Osteoarthritis (OA) is one of the most common chronic, painful conditions recognized in dogs and cats. Challenges in management arise because of lack of early recognition and progressive pathological changes.
Etiology and Pathophysiology of Osteoarthritis in Dogs and Cats
In dogs with OA, unlike in humans, the inflammatory and degenerative process very often begins quite early in life and depends in large measure on heritable, appendicular skeletal conformational abnormalities.
The pathophysiology of OA in cats is poorly understood, but the disease can also be present when cats are young. In cats, except in Maine Coon Cats, which do get hip dysplasia, OA is not generally related to orthopedic conformation.
In OA, progressive deterioration of articular cartilage in diarthrodial joints is characterized by hyaline cartilage clefts and thinning, joint effusion, and periarticular osteophyte formation. Joint degeneration can be caused by trauma, infection, immune-mediated diseases, or (in the dog, most commonly) developmental malformations. The inciting cause initiates chondrocyte necrosis; release of degradative enzymes and proinflammatory, pronociceptive mediators; and synovitis, which in turn leads to continued cartilage destruction, creating a circular and ever-advancing disease state.
The pain of OA is felt less at the damaged articular surfaces than in the peri- and subarticular structures. Contributors to pain include the following:
inflamed synovium (synovitis, which can be pronounced, with great fronds of richly innervated neovascularization, and is a key feature driving OA pathophysiology)
eventual exposure of innervated subchondral bone
inflamed and fibrotic joint capsule
exertion on weakened ligaments, tendons, and muscle
Abnormal cartilage congruency and joint capsule anatomy can further lead to alteration in normal joint biomechanical function.
Pain and lameness develop secondary to joint dysfunction or muscle atrophy and to disuse of affected limbs; weight redistribution to, and consequent strain on, alternative limbs also leads to progressive disability. Thus, OA is a disease of the entire joint organ and indeed of the entire musculoskeletal system.
Furthermore, in approximately one-quarter of any given cohort of affected patients, OA has a maladaptive, if not abjectly neuropathic pain, component. During its lifetime, any individual patient will likely develop this exaggerated pain-processing component.
Epidemiology for Osteoarthritis in Dogs and Cats
Risk factors for OA in dogs begin with breed predisposition (see the table Heritable Conformational Conditions Resulting in Canine Osteoarthritis) and extend to breed dispositions for a variety of other painful orthopedic conditions, injuries, and inflammatory joint diseases.
Heritable Conformational Conditions Resulting in Canine Osteoarthritis
Condition | Common Breeds with Highest Odds Ratio |
|---|---|
Legg-Calvé-Perthes disease (avascular necrosis of the femoral head) | Australian Shepherd, Chihuahua, Miniature Pinscher, Pug, Toy Poodle, West Highland White Terrier, Yorkshire Terrier |
Elbow dysplasia | |
Fragmented medial coronoid process | Bernese Mountain Dog, Bullmastiff, German Shepherd Dog, Irish Wolfhound, Labrador Retriever, Rottweiler, Saint Bernard |
Ununited anconeal process | Bernese Mountain Dog, Mastiff, Rottweiler |
Osteochondritis dissecans (OCD) | |
Shoulder | Bernese Mountain Dog, Great Dane, Great Pyrenees, Irish Wolfhound, Labrador Retriever Large-breed dogs, especially German Shepherd Dog, Rottweiler Sporting breeds |
Elbow | Chow Chow, Golden Retriever, Great Dane, Labrador Retriever, Newfoundland, Rottweiler |
Stifle | Boxer, Bulldog, Great Dane, Irish Wolfhound, Mastiff, Rottweiler |
Hock | Bullmastiff, Labrador Retriever, Rottweiler |
Medial shoulder instability/subluxation | Chihuahua, Dachshund, Pekinese, Shetland Sheepdog, Toy Poodle |
Angular limb deformity (premature growth plate closure) | |
Pes varus | Dachshund |
Pes valgus | Collie, Newfoundland, Rottweiler, Shetland Sheepdog |
Genu valgum (knock-knee) | Small-breed dogs |
Genu varum (bowlegs) | Large-breed dogs |
Luxating patella | |
Medial | Maltese, Pomeranian, Toy Poodle, Yorkshire Terrier |
Lateral | Akita, Bulldog, Cavalier King Charles Spaniel, Chihuahua, Chinese Shar-Pei, Great Pyrenees |
Poor tibial plateau angle resulting in cranial cruciate ligament injury/rupture | Airedale Terrier, Alaskan Malamute, American Staffordshire Terrier, Boxer, Chow Chow, Labrador Retriever, Newfoundland, Rottweiler, Saint Bernard Neutered male, spayed female, and sexually intact female dogs predisposed Akita, Chesapeake Bay Retriever, and Mastiff were also predisposed; obesity a risk factor |
In dogs, the highest prevalence of hip dysplasia is in breeds that tend to be stocky, round, and heavy (eg, German Shepherd Dog, Labrador Retriever). The lowest prevalence is in slender, trim, fleet-footed, and highly coordinated breeds (eg, Greyhound, Whippet).
