Canine osteoarthritis is a common chronic degenerative joint condition that affects the whole joint but the most prominent symptom is the loss of articulate cartilage.

OA causes pain, lameness, decreased mobility, and if not managed on time and correctly the symptoms will escalate to muscular atrophy, joint effusion, incorrect joint articulation, etc. Dogs that experience chronic pain often develop other conditions such as fear, depression and anxiety, moreover, OA becomes a contributing factor to the decision of euthanasia, especially in older dogs. There are two types of OA: primary, cause of which is unknown but could be associated with the animal’s age and weight, and secondary, which is a result of trauma, inflammatory arthritis, abnormal development of the joint, like in hip or elbow dysplasia, or metabolic diseases with the pathogenesis possibly having a genetic component to it.

Studies on the prevalence of OA in the UK reported that between 2.5% to 6.6% of dogs in primary veterinary care will develop the disease (1, 2). A similar study in the US from 1997 by Johnson et al. (3) estimated the number to be 20%. However, the real prevalence numbers might be much higher. Considering the total number of dogs in these countries (12.5mln in UK and 77mln in US respectively), canine OA represents a welfare problem with a significant number of pet owners affected and the overall cost of a life-long treatment and management of the symptoms.

OA risk factors.

Since secondary canine OA is the most prevalent type, it is important to consider the risk factors in order to diagnose and manage OA at early stages. Some dog breeds are especially prone to developing OA at as early as several months old due to their genetic factors as well as body features which are required by the breed standards such as size, joint angles, leg size. Among the breeds that have an increased risk of cruciate ligament rupture are Golden Retriever, Rottweiler and Labrador Retriever (4-7); German Shepherds, Golden Retrievers, Labrador Retrievers, Mastiffs, Bernese Mountain dogs have an increased risk of hip and elbow dysplasia (8-11), while smaller breeds like Pomeranians, Chihuahua, Yorkshire Terrier might develop a condition called luxating patellar or a tricking knee (12). Diet might also be a contributing factor. For example, it was found that high-fat diet and unrestricted diet during the growth period are associated with higher risk of elbow and hip dysplasia (13).

Diagnosis of OA

The diagnosis of canine OA includes physical examination, radiography, synovial fluid analysis, arthroscopy and CT or MRI scans for more accurate visualization of joints. The main strategy of conventional OA management is to slow down disease progression, pain alleviation and anti-inflammatory therapy. The ABCDE approach which stands for analgesia, bodyweight control, disease modification and exercise can also be applied for the management of canine OA. Analgesia, or pain management, is especially important because it improves the quality of life of a dog suffering from OA.

Current treatment strategies:

NSAIDS

NSAIDs are quite effective at addressing both pain and inflammation, so among most commonly prescribed medicines are meloxicam, carprofen, firocoxib, maxacoxib. However, prolonged treatment with NSAIDs can cause damage to the GI tract and in extreme cases lead to liver and kidney failure and even death of an animal. Other drugs such as an anticonvulsant medication gabapentin, an antiviral amantadine or an opioid tramadol can be prescribed alongside NSAIDs. However, these compounds might also have behavioral and physiological side effects.

Nutraceuticals

Nutraceuticals, despite the lack of scientific evidence of their efficacy can also be prescribed together with pain relief medication and other measures. Among the most commonly used supplements for OA are glucosamine, chondroitin, methylsulfonylmethane (MSM). A study on the effect of Omega-3 fatty acids demonstrated that 127 dogs fed a diet rich in Omega-3 had a significant improvement of mobility and the tests showed reduced levels of arachidonic acid in the blood serum which indicates lower inflammation of the joints (14).

