Treating Canine Osteoarthritis

Osteoarthritis (OA), also known as degenerative joint disease (DJD), is a debilitating disorder that can affect many animal species.

Related Article: Feline Degenerative Joint Disease Part 1: Diagnosis

OverviewIn dogs, OA commonly causes joint dysfunction with stiffness, loss of mobility, and varying degrees of inflammation and pain. OA is typically a result of joint instability from ligament laxity, strains, direct or indirect injury, or faulty bone and cartilage development.

Less efficient repair processes in older patients make age a contributing factor, and the condition may be exacerbated by obesity and/or overexertion. OA may affect up to 20% of dogs over 1 year of age,¹ and nearly 50% of musculoskeletal disorders identified in a 10-year span in 16 veterinary hospitals resulted from joint disease.¹

Clinical SignsOnce joint cells are stressed or damaged, enzymes that fray and ulcerate joint cartilage and compromise the lubricants of the joint fluid are released. This damage causes the joint lining and capsule to become inflamed and bone that is underlying the cartilage to become less resilient.

Related Article: Treatment of Feline Degenerative Joint Disease

When the sensitive tissues of both joint capsule and bone are affected (usually after significant articular cartilage damage), signs of pain, lameness, swelling, stiffness, and muscle atrophy are typically apparent. The body then reacts with an ossification process (ie, laying down bone) in the attempt to stabilize the joint, reduce movement, and potentially lessen pain. However, this degenerative process may still result in lifelong pain.

DJD = degenerative joint disease, OA = osteoarthritis

DiagnosisThe initial stages of OA are not readily apparent, but once deterioration has reached the synovial membrane and/or bone beneath joint cartilage, painful inflammation begins. The first visible signs of OA pain may include lameness; apparent pain with range of motion (ROM); sensitivity to palpation of the affected area; decreased activity; stiffness (especially after rest); difficulty rising, lying down, or climbing stairs; or inability or reluctance to jump.

Radiographs can reveal and help confirm preliminary indicators of OA (eg, joint effusion) or more advanced changes (eg, calcification within and around the joint, often appearing as osteophytes).

Arthrocentesis can help rule out other causes of joint effusion or pain. For example, if nondegenerate neutrophils are present on joint fluid cytology and analysis, immune-mediated and/or tick-borne diseases are more likely. In contrast, the presence of significant monocytic inflammation (ie, high mononuclear cells) often confirms DJD or classic OA.

It is important to identify and treat underlying joint instabilities or pathologies, including fragmented coronoid process, osteochondrosis dissecans, ruptured cranial cruciate ligament, meniscal injury, or collateral ligament injury.

DJD = degenerative joint disease, HA = hyaluronic acid, OA = osteoarthritis, PSGAG = polysulfated glycosaminoglycan, ROM = range of motion

Related Article: Omega-3 Benefits & Osteoarthritis

How I Treat Canine OA

Treat and remove underlying joint pathology to ensure treatment success.

Administer slow-acting, disease-modifying OA agents.

• Injectable products include polysulfated glycosaminoglycan (PSGAG; Adequan) and intraarticular hyaluronic acid (HA; Hylartin V).

• As OA advances, weekly to monthly injections of PSGAG can help lessen joint pain.

• Intraarticular HA injections can help reduce joint pain and inflammation and reestablish normal joint environment.

• Oral products include glucosamine hydrochloride and chondroitin sulfate, methylsulfonylmethane, and long-chain omega-3 fatty acids (eg, docosahexaenoic acid, avocado soybean unsaponifiables, eicosapentaenoic acid [Cosequin, Dasuquin, or Welactin]).

• Start patients on oral glucosamine-chondroitin sulfate and omega-3 fatty acid supplements at the first signs of OA.

• Athletic patients can be started earlier in life to help lower the incidence of OA from joint overexertion.

Consider intraarticular steroid injections (eg, methylprednisolone, triamcinolone).

• These injections can be used to reduce pain and inflammation in refractory patients.

