Contributors: Eithne Comerford, David Godfrey, John Innes, Melvyn Pond, Jo Murrell

 Species: Feline   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading

Introduction

  • Progressive disorder of movable joints characterized by degeneration of articular cartilage and production of new bone at articular margins - the end-stage of a variety of pathological processes.
  • The most frequently encountered joint disease - synonyms are:
    • Osteoarthritis: emphasizes the inflammatory nature of condition.
    • Degenerative joint disease (DJD): deliberately broad term that encompasses osteoarthritis along with other predominantly degenerative conditions.
    • Osteoarthrosis: pathological process different from acute inflammatory process.
    • Secondary joint disease: initiating factors have been identified, eg joint instability due to abnormal conformation, ligament rupture or intra-articular fractures.
  • Osteoarthritis classification may be primary (idiopathic) or secondary (to an identifiable joint disease).
  • Cause: in cats this is not well established but it appears to be idiopathic in the considerable majority of cases. In other species it is often multifactorial: congenital/developmental abnormalities, obesity, trauma and other acquired disease are significant factors.
  • Signs: insidious onset change in normal behavior with a reduction in activity levels is the commonest sign observed by owners, lameness of one or more limbs, pain on palpation/manipulation, change of temperament, and poor grooming.
  • Treatment: environmental modification and medical treatments are usual. Surgical treatment would be rare. No treatment is required for pure radiographic signs if no clinical signs are evident but a short trial treatment with an analgesic may be appropriate to ensure that clinical signs have not gone unobserved.
  • Prognosis: this is a slowly progressive condition that often goes unnoticed by owners. Medical and/or surgical treatment may alleviate pain, decrease inflammation, improve function and slow progress of degenerative joint disease (DJD).
  • One of the commonest clinical problems of cats. Much overlooked and underdiagnosed in the past. The commonest musculoskeletal condition in cats.
Use the interactive tool from ROYAL CANIN® UK  to explain cat anatomy and disease conditions to your client. Visit ROYAL CANIN Natom Explorer to find out more.

Presenting Signs

Chronic

Cats that actually do have clinical signs of DJD often are presented to the practice for another reason (routine check, evaluation for another condition). Signs of DJD will only become clear if the veterinary surgeon asks appropriate questions of the owner.

  • Reduced activity levels usually with insidious onset.
  • Insidious onset lameness of one or more legs.
  • Jumping height progressively lowered or makes a jump up or down in stages where possible.
  • Change of temperament, depressed or aggressive when handled.
  • Accidents outside litter box.
  • Poor grooming habits.
  • Stiffness or limited range of movement.
  • Thickened joints.
  • Crepitus if severely damaged joint.
  • It is expected that clinical signs will become less severe or disappear within a day or two of starting an analgesic (see below).

Acute Presentation

  • Sudden onset lameness - presumably following trauma to already diseased joint.

Age Predisposition

  • Incidence has been shown to increase with increasing age.

Breed Predisposition

Primary OA

  • Maine Coons Maine Coon have been reported as predisposed to hip dysplasia, which is expected to predispose them to hip DJD although this has not yet been demonstrated.
  • Burmese Burmese have anecdotally been suggested to be predisposed to DJD or perhaps just to elbow DJD.

Pathogenesis

Etiology

  • Unproven in cats although at least 80% of cases seem to be idiopathic.
  • Trauma: a single severe injury or low-grade repeated trauma, eg abnormalities of joint anatomy/structure, conformational abnormalities, instability due to severe joint trauma, contra-lateral amputation.
  • Repetitive joint concussion if unproven to be important in cats.
  • ?Genetic - primary OA - has not been shown to occur in cats.
  • Obesity Obesity is suspected to be a significant factor but this has not yet been proven in cats.

Predisposing Factors

General

  • Joint instability as a result of ligamentous damage,  eg carpal collapse syndrome with diabetes mellitus, or cranial cruciate ligament damage are potential causes.
  • Joints most commonly affected are the elbow and hip. The shoulder, stifle and tarsus seem to be more commonly affected than the carpus or the digital joints.