Physical therapy and surgery

Appropriate exercise and physiotherapy are also critical for OA patients once the acute phase of the disease has passed, since reduced mobility further exacerbates the symptoms and can lead to muscle atrophy. Other types of physical rehabilitation such as cryotherapy, extracorporeal shock wave therapy, transcutaneous electrical nerve stimulation, therapeutic laser treatment can be offered to the owner. In cases when no other therapy is effective, surgical intervention can also be performed, which can include complete joint replacement, osteotomy or arthrodesis (joint fusion).

Biologics

It is important to remember that the traditional treatment strategies of OA only slow down (at best) the disease progression and alleviate the symptoms, but do not provide tissue regeneration, neither stop the degradation of the damaged cartilage. Currently some veterinary clinics offer experimental treatment of OA which includes the use of biologics, such as structure modifying OA drugs (SMOADs), platelet-rich plasma, gene therapy and mesenchymal stem cells (reviewed in 15). SMOADs are supposed to stabilize and repair OA lesions (pentosan polysulphate, polysulphated glucosaminoglycans, hyaluronic acid, etc) however, there is little robust scientific evidence of the efficacy of this class of OA medication. Platelet-rich plasma (PRP) is obtained from the OA affected dog by drawing blood and then injecting the processed plasma into the joint.

Growth factors released by platelets can stimulate chondrocyte proliferation and inhibit chondrocyte apoptosis. Anti-inflammatory cytokine plasmid DNA therapy is aimed at increasing the levels of anti-inflammatory cytokines which can inhibit the production of inflammatory cytokines and hence reduce the chondrocyte apoptosis, however, there have been very few studies on this therapy and further investigation is required. Studies on using mesenchymal stem cells for reverting canine OA showed very promising results. You can refer to these studies by our group (16, 17) as well as published studies from others (18-20) to learn more about our technology and benefits of stem cells for treating OA.

Early diagnosis and management of OA are paramount

If you notice any of the symptoms like lameness, reluctance to run and walk, unusual gait, difficulties to do certain movements (jumping, climbing stairs, etc), or in case the breed of your dog is highly susceptible to this disease, you should take your dog to a veterinary clinic. All medication for pain management and even supplements might have side effects, or certain forms of physiotherapy might not be suitable, so it is important that they are prescribed by a professional. Depending on the severity of the disease and other factors such as weight, age, breed, etc., your veterinarian will recommend an optimal OA management strategy for your dog and by observing its effectiveness might later adjust the treatment, because there is no universal solution for OA.

Since most of the conventional treatment methods can only alleviate pain and slow the progression of the disease but not cure it, you might want to ask your vet for information about experimental treatment options. 

References:

1. Anderson KL, O’Neill DG, Brodbelt DC, Church DB, Meeson RL, Sargan D, et al.. Prevalence, duration and risk factors for appendicular osteoarthritis in a UK dog population under primary veterinary care. Sci Rep. (2018) 8:5641. 10.1038/s41598-018-23940-z
2. O’Neill DG, Church DB, McGreevy PD, Thomson PC, Brodbelt DC. Prevalence of disorders recorded in dogs attending primary-care veterinary practices in England. PLoS ONE. (2014) 9:e90501 10.1371/journal.pone.0090501
3. Johnston SA. Osteoarthritis. Joint anatomy, physiology, and pathobiology. Vet Clin North Am Small Anim Pract. (1997) 27:699–723. 10.1016/S0195-5616(97)50076-3
4. Taylor-Brown FE, Meeson RL, Brodbelt DC, Church DB, McGreevy PD, Thomson PC, et al.. Epidemiology of cranial cruciate ligament disease diagnosis in dogs attending primary-care veterinary practices in England. Vet Surg. (2015) 44:777–83. 10.1111/vsu.12349
5. Grierson J, Asher L, Grainger K. An investigation into risk factors for bilateral canine cruciate ligament rupture. Vet Comp Orthop Traumatol.
6. Necas A, Zatloukal J, Kecova H, Dvorak M. Predisposition of dog breeds to rupture of the cranial cruciate ligament. Acta Veterinaria Brno. (2000)
7. Whitehair JG, Vasseur PB, Willits NH. Epidemiology of cranial cruciate ligament rupture in dogs. J Am Vet Med Assoc. (1993) 203:1016–9.
8. Coopman F, Verhoeven G, Saunders J, Duchateau L, van Bree H. Prevalence of hip dysplasia, elbow dysplasia and humeral head osteochondrosis in dog breeds in Belgium. Vet Rec. (2008) 163:654–8. 10.1136/vr.163.22.654
9. Hou Y, Wang Y, Lu X, Zhang X, Zhao Q, Todhunter RJ, et al.. Monitoring hip and elbow dysplasia achieved modest genetic improvement of 74 dog breeds over 40 years in USA. PLoS ONE. (2013) 8:e76390. 10.1371/annotation/92e1aa00-169b-45dc-9866-61034e061f6d
10. Lavrijsen ICM, Heuven HCM, Meij BP, Theyse LFH, Nap RC, Leegwater PAJ, et al. Prevalence and co-occurrence of hip dysplasia and elbow dysplasia in Dutch pure-bred dogs. Prevent Vet Med. (2014) 114:114–22. 10.1016/j.prevetmed.2014.02.001
11. Witsberger TH, Villamil JA, Schultz LG, Hahn AW, Cook JL. Prevalence of and risk factors for hip dysplasia and cranial cruciate ligament deficiency in dogs. J Am Vet Med Assoc. (2008) 232:1818–24. 10.2460/javma.232.12.1818
12. O’Neill DG, Meeson RL, Sheridan A, Church DB, Brodbelt DC. The epidemiology of patellar luxation in dogs attending primary-care veterinary practices in England. Canine Genet Epidemiol. (2016) 3:4. 10.1186/s40575-016-0034-0
13. Sallander MH, Hedhammar A, Trogen MEH. Diet, exercise, and weight as risk factors in hip dysplasia and elbow arthrosis in Labrador Retrievers. J Nutr. (2006) 136:2050–52S. 10.1093/jn/136.7.2050S
14. Roush J, Dodd CE, Fritsch D, Allen T, Jewell D, Schoenherr WD, Richardson D, Leventhal PS, Hahn K. Multicenter veterinary practice assessment of the effects of omega-3 fatty acids on osteoarthritis in dogs. Journal of the American Veterinary Medical Association (2010) DOI:10.2460/javma.236.1.59 Corpus ID: 11902033
15. Pye C, Bruniges N, Peffers M, Comerford E. Advances in the pharmaceutical treatment options for canine osteoarthritis. J Small Anim Pract. (2022) 63(10):721-738. doi: 10.1111/jsap.13495.
16. Kriston-Pal E, Czibula A, Gyuris Z, Balka G, Seregi A, Sukosd F, Suth M, Kiss-Toth E, Haracska L, Uher F, Monostori E. Characterization and therapeutic application of canine adipose mesenchymal stem cells to treat elbow osteoarthritis. Can J Vet Res(2017) 81(1):73-78.
17. Kriston-Pal E, Haracska L, Cooper P, Kiss-Toth E, Szukacsov V, Monostori E. A Regenerative Approach to Canine Osteoarthritis Using Allogeneic, Adipose-Derived Mesenchymal Stem Cells. Safety Results of a Long-Term Follow-Up. Front. Vet. Sci., (2020) doi: 10.3389/fvets.2020.00510
18. StemCellX. What Are Stem Cells And How Are They Used? https://stemcellx.com/what-are-stem-cells-and-how-are-they-used/. Accessed: 02.11.2022
19. StemCellX. Use Of Mesenchymal Stem Cells (MSCs) In Regenerative Medicine. https://stemcellx.com/use-of-mesenchymal-stem-cells-mscs-in-regenerative-medicine/. Accessed: 02.11.2022
20. StemCellX. Our Technology. https://stemcellx.com/technology/. Accessed: 02.11.2022