• Evidence suggests that intraarticular steroids can protect articular cartilage in experimental canine OA; however, repeated use may also have deleterious effects on joint tissue from suppression of cartilage matrix synthesis.^2-4

• Benefits typically outweigh risks.

• Strict aseptic technique is essential to avoid iatrogenic septic arthritis.

Provide or refer for rehabilitation therapy.

• Therapy should begin with modality treatment, such as cold laser and transelectrical neuromuscular stimulation, to help reduce inflammation, effusion, and pain.

• Home exercise programs should include passive ROM to improve and maintain full-joint ROM, as well as muscle-building exercises to improve potential muscle atrophy.

• Once pain and discomfort have been reduced and controlled, hydrotherapy (eg, underwater treadmill, deep water or swim therapy) can help increase joint ROM and muscle building, and hydrostatic pressure and warm water temperatures may help lessen joint effusion and chronic pain.

Recommend weight loss and exercise, if indicated.

Consider alternative therapies:

• Acupuncture to decrease chronic pain

• Stem cell and/or platelet-rich plasma therapy

Institute medical management.

• NSAIDs are commonly used to treat OA.

• Many NSAIDs may produce adverse effects (eg, GI,liver, kidney damage) with long-term use.

• NSAIDs should be used sparingly but can be offeredfor breakthrough pain or when other therapies are insufficient.

• Although NSAIDs should not be used concurrently with systemic steroids, they can be used concurrently with intraarticular steroid injections.

• Tramadol (an opioid derivative that acts on serotonergic and α-adrenergic systems) and gabapentin or amantadine (neuropathic, musculoskeletal pain cascade-blocking agents [N-methyl-d-aspartate] receptor antagonists) can be used in conjunction with NSAIDs when refractory pain is suspected.

DEBRA A. CANAPP, DVM, CCRT, CVA, DACVSMR, is coprincipal and medical director of Veterinary Orthopedic & Sports Medicine Group, through which she provides sports medicine and rehabilitation care to canine athletes, working dogs, and companion animals. Dr. Canapp has lectured across the globe, including at the NAVC Conference, ACVS Symposium, AVO (in Germany), and NAHA (in Japan). She specializes in small animal musculoskeletal diagnostics, therapeutic ultrasonography, and ultrasound-guided regenerative medicine injections.

CANINE OSTEOARTHRITIS • Debra A. Canapp

References

1. Incidence of canine appendicular musculoskeletal disorders in 16 veterinary teaching hospitals from 1980 through 1989. Johnson JA, Austin C, Breur GJ. Vet Comp Orthop Trauma 7:56-69, 1994.2. The in vivo effects of intraarticular corticosteroid injections on cartilage lesions, stromelysin, interleukin-1 and oncogene protein synthesis in experimental osteoarthritis. Pelletier JP, Di Battista JA, Raynauld JP, et al. Lab Invest 72:578-586, 1995.3. Intraarticular injections with methylprednisolone acetate reduce osteoarthritic lesions in parallel with chondrocyte stromelysin synthesis in experimental osteoarthritis. Pelletier JP, Mineau F, Raynauld JP, et al. Arthritis Rheum 37:414-423, 1994.4. Intraarticular corticosteroid for treatment of osteoarthritis of the knee. Bellamy N, Campbell J, Robinson V, et al. Cochrane Database Syst Rev 19:CD005328, 2005.