In cats, hip dysplasia is found predominately in Maine Coon Cats.
Physical examination in puppies at risk for hip dysplasia should include the Ortolani maneuver; elicitation of a characteristic pop or thunk indicates hip laxity and likely early development of OA. The PennHIP radiographic technique can detect hip laxity in young dogs but requires sedation, a distraction device, and training to accomplish.
The Orthopedic Foundation of America (OFA) will certify hip and elbow character (and give preliminary evaluations between 4 and 24 months) with specifically positioned radiographs of dogs 2 years and older.
Interestingly, hip dysplasia is not reported in wild, undomesticated carnivores. It has been speculated that this is because they often mature slowly due to poor nutrition, although genetics may play an important role.
Nutrition has been shown to play a role in development of hip dysplasia in domesticated dogs. Caloric restriction over a 5-year period in dogs at risk for hip dysplasia was found to minimize development of coxofemoral OA (1).
Other historical and environmental factors also impact development of hip dysplasia in dogs. One report of 501 dogs found increased risk of developing a dysplastic phenotype in puppies allowed to take stairs at or before 3 months old. The study found diminished radiographic evidence of hip dysplasia in puppies that were allowed off-leash before 3 months and those born on a farm or in the spring or summer (2).
Although up to 40% of dogs aged 8 months–4 years have OA (3), clinical signs are generally not identified until dogs are 5–13 years old (4). Similarly, OA is underrecognized in cats: approximately 60% of all cats, and over 90% of cats > 12 years old, can be identified as having degenerative joint disease (DJD) (5).
Clinical Signs of Osteoarthritis in Dogs and Cats
Lameness is a key clinical sign associated with OA. Importantly, lameness may be less apparent than expected—not only with early disease but even with advanced bilateral disease.
Common clinical signs include slowness to rise, especially after extended rest; initiating with forelimbs, then hoisting up hindlimbs, or vice versa; difficulty going up or down stairs; and limited jumping or playing.
Physical examination findings can include the following:
joint and periarticular swelling, with asymmetry to the contralateral joint (eg, medial buttress on the stifle)
muscle atrophy
abnormal conformation, such as kyphosis
straight rear limb
abducted elbows
crepitation and resistance to range of motion from synovitis, osteophytosis, or pericapsular fibrosis
Diagnosis of Osteoarthritis in Dogs and Cats
Radiographic changes in degenerative joint disease include joint effusion, periarticular soft tissue swelling, osteophytosis, subchondral bone sclerosis, and possibly narrowed joint space (see DJD radiographs, ventrodorsal and lateral). Arthrocentesis may be unremarkable or yield minor changes in color, turbidity, or cell counts of synovial fluid.
Courtesy of Dr. Ronald Green.
Courtesy of Dr. Ronald Green.
Force-plate and gait analysis technology can provide objective data regarding patient weight bearing and stride abnormalities during a controlled walk. Limitations exist with bilateral joint disease, poor patient cooperation, and restricted availability outside the research setting. Artificial intelligence technology has the promise to overcome these barriers, including the prospective ability to generate objective data from at-home video images.
Validated clinical metrology instruments (CMIs) allow for semi-objective scoring of owner-observed, DJD-related pain as it affects mobility and other activities of daily living. CMIs include the following:
For dogs:
For cats:
The Canine Osteoarthritis Staging Tool (COAST) has been developed to promote a standardized approach to diagnosis and monitoring of OA by characterizing an individual dog on a 0–4 scale based on risk factors, owner's observations, physical examination findings, and radiographic results (4). In brief, the stages of the COAST guidelines are as follows:
COAST Stage 0: Clinically normal with no risk factors
COAST Stage 1: Clinically normal but with one or more risk factors (breed disposition, history of prior joint injury, overweight, highly active instead of sedentary, older)
COAST Stage 2: With risk factors and mild clinical signs
COAST Stage 3: With risk factors and moderate clinical signs
COAST Stage 4: Severe clinical signs
Treatment of Osteoarthritis in Dogs and Cats
Given the variable interpatient biological nature of OA, paucity of properly designed multimodal treatment studies in dogs and cats, and widely divergent values among clients and veterinarians, formulating a standard approach is difficult.
The AAHA Pain Management Guidelines and the WSAVA Global Pain Council’s Guidelines for Recognition, Assessment, and Treatment of Pain provide guidelines for assessment and management of acute and chronic pain in dogs and cats (6, 7).
