogs with chronic induced stifle OA. A recent study arm on this dog colony evaluated Dasuquin® (Nutramax Labs), a nutraceutical containing Glu + CS + ASU + EGCG. Dogs treated with Dasuquin® showed increased peak vertical force similar to that seen with various NSAIDs in a previous study arm.11 Though the small study population does not permit meaningful statistical analysis, these data suggest the need for larger scale and longer term in vivo evaluation of Dasuquin® in the restoration of function and pain relief of dogs with chronic OA. It is important to evaluate these supplements with a placebo control and with objective measurements of function. Many studies are lacking this, which is why the evidence for the efficacy of these nutraceuticals in managing osteoarthritis is considered moderate. There is much less data supporting their efficacy for prevention of disease compared to treatment. These are very safe; thus, they are worth trying if there are no other limitations.

Omega-3 Fatty Acids

Clinical trials that suggest a therapeutic effect of omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) upon OA are frequently reported. One such study of dietary supplementation with fish oil omega-3 fatty acids in osteoarthritic dogs showed a significant improvement in weightbearing (peak vertical force - PVF) as compared to the control-group diet.12 The magnitude of improved weightbearing (+ 5.6%) was of similar magnitude reported in many NSAID trials. Improved PVF was noted in 82% of osteoarthritic dogs fed the omega-3 supplemented diet as compared to 38% fed the control diet.12

A similar study design was used to compare the effects of a test food supplemented with fish oil omega-3 fatty acids and a control diet on serum fatty acid concentrations and owner- and veterinary-assessed severity of OA.13 They reported that the test diet raised blood concentrations of omega-3 fatty acids and improved the owner-assessed ability to rise from a resting position, play, and walk compared with control dogs (who showed no improvement).13 Another study showed that a diet supplemented with omega-3 fatty acids allowed for more rapid reduction in carprofen dosage in osteoarthritic dogs as compared to dogs fed a diet with a low omega-3 fatty acid content.14 The recommended dose is 230 to 370 mg EPA and DHA per kg of metabolic bodyweight. It is easier to achieve this dose via enriched diets (especially if clinically tested) than supplementing, since fish oil supplements provide approximately 9 kcal per gram and can easily unbalance the ration.

Weight Loss Plan

Weight loss is a priority. Weight loss improves signs associated with joint disease. The options are: 1) use a weight-loss therapeutic diet, fortified in nutrients and low in energy density; 2) use a joint diet; and 3) use a joint diet also formulated for weight loss. For options 1 and 3, a rate of weight loss of 1–2% bodyweight per week is recommended. Only 0.5% for option 2, to avoid nutrient deficiencies in a non-fortified diet fed below energy requirements. To start, offer RER (70 x bodyweight (kg)0.75 kcal per day), and adjust twice a month to achieve the desired rate of weight loss. For option 1, once a BCS of 4/9 is achieved, a joint diet can be used, fed in controlled amounts for weight stability.

References

References are available upon request.

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

R. Palmer, DVM, MS (Physiology), DACVS
Veterinary Teaching Hospital
Colorado State University
Fort Collins, CO, USA


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