Suggested Reading

Beyond NSAIDs for canine osteoarthritis patients: What other drug options exist? Lascelles DBX. Symposium: A Multimodal Approach to Treating Osteoarthritis, 2007, pp 8-12.Comparison of polysulphated glycosaminoglycan and sodium hyaluronate with placebo in treatment of traumatic arthritis in horses. Gaustad G, Larsen S. Equine Vet J 27:356-362, 1995.Effect of intraarticular HA injection on the synovial fluid of OA joints. Smith GN Jr, Mickler EA, Myers SL, Brandt KD. ORS Proceedings, 2000, p 233.Effect of intraarticular hyaluronan injection in experimental canine osteoarthritis. Smith GN Jr, Myers SL, Brandt KD, Mickler EA. Arthritis Rheum 41:976-985, 1998.Effects of an oral chondroprotective agent (Cosequin) on cartilage metabolism and canine serum. McNamara PS, Barr SC, Idouraine A, Lippiello L. Veterinary Orthopedic Society Proceedings, 1997, p 35.Effects of intramuscular administration of glycosaminoglycan polysulfates on signs of incipient hip dysplasia in growing pups. Lust G, Williams AJ, Burton-Wurster N, et al. Am J Vet Res 53:1836-1843, 1992.Evaluation of polysulfated glycosaminoglycan for the treatment of hip dysplasia in dogs. de Haan JJ, Goring RL, Beale BS. Vet Surg 23:177-181, 1994.Hyaluronan in canine arthropathies. Arican M, Carter SD, May C, Bennett D. J Comp Pathol 111:185-195, 1994.Intraarticular sodium hyaluronate injections in the Pond-Nuki experimental model of osteoarthritis in dogs. I. Biochemical results. Abatangelo G, Botti P, Del Bue M, et al. Clin Orthop Relat Res 278-285, 1989.Long-term effect on nonsteroidal anti-inflammatory drugs on the production of cytokines and other inflammatory mediators by blood cells of patients with osteoarthritis. González E, de la Cruz C, de Nicholäs R, et al. Agents Actions 41:171-178, 1994.NSAIDs and nutraceuticals: What’s the evidence? Fox, SM. Symposium: A Multimodal Approach to Treating Osteoarthritis, 2007, pp 2-5.Nutraceuticals as therapeutic agents in osteoarthritis. The role of glucosamine, chondroitin sulfate, and collagen hydrolysate. Deal CL, Moskowitz RW. Rheum Dis Clin North Am 25:379-395, 1999.Oral treatment with a glucosamine-chondroitin sulfate compound for degenerative joint disease in horses: 25 cases. Hanson RR, Smalley LR, Huff GK, et al. Equine Practice, 19:16-22, 1997.Pharmacologic and clinical aspects of intraarticular injection of hyaluronate. Iwata H. Clin Orthop Relat Res 285-291, 1993.Rapid and sustained rise in the serum level of hyaluronan after anterior cruciate ligament transection in the dog knee joint. Manicourt DH, Cornu O, Lenz ME, et al. J Rheumatol 22:262-269, 1995.Scintigraphic evaluation of dogs with acute synovitis after treatment with glucosamine hydrochloride and chondroitin sulfate. Canapp SO Jr, McLaughlin RM Jr, Hoskinson JJ, et al. Am J Vet Res 60:1552-1557, 1999.Slow acting, disease-modifying osteoarthritic agents. McNamara PS, Johnston SA, Todhunter RJ. Vet Clin North Am Small Anim Pract 27:863-881, 1997.Stimulation of proteoglycan production by glucosamine sulfate in chondrocytes isolated from human osteoarthritic articular cartilage in vitro. Bassleer C, Rovati L, Franchimont P. Osteoarthritis Cartilage 6:427-434, 1998.Systemic administration of glycosaminoglycan polysulphate (arteparon) provides partial protection of articular cartilage from damage produced by meniscetomy in the canine. Hannan N, Ghosh P, Bellenger C, Taylor T. J Orthop Res 5:47-59, 1987.The effect of additive hyaluronic acid on animal joints with experimentally reduced lubricating ability. Mabuchi K, Tsukamoto Y, Obara T, Yamaguchi T. J Biomed Mater Re_s 28:865-870, 1994.Treatment of degenerative joint disease. Manley, PA. In Bonagura JD, Kirk RW (eds): _Kirk’s Current Veterinary Therapy XII—Philadelphia: W.B. Saunders, 1995, pp 1196-1199.Treatment of osteoarthritis with chondroprotective agents. Hungerford DS. Orthopedics Special Edition 4:39-42, 1998.