Feline Osteoarthritis (OA)

Diagnosis

Clinical Examination and Pain Assessment in Cats with Suspected Osteoarthritis

Conducting an orthopedic examination in cats can be particularly challenging and requires a low-stress, feline-friendly environment to improve accuracy and minimize behavioral confounders. It is possible to mistake fear-based behaviors for pain responses in a clinical setting.

General Appearance and Behavior

Postural and activity changes suggestive of discomfort or pain may include:

• Hunched or crouched posture
• Dorsolateral recumbency
• Abdominal muscle tension
• Vocalization
• Dull mentation or decreased responsiveness
• Restlessness or agitation

Behavioral alterations and environmental interaction cues often include:

• Withdrawal or reduced interest in surroundings
• Facing the back of the cage
• Reluctance to move after stimulation
• Attempting to hide or escape
• Irritability or aggression
• Changes in grooming behavior (either excessive or markedly reduced)

Facial expressions associated with discomfort may consist of:

• Ears pulled laterally or flattened
• Partially closed (squinting) eyes
• Tense muzzle
• Straightened whiskers
• Lowered head posture

Gait and Joint Evaluation

Gait evaluation in cats is notoriously difficult, as lameness is uncommonly reported and visual assessment in a clinical setting is often unreliable. When feasible, videos captured by owners of the cat ambulating in their home environment can provide valuable supplementary information.

Joint-specific examination involves palpation of individual joints, typically beginning with those suspected to be least painful and progressing to the most affected. Unfortunately, in feline patients, indicators such as joint pain, crepitus, effusion, thickening and decreased ROM are inconsistent and not as helpful for OA diagnosis as they are in other species.

Goniometric measurements of joint ROM can aid in identifying joints less likely to be affected by OA. In general, higher ROM values in joints that are non-painful on examination correlate with radiographically normal joints, making goniometry a potentially useful screening tool.¹⁶

Adjunctive Pain Monitoring Tools

Several objective tools are emerging to assess chronic pain in cats with OA, including:

• Collar-mounted accelerometers, which detect changes in activity patterns in response to analgesic treatment
• Piezoelectric activity monitors, which convert force, pressure, acceleration, and vibration into electrical signals to track movement patterns over time

Thermal and sensory threshold testing, which may help assess altered nociception in affected individuals

Radiographic imaging

Radiographic evidence suggests that approximately 91% of cats have osteoarthritis (OA) in at least one appendicular joint, with the shoulders, elbows, hips, stifles, and tarsi being the most frequently affected sites.1 Additionally, vertebral column OA is observed in 40–55% of cats, most commonly involving the lumbosacral joint. ^1,8

The radiographic manifestations of OA in cats are unique compared to other species. In cats, the most common findings include periarticular new bone formation and joint-associated mineralization. Features such as joint effusion, osteophyte formation, and subchondral bone changes (commonly observed in canine OA) are less frequently detected in cats.¹⁷

Radiographic presentation of hip dysplasia also differs between species. In cats, the acetabulum often appears shallow, with remodeling and proliferative changes primarily affecting the cranio-dorsal acetabular margin, while remodeling of the femoral neck is typically minimal. Degenerative changes of the femoral head and neck develop slowly.¹⁸

Radiographs are not a reliable diagnostic for OA in cats as there is poor correlation between radiographic abnormalities and both clinical signs and cartilage damage in cats. Certain joints demonstrate a high prevalence of cartilage lesions even in the absence of radiographic evidence of disease including¹⁷:

• 71% of stifles
• 57% of coxofemoral joints
• 57% of elbows
• 46% of tarsal joints

There does appear to be a linear correlation between bone mineral density and degree of OA in the cat.¹⁸

Mechanism of Action

Pathophysiology of OA

In feline OA, cytokine profiling has revealed increased concentrations of inflammatory mediators, including tumor necrosis factor-alpha (TNF-α) and interleukin-2 (IL-2).¹³ Genomic studies have identified dysregulated immunomodulatory pathways related to antigen presentation (via MHC molecules), T-cell receptor signaling, and oxidative phosphorylation in cats with OA.¹⁴ Additionally, proteomic analyses have identified numerous differentially expressed proteins associated with feline OA and OA-related pain. These proteins are implicated in pathways such as the acute phase response and complement system activation, reinforcing the role of inflammation in disease progression.¹⁴

Given the relative avascularity and therefore the lack of systemic regulation, the repair capacity of cartilage is very limited. Over time, fibrous tissue forms with different functional properties then that of native hyaline cartilage, promoting joint degeneration.¹⁵

Current medical therapies

A multimodal approach is typically required to manage OA which often includes various combinations of non-steroidal anti-inflammatories (i.e meloxicam/ Metacam®, robenacoxib/ Onsior®), monoclonal Ab (frunevetmab/ Solensia®), pain medications (gabapentin/pregabalin, tramadol, buprenorphine, butorphanol, amantadine), and joint supplements (omega-3 fatty acids, chrondroitin-sulfate, other nutraceuticals). There are a small number of studies exploring the use of platelet-rich plasma (PRP) in cats.¹⁹ Adjunctive therapies, including physiotherapy and acupuncture, are also used in some cats. Most of these therapies typically work by blocking pain and inflammatory pathways to improve symptoms, as none have been shown to improve cartilage damage.²⁰ Unfortunately this typically results in underlying disease progression even if the cats feel less painful.

Investigational Use of Mesenchymal Stem Cell Therapy in Feline Osteoarthritis

Mesenchymal stem cell (MSC) therapy is an emerging therapeutic approach currently under investigation for the treatment of osteoarthritis (OA) in cats. A pilot study evaluating allogeneic (donor is the same species as the recipient) adipose-derived MSCs in a small cohort of feline OA patients demonstrated increased activity levels in all treated cats, with two cats able to discontinue adjunctive medications and supplements.²² Importantly, no short-term or long-term adverse effects were reported.

The therapeutic effects of MSCs are believed to be mediated primarily through paracrine mechanisms, involving the secretion of bioactive molecules that modulate the local microenvironment. Studies in other species, including dogs and humans, have shown that MSC administration can suppress pro-inflammatory mediators, promote local tissue repair, and facilitate cartilage regeneration. Additionally, upregulation of genetic markers associated with chondrogenesis has been identified following MSC administration in canine models, supporting their potential to induce cartilage repair at a molecular level.

Unlike conventional OA therapies, MSCs offer a potential disease-modifying approach through their ability to restore joint homeostasis and stimulate cartilage regeneration. This unique regenerative mechanism distinguishes stem cell therapy from standard symptomatic treatments and positions it as a candidate for long-term management of feline OA.

Uterine derived MSCs

Additionally, MSCs derived from the uterus tend to have low expression of major histocompatibility complex (MHC) antigens, which makes them less likely to be recognized and attacked by the recipient’s immune system.

Available data to date suggests that use of MSCs could provide a novel treatment option  for cats with OA, going beyond treatment of individual clinical signs to target the source of the disease, potentially enhancing their quality of life.

A deeper look into the life organ

Manufacturing and Potency

Allogeneic cells from a FDA qualified donor