Pathophysiology

These theories are extrapolated from other species.

  • Stress on normal or abnormal cartilage    →   enzymatic degradation of articular cartilage    →   softening of cartilage    →   progressive cartilage degradation    →   remodeling and osteophytosis.
  • Represents the end-stage of a variety of pathological processes: likely that both biochemical and biomechanical processes are involved    →   degeneration of articular cartilage and production of new bone at articular margins.

Biochemical theory

  • ?Cartilage wear particles    →   released into synovial fluid    →   irritant stimulation of resident joint cells    →   to produce mediators of connective tissue remodeling    →   biochemical cartilage degradation.
  • Intrinsic (arising from cartilage itself - chondrocytes more likely) or extrinsic (arising from synovial tissue) degradative enzymes (aggrecanases (especially), neutral proteases)    →   proteoglycan degradation    →   massive decrease in molecular weight of proteoglycan-hyaluronate aggregates    →   increase in water from articular cartilage and loss of stiffness of collagen network    →   increased friction    →   increased probability of mechanical disruption of cartilage    →  cartilage erosion.
  • Blood vessel proliferation in region of cartilage erosion; or venous congestion; or stimulation of peripheral cells to undergo endochondral ossification by low grade synovitis at joint margins (joint movement seems to be involved - immobilization markedly reduces osteophyte formation)    →    new bone production:osteophyte formation    →   subchondral bone remodeling.
  • Severe joint trauma    →   abnormalities of joint anatomy/conformation or joint instability    →   amplify wear and tear on joint surfaces    →   abnormal distribution of forces across joint surfaces.
  • Synovial membrane cells    →   activated by repeated trauma    →   stimulates release of interleukin    →   prostaglandin and neutral metalloproteinases by chondrocytes    →   pain and cartilage degradation.

Biomechanical theory

  • ?Repetitive concussion to joints    →   trabecular microfractures or direct stimulation to bone deposition    →   remodeling of subchondral bone    →   increased stiffness and reduced shock absorbing capacity    →   increased forces absorbed by articular cartilage    →   mechanical fragmentation of cartilage.
  • Biochemical and biomechanical theories of OA are not mutually exclusive and it is likely that both act in concert in OA.

Timecourse

  • Months to years. Although, radiographically and histopathologically, features of DJD can be seen within days of experimentally-induced joint instability.

Diagnosis

Presenting Problems

  • Lameness.
  • Presented for evaluation of an unrelated issue.
  • Decreased or altered activity.

Client History

  • Insidious onset or sudden onset lameness in one or more limbs. Other joint condition, eg injury, chronic inflammation.
  • Reduced activity levels usually with insidious onset.
  • Slower running, eg towards food, or away from a dog.
  • Jumping height progressively lowered, or makes a jump up or down in stages, where possible. If there is a greater incentive then the cat will be able to move more quickly and jump further than it might generally choose.
  • Change in temperament.
  • Litter box accident.
  • Signs of discomfort on handling.

Clinical Signs

  • Pain in affected joint(s) on palpation/manipulation.
  • Thickened joints if advanced case - peri-articular new bone formation, fibrosis and synovial effusion.
  • Restricted extension or flexion.
  • Crepitus in severely damaged joint.
  • Crouched position if cat is protecting affected joint.

Diagnostic Investigation

Physical examination

  • Watch cat from behind a door or get the owners to video the cat's behavior.
  • Palpate for muscle atrophy with the cat in a sitting position.
  • Place cat on affected side and examine every joint in detail leaving most suspected affected joint until last. Record any other "clinical signs" listed above.