Specifically for OA in dogs, treatment guidelines based on the COAST stages have been developed (4). Whereas treatment should be based on clinical signs rather than radiographic findings, the COAST Development Group's treatment recommendations are organized by the COAST stage determined after radiography is excluded.
Pearls & Pitfalls
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Similar consensus guidelines for treatment of OA in cats have not been published.
Weight Optimization
Weight optimization, the primary preventive method to slow development of OA in dogs, is imperative if the patient is already overweight. Adipose tissue is the body’s largest endocrine organ and secretes a variety of proinflammatory, pronociceptive mediators and cytokines, driving both pain and pathophysiological changes. The primacy of even very modest weight loss to improving function in overweight dogs with OA is well established. For overweight dogs with moderate to severe clinical signs from OA (COAST stages 3 and 4), gaining a leaner body condition is crucial.
The role of excess weight in OA-related pain and pathophysiology is less clear in cats than in dogs; however, in cats with OA and other health risks, maintaining a lean body condition is advised.
Regular, Controlled Exercise
Exercise elicits hypoalgesia through a variety of mechanisms, including spinal-level blockade of nociceptive signaling in favor of touch, pressure, and proprioception (according to gate control theory); activation of the endogenous cannabinoid system; and increased strength and microstability of joint soft tissue structures. In dogs at risk, exercise may be protective for hip dysplasia.
Fatty Acid Supplementation
In dogs, eicosapentaenoic acid (EPA) supplementation (50–100 mg/kg, PO, every 24 hours) and EPA-rich diets have been demonstrated to elicit improved gait and mobility and to have an NSAID-sparing effect.
Diets rich in the omega-3 fatty acid docosahexaenoic acid (DHA) are commercially valuable for cats, but evidence supporting effectiveness in OA in cats is not clear.
NSAID Therapy
NSAIDs (including the subclass of prostaglandin E2 type 4 [EP4] receptor antagonists) are the most predictably effective treatment for OA. In dogs with mild clinical signs from OA (COAST stage 2), ≥ 1 month of treatment with NSAIDs may be required before attempting withdrawal. In dogs with moderate to severe clinical signs from OA (COAST stages 3 and 4), NSAIDs may be used on a more sustained, longterm basis.
In cats, utility and safety of longterm use of low-dose meloxicam (0.02 mg/kg, PO, every 24 hours) and robenacoxib (2 mg/kg, PO, or 1 mg/kg, SC, every 24 hours and then adjusted to the lowest effective dose) have been established. This is the case even in cats with International Renal Interest Society (IRIS) stage 1 and 2 chronic kidney disease that is stable (unchanged weight, renal marker concentrations, urinary protein:creatinine concentration ratio, and blood pressure over the previous 2-month period). Safety is less certain in cats with IRIS 3 and 4. This usage is on an extralabel basis in the US. In the EU, meloxicam (0.05 mg/kg, PO, every 24 hours longterm) is labeled for chronic musculoskeletal pain in cats. Consensus guidelines on the longterm use of NSAIDs in cats have been developed (8).
Chondroprotectants
Glucosamine and chondroitin sulfate are among the most common nutraceuticals used in pain management in dogs and cats with OA. However, a systematic review of nutritional supplements and meta-analysis of the published literature (9) found no evidence of a beneficial effect and concluded that the available evidence did not support the use of these supplements for pain management in OA in dogs and cats. Commercial glucosamine and chondroitin sulfate nutritional supplements may contain other ingredients (eg, avocado and soybean unsaponifiables, type II collagen, eggshell membrane) that are possibly efficacious in treating OA.
In dogs, polysulfated glycosaminoglycan (PSGAG; 4.4 mg/kg, IM or SC, twice weekly for up to 8 treatments) or pentosan polysulfate (PPS; 3 mg/kg, SC or IM, every 5–7 days for up to 4 treatments) may be more beneficial in the earlier stages of OA.
In cats, PSGAG (5 mg/kg, SC, twice weekly for 4 weeks, then once weekly for 4 weeks, then once monthly) distributes effectively to joints.
Although commercial hyaluronic acid products exist for humans and animals, their benefit in treating OA remains questionable.
Anti–Nerve Growth Factor Monoclonal Antibodies
Bedinvetmab (0.5 mg/kg, SC, every 30 days) is useful for dogs with moderate to severe clinical signs from OA (COAST stages 3 and 4). Use can be considered in dogs with mild clinical signs from OA (COAST stage 2) but remains controversial.
Analysis of pharmacovigilance data from 3 years of bedinvetmab use in Europe and since the drug's approval in the US has resulted in the addition of 3 potential adverse events: injection site reaction (uncommon), polydipsia-polyuria (rare), and systemic reaction (very rare). In Canada, neurological disease is noted as a potential adverse effect, but causation related to administration of bedinvetmab remains uncertain.
The anti–nerve growth factor monoclonal antibody (NGF mAb) frunevetmab (1–2.8 mg/kg, SC, every 30 days) has become a valuable treatment in cats with OA.
Whereas NSAIDs address the underlying inflammatory process that emanates from cartilage damage, anti-NGF mAbs address neurogenic inflammation and peripheral sensitization. A drug-drug interaction (DDI) between the two drug classes is not known to occur in dogs and cats, and some patients will likely benefit from using both.
Other Pain-Modifying Analgesic Drugs
Limited data on other pain-modifying analgesic drugs are available for dogs and cats. However, for dogs with moderate to severe clinical signs from OA (COAST stages 3 and 4), the following modalities can be considered:
Amantadine (3–5 mg/kg, PO, every 12–24 hours) is a weak N-methyl-D-aspartate (NMDA)-receptor antagonist.
Gabapentin (10–20 mg/kg, PO, every 8–12 hours) and pregabalin (2–5 mg/kg, PO, every 8–12 hours) work through downregulation of calcium channels.
Ketamine (subanesthetic doses; no unifying protocol has been devised) is a potent NMDA-receptor antagonist.
Among pain-modifying analgesic drugs, gabapentin (10 mg/kg, PO, every 12 hours longterm) has been the most commonly used medication to treat OA in cats, and some limited data suggest clinical utility. One study demonstrates the possible utility of amantadine (3–5 mg/kg, PO, every 12–24 hours) as an adjunctive treatment.
For dogs with severe clinical signs from OA (COAST stage 4), additional treatments can be considered, although depending on the treatment, limited to no data exist supporting efficacy, safety, or dose titration:
selective serotonin norepinephrine reuptake inhibitors (SSNRIs), such as venlafaxine (1–4 mg/kg, PO, every 24 hours)
tapentadol (10 mg/kg, PO, every 24 hours; note that tramadol has poor pharmacokinetics in dogs compared with humans and is ineffective in canine arthritis)
cannabinoids (evidence remains mixed at this time; quality control and regulatory issues pose challenges for use)
acetaminophen (10–15 mg/kg, PO, every 8–12 hours; dogs only), with or without codeine (1–2 mg/kg, PO, every 8–12 hours); although likely safe with judicious use, evidence is mixed as to bioavailability and clinical effectiveness of codeine, and it poses risk for diversion
low-dose naltrexone (0.02 mg/kg, PO, every 24 hours); based on human data—limited data in animals
Tramadol (2 mg/kg, PO, every 12 hours longterm) has favorable pharmacokinetics and appears effective in cats with OA but is quite bitter. Limited data exist regarding the use of other pain-modifying analgesic agents (eg, cannabinoids, SSRIs, opioids, and ketamine) for chronic OA-related pain in cats. Acetaminophen is contraindicated in cats.
Interventional Joint Treatments
Interventional (intra-articular) joint treatments include biologics, radiation (ablates synovitis), and corticosteroids.
Investigational biologics represented in the literature, with some in clinical use, include the following:
autologous mesenchymal stem cells
platelet-rich plasma
adipose-derived stromal vascular fraction
microfragmented adipose tissue
autologous protein solution
autologous conditioned serum (IL-1 antagonist)
plasmid-derived IL-10
resiniferatoxin (transient receptor potential vanilloid 1 [TRPV1] agonist)
These products have noteworthy interproduct heterogeneity.
Evidence supports use of radiation as a therapeutic modality (ablating synovitis) for OA, including external beam radiation (10) or via joint injection of tin-117m radionuclide (an FDA-approved device for treatment of canine elbow OA) (11).
Corticosteroids are a first-line palliative agent in humans (often pending joint replacement). Intra-articular corticosteroids are chondrotoxic and generally not advised in dogs and cats except as a salvage treatment.
Surgical Options
With surgery, the prognosis is variable and depends on the arthropathy's location and severity. Surgical interventions include the following:
joint fusion (arthrodesis, most frequently performed on the carpus and tarsus)
joint replacement (eg, total hip replacement)
joint excision (eg, femoral head and neck osteotomy)
amputation
Other Nonpharmacological Interventions
Other nonpharmacological interventions in dogs include, but are not limited to, the following:
therapeutic laser
pulsed electromagnetic field therapy
acupuncture
household enrichment and accommodations
Data are limited regarding nonpharmacological interventions with OA in cats, but they can be deployed at the clinician's discretion. Therapeutic household enrichment and exercise opportunities have benefits in cats similar to those in dogs.
Key Points
Osteoarthritis is a lifetime disease, with subtle clinical signs in patients existing long before they become obvious.
Preventive and therapeutic measures should begin far earlier than has historically been the case.
For More Information
References
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