Radiography of affected joint 

  • Osteophytes at characteristic sites in individual affected joints. In severe cases: quite large deposits of new bone Stifle: osteoarthritis - radiograph lateral but osteophytes are generally considered to be less obvious in cats than in dogs. 
  • Increased opacity of subchondral bone or attrition of subchondral bone on weight-bearing surface. Sclerosis is generally considered more reliable and more significant in cats than in dogs. It is not possible to distinguish between face-on osteophytes and sclerosis if only one view is seen.
  • Watch for the sesamoid in the supinator muscle located near the proximal radius, this can be mistaken for an osteophyte. However, it may be that this sesamoid is more likely to be prominent or irregular in shape in joints with DJD.
  • Calcification of intra-articular or peri-articular soft tissues.
  • Subchondral bone cysts can occur in cats but are uncommon.
  • Periarticular soft tissue swelling, eg synovial effusion  Stifle: osteoarthritis - radiograph CrCd  Stifle: normal - CrCd radiograph  is more a feature of other arthropathies. In DJD it is seen most often in the more peripheral joints, eg the tarsus. 
  • Perisosteal proliferation.
    Degree of lameness correlates poorly with severity shown radiographically in other species and this is likely to also be the case in cats.

Cytopathology

  • Arthrocentesis Synovial fluid: sampling - synovial fluid from several larger joints, especially those with palpable effusion.
  • Consider infective arthritis  Arthritis: infective when the cat is acutely ill and there is recent history to support this or immune-mediated arthritis if more than one joint is involved especially the carpi and tarsi.
  • DJD may have marginally increased total nucleated cell count Synovial fluid: differential cell count and viscosity  (< 5000 cells/mm3) predominantly mononuclear cells typical of normal fluid and increased [total protein]  Synovial fluid: protein. The fluid is typically straw colored and viscous  Synovial fluid: normal and abnormal  Synovial fluid: normal .

Other

Gross Autopsy Findings

  • Peri-articular thickening, lipping and proliferation  Stifle: osteoarthritis - pathology 01  Stifle: osteoarthritis - pathology 02 .
  • Cartilage softening or fissuring.
  • Osteophyte formation.
  • Peri- or intra-articular calcification in severe cases.

Histopathology Findings

  • Hyperplasia and hypertrophy of synovial lining cells.
  • Lymphocytic, plasmacytic infiltration.
  • Peri-articular fibrosis.

Differential Diagnosis

Causes of reduced activity/agility in an old cat

  • Common causes of systemic illness/muscle loss, eg neoplasia - lung, liver, gastrointestinal tract, lymphoma, liver disease, inflammatory bowel disease, chronic renal failure, diabetes mellitus, hyperthyroidism, etc.

Metabolic diseases causing locomotor dysfunction

Causes of primary musculoskeletal disease

Polyarthropathies - inflammatory joint diseases

Treatment

Initial Symptomatic Treatment

Management

Environmental modification

  • Arrange food bowls in places that do not require leaping or stair climbing.
  • Build ramps leading to favorite sitting places.
  • Make sure that daily routine is not a difficult obstacle course.

Obesity

  • Light/reduced calorie diet.
  • Avoid ad libitum feeding.
  • Stress to owners how important weight control is in the management of OA.

Encourage movement

  • Create environment in home to allow easy movement.

Pain control 

  • The only appropriate NSAIDs for treating DJD in cats currently are meloxicam Meloxicam and Robenacoxib Robenacoxib Therapeutics: musculoskeletal system.
  • Meloxicam (Metacam 5 mg/ml solution for injection for dogs and cats or 2 mg/ml solution for cats) is licensed for a single use SC injection at a dose of 0.3 mg/kg SC.
  • Meloxicam (Metacam 0.5 mg/ml oral suspension for cats) is licensed for indefinite use in cats that are benefiting from treatment. Initial treatment of a single dose of 0.1 mg/kg bodyweight orally or in food is continued at 0.05 mg/kg bodyweight per day (although lower doses or frequencies might be appropriate for some cats). The same precautions and contra-indications apply as for other NSAIDs and are detailed in the data sheet. A trial treatment might be used as part of the work-up of a cat with suspected clinical DJD (See above).
  • Robencoxib tablets (Onsior) are licensed for the management of chronic musculoskeletal conditions in cats at a dose of 1-2 mg/kg per day. The interchangeable use of Onsior tablets and Onsior solution for injection has been tested in target animal safety studies and was shown to be well tolerated by cats. The same precautions and contra-indications apply as for other NSAIDs and are detailed in the data sheet. 
  • Toxic effects of NSAIDs are caused partly by inhibition of the production of prostaglandins that protect homeostasis of the kidneys and gastrointestinal tract.  
  • The cat is particularly susceptible to the toxic effects of some NSAIDs due to its deficiency of the hepatic glutathione-dependent enzyme system which is involved in metabolism of many of the NSAIDs. This leads to build-up of toxic levels of active compounds when cats are given the drugs at doses and frequencies safe in other species.
  • Toxicity may be exacerbated by using more than one NSAID concurrently, or within 24 hours of dosing with a different NSAID or corticosteroid, or administering to a dehydrated, hypovolemic or hypotensive animal.
  • Toxic side-effects include:
    • Gastric irritation, progressing to vomiting, ulceration and hemorrhage.
    • Enteritis leading to diarrhea.
    • Blood dyscrasias.
    • Occasionally hepatotoxicity and/or nephrotoxicity.
    • Nephrotoxicity is more likely in dehydrated, hypovolemic or hypotensive animals, those undergoing anesthesia, or in animals being treated with other drugs which are potentially nephrotoxic. Use of NSAIDs should generally be avoided in these circumstances.

Cats should be evaluated for dehydration, renal insufficiency and liver damage by clinical examination and routine blood and urine analysis prior to starting treatment with a NSAID and periodically through the treatment.

Other analgesics

  • Frunevetmab Frunevetmab: this is a licensed felinized monoclonal antibody to Nerve Growth Factor. It captures free Nerve Growth Factor and neutralizes its effect in the peripheral nervous system. Nerve Growth Factor is responsible for driving peripheral sensitization and in turn central sensitization of the pain pathways via binding to TrKA receptors on peripheral afferent fibers. It is given as a once monthly SC injection. Side-effects are reported to be minimal, with no reported effects on cardiac, renal or hepatic function.
  • Amantadine Amantadine: Amantadine has recently been trialed to manage pain associated with osteoarthritis in cats. In a small study, at a dose of 5 mg/kg once daily orally, amantadine increased quality of life and improved Client Specific Outcome Measures (an owner questionnaire designed to assess pain associated with osteoarthritis) to a greater extent than placebo treatment. However activity counts decreased compared to placebo suggesting that amantadine was also associated with sedation. Amantadine is thought to be renally excreted therefore caution should be exercised using amantadine in cats with significant renal dysfunction. Amantadine is unlicensed in cats and it likely takes 2-3 weeks before beneficial effects of treatment with amantadine are seen.
  • Gabapentin Gabapentin: although gabapentin is a structural analogue of GABA it does not act at GABA receptors, instead it selectively inhibits voltage gated calcium channels containing the alpha-2 delta-1 subunit. This serves to decrease nociceptive transmission by decreasing the excitability of dorsal horn neurons and also stimulates descending inhibition by increasing glutaminergic neurotransmission in the locus coeruleus. In a small cross over study cats with osteoarthritis were randomly assigned to receive gabapentin 10 mg/kg orally or placebo. Cats treated with gabapentin were less active compared to placebo due to associated sedation. Some owners reported an improvement in quality of life in their cat during gabapentin treatment compared to placebo, changes in Client Specific Outcome Measures were not significant between placebo and gabapentin treatment.

Standard Treatment

Surgery

  • Not really an option unless as a salvage procedure to manage severe unremitting pain - arthrodesis, excision arthroplasty or amputation may be considerations.

Chrondroprotective agents 

  • May be the first option Therapeutics: oral chondroprotectants tried in cats with significant concurrent diseases that contraindicate the use of NSAIDs or in cats with mild (but proven) signs. Although with the licensing of frunevetmab alternative licensed treatments to NSAIDs are available.
  • Essential fatty acids Omega-3 fatty acids may reduce joint inflammation.
  • Substances which promote anabolic processes (unproven in clinical cases) of cartilage homeostasis and inhibit factors causing cartilage breakdown:
    • Pentosan polysulfate Pentosan polysulfate 3 mg/kg SC q5-7 days on four occasions and repeated as a course or as a single "booster" dose as necessary according to clinical effect.
    • Polysulfated glycosaminoglycan Polysulfated glycosaminoglycan 1.1-4.8mg/kg IM every 4 days for 6 doses, may increase bleeding times.
    • Cosequin (glucosamine Glucosamine and chondroitin sulfate Chondroitin sulfate). One regular strength capsule daily for 4 weeks then 1/2 capsule daily. May take 4-6 weeks to become effective. Also Cosequin for Cats 1-2 capsules daily for 4-6 weeks then 1 capsule daily or every other day.
    • Glucosamine Glucosamine: amino sugar synthesized by chondrocytes from glucose and glutamine. Important intermediate in synthesis of glycosaminoglycans (GAGs). Manufacturer's recommended doses should be followed for the various preparations.
    • Chondroitin sulfate Chondroitin sulfate: most abundant of all GAGs. Chains bind with collagen to form a matrix which provides the characteristics of articular cartilage. Manufacturer's recommended doses should be followed for the various preparations.
    • Avocado/soybean unsaponifiables (ASU) Avocado/soybean unsaponifiables : a mixture of unsaponifiables from avocado and soybean. Available in combination with glucosamine and chondroitin sulfate. Manufacturer recommended doses should be followed for the various preparations.

Opioids

  • Buprenorphine Buprenorphine: 0.02mg/kg IV or IM or sublingual q6-7 hours. Transdermal patch: 25 ug patch for 3.5-5.0 kg cats for continued release, although there is no evidence to support the efficacy of buprenorphine transdermal patches for the management of osteoarthritis pain in cats.
  • Tramadol Tramadol has been used for the management of pain associated with DJD in cats and licensed oral and injectable preparation are available in some countries (eg Tralieve, UK). One study found oral tramadol 2 mg/kg twice daily increased activity levels in cats with osteoarthritis compared to placebo and improved quality of life. However side-effects were common (euphoria, dysphoria, sedation, decreased appetite and diarrhea) and resulted in some cats being withdrawn from the study. Another study investigated tramadol 3 mg/kg twice daily orally and similarly found an improvement in outcome measures associated with osteoarthritis with no clinically relevant adverse effects in this study. It is worth noting that oral tramadol tablets are very bitter so repeated dosing with tramadol orally in cats can be problematic.

Corticosteroids

  • Prednisolone Prednisolone: 2 mg q12-24 hours then taper to q48 hours.
  • Controversial: for symptomatic relief if all other forms of treatment have failed.
  • Must not be used concurrently with NSAIDs (wash out period required).
  • May be most appropriate when the cat requires systemic corticosteroid treatment for a concurrent condition.

Subsequent Management

Monitoring

  • For steady and maintained weight loss.
  • For control of pain - if this is not occurring reassess management program, eg use Client Specific Outcome Measures or the Feline Musculoskeletal Pain Index Pain: assessment.
  • Regular (3-6 monthly) monitoring of hepatic and renal function if receiving chronic NSAID medication.
  • For side-effects of therapy - may require alternative medication.
  • Repeat radiography is not likely to be rewarding unless further diagnostic evaluation is required.

Outcomes

Prognosis

  • Guarded: medical treatment is unlikely to stop or slow progression of OA but may give good symptomatic improvement.
  • Most animals able to lead a good quality of life with appropriate management.
  • Medical options limited if renal or hepatic dysfunction.

Expected Response to Treatment

  • Improved exercise tolerance.
  • Reduced joint pain.
  • Change in temperament.
  • The owner may report that the cat appears to behave as a younger animal.

Reasons for Treatment Failure

  • Misdiagnosis, eg infective arthritis, immune-mediated polyarthritis.
  • Poor compliance with medical treatment.
  • Unrecognized or untreated primary condition, eg hip dysplasia Hip: dysplasia or patellar luxation Patella: luxation.
  • Unrecognized concurrent condition also causing non-specific signs of ill health such as inactivity.
  • Severe end-stage disease.
  • Owner non-compliance with weight reduction program or exercise regime.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Shipley H, Flynn K, Tucker L et al (2021) Owner evaluation of quality of life and mobility in osteoarthritic cats treated with amantadine or placebo. J Feline Med Surg 23, 568-574 PubMed.
  • Guedes A G P, Meadows J M, Pypendop B H, Johnson E, Zaffarano B (2018) Assessment  of the effects of gabapentin on activity levels and owner-perceived mobility impairment and quality of life in osteoarthritic geriatric cats. J Am Vet Med Assoc 253, 579-585 PubMed
  • Guedes A G P, Meadows J M, Pypendop B H, Johnson E (2018) Evaluation of tramadol for treatment of osteoarthritis in geriatric cats. J Am Vet Med Assoc 252, 565-571 PubMed
  • Monteiro B P, Klinck M P, Moreau M et al (2017) Analgesic efficacy of tramadol in cats with naturally occurring osteoarthritis. PLoS One 12 (4), e0175565 PubMed
  • Au R Y, al-Tabib T K, Au A Y et al (2007) Avocado soybean unsaponifiables (ASU) suppress TNF-alpha, IL-1beta, COX-2, iNOS gene expression, and prostagalndin E2 and nitric oxide production in articular chondrocytes and monocyte/macrophages. Osteoarthritis Cartilage 15 (11), 1249-1255 PubMed.
  • Clarke S P & Bennett D (2006) Feline osteoarthritis: a prospective study of 28 cases. JSAP 47 (8), 439-445 PubMed.
  • Clarke S P, Mellor D, Clements D N et al (2005) Prevalence of radiographic signs of degenerative joint disease in ahospital population of cats. Vet Rec 157 (25), 793-799 PubMed.
  • Godfrey D R (2005) Osteoarthritis in cats: a retrospective radiological study. JSAP 46 (9), 425-429 PubMed.
  • Leonard C A & Tillson M (2001) Feline Lameness. Vet Clin North Am Small Anim Pract 31 (1), 143-163 PubMed.
  • Bardet J F (1998) Diagnosis of shoulder instability in dogs and cats - a retrospective study. JAAHA 34 (1), 42-54 PubMed.
  • Hulse D (1998) Treatment methods for pain in the osteoarthritis patient. Vet Clin North Am Small Anim Pract 28 (2), 361-375 PubMed.
  • Langenbach A, Green P, Giger U et al (1998) Relationship between degenerative joint disease and hip joint laxity by use of distraction index and Norberg angle measurement in a group of cats. JAVMA 213 (10), 1439-1443 VetMedResource.
  • Boon G K (1997) Synovial fluid analysis - a guide for small-animal practitioners. Vet Med 92 (5), 443-451 AGRIS FAO.
  • Hardie E M (1997) Management of osteoarthritis in catsVet Clin North Am Small Anim Pract 27 (4), 945-953 PubMed.
  • Harari J (1997) Clinical evaluation of the osteoarthritic patient. Vet Clin North Am Small Anim Pract 27 (4), 725-734 PubMed.
  • Hoskins J D, Kerwin S C (1997) Musculoskeletal system. Joint and vertebral column diseases. Vet Clin North Am Small Anim Pract 27 (6), 1433-1449 PubMed.
  • Johnston S A (1997) Osteoarthritis - joint anatomy, physiology and pathobiology. Vet Clin North Am Small Anim Pract 27 (4), 699-723 PubMed.
  • Johnston S A & Fox S M (1997) Mechanisms of action of anti-inflammatory medications used for the treatment of osteoarthritis. JAVMA 210 (10), 1486-1492 PubMed.
  • Ellison R S (1988) The cytologic examination of synovial fluid. Semin Vet Med Surg (Small Anim) (2), 133-139 PubMed.

Other sources of information

  • Punke J P, Au R Y, Au A Y, Phan  P, Budsberg S C & Frondoza C G (2007) Modulation of protstaglandin E-2 production in feline articular chondrocytes propagated in monolayer and dynamic microcarrier culture. American College of Veterinary Surgeons Symposium, poster.

Other Sources of Information