Managing OA requires controlling inflammation

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At least one in four adult dogs suffers from canine osteoarthritis (OA),1 with more than 50 percent of the cases diagnosed between eight and 13 years old,2 typically long after joint degeneration has started. OA is the number one cause of chronic pain in dogs,3 and while sometimes called an “old dog disease,” many are surprised to learn joint inflammation and OA can impact patients as early as one year of age.4 In addition, roughly 40 percent of dogs have radiographic evidence by age four.4 Regardless of age, any dog may be susceptible to OA; risk factors include breed, intense activity, obesity, joint injury, and joint surgery.2

Unfortunately, dogs cannot tell us when they are hurting, and some may even try to hide their pain. As veterinarians, it is important to keep an eye out for OA in dogs–treating both their pain and underlying inflammation. Starting the discussion about this disease early can help with the patient’s quality of life.

Signs of canine OA

In dogs of any age, it is important to help pet owners recognize early signs so there can be a timely initiation of a management plan aimed at controlling pain and inflammation, building muscle strength and maximizing range of motion and mobility. Warning signs of OA can include:

  • A decrease in overall activity, abnormalities in static posture or gait, lameness, reluctance to exercise, difficulty jumping or climbing stairs, or pain upon joint manipulation.
  • Bunny hopping (using both hind legs at once to move forward–especially going up or down stairs).
  • Significant hip swaying or butt wiggling while walking is commonly associated with hip dysplasia, which can cause OA in a dog’s hip joints.

Treating the source—inflammation

Canine OA is characterized by a vicious cycle of inflammation and pain that requires a multimodal approach. Use of pharmacologic and non-pharmacologic modalities is recommended for OA treatment.5 Together, these regimens target joint inflammation, which is critical to managing OA and pain,6-8 and promote an active lifestyle for the patient.

In the arthritic joint, inflammatory mediators (e.g. PGE2, IL-1) play a pivotal role in OA pathogenesis and pain. Increased PGE2 in the joint leads to sensitization, or windup, and can lead to heightened pain sensation and chronic pain, which can be difficult to treat. Once OA is diagnosed, dogs require proven effective treatment, such as non-steroidal anti-inflammatory drugs (NSAIDs), because joint supplements alone cannot address pain and inflammation associated with disease. For this reason, NSAIDs have historically been, and remain, the cornerstone of treatment.

Chronic disease requires chronic treatment

A variety of canine NSAIDs are available on the market today. NSAIDs work by either blocking the production of PGE2 or blocking the downstream effects of PGE2 via specific and selective receptor antagonism. PGE2 is an important pro-inflammatory mediator and contributor to OA pain, but also plays a role in normal homeostatic function for multiple organs.

In recently published consensus guidelines for canine OA treatment, experts in orthopedic disease from around the world unanimously agreed that one to three months of daily NSAID therapy is warranted in newly diagnosed cases before considering tapering, with moderate to severe cases often requiring lifelong daily treatment.9-11

Don’t bypass NSAIDs for anti-nerve growth factor monoclonal antibodies

After initiating anti-inflammatory treatment, experts unanimously agree that targeting nerve growth factor (NGF) is also an effective means for controlling pain, but not inflammation, associated with canine OA.10,11 Nerve growth factor, similar to PGE2, contributes to peripheral sensitization, or increased sensitization of peripheral nerves.7,12

Monoclonal antibody treatment targeting NGF has recently become available and represents an important addition to the available therapeutic options for managing canine OA. Nerve growth factor is known to contribute to neurogenic inflammation through the binding of the TrkA receptor.

Unlike classic inflammation, which is responsible for synovitis and degradative changes in arthritic joints, neurogenic inflammation is a subset of inflammation confined to the nervous system that results in heightened pain sensation.

Given anti-NGF monoclonal antibodies primarily treat pain and are not considered potent anti-inflammatories, there is not unanimous expert agreement about their use as a first-line treatment in mild (stage 2) osteoarthritis.10, 11

The best opportunity to limit the negative impact of joint inflammation on cartilage degeneration and disease progression with NSAIDs is early in the course of the disease. Anti-NGF monoclonal antibody is unanimously supported in later stages of the disease, when more dogs are expected to have a neurogenic component to their pain that is not being adequately controlled with NSAIDs alone.

At this time, there is limited information regarding the long-term safety of NGF inhibition in dogs. Due to the important role NGF plays in maintenance and repair of the nervous system, as well as other homeostatic processes related to bony metabolism and other body systems, the combination of NSAIDs and anti-NGF monoclonal antibodies should be approached on a case-by-case basis with informed client consent.

Back to the basics

Along with NSAID therapy as soon as clinical signs of OA develop, experts also unanimously support a three-pronged nonpharmaceutical core approach to therapy that involves:

  1. Weight optimization. This can be one of the most effective steps for the long-term health of a dog. Extra weight puts unnecessary pressure on the joints, which can increase inflammation and pain. In addition, fat tissue itself can lead to more inflammation.
  2.  Exercise appropriate for stage of disease. Physical pain-relieving therapies can improve mobility and range of motion as well as relieve muscle tension. This can also work safely with other types of pain relief.
  3. Feeding an EPA-rich supplement or diet, targeting a minimum daily dose of 100 mg/kg DHA/EPA.10, 11 The inclusion of an EPA-rich supplement or diet into a dog’s treatment plan can create a multitiered therapy approach that can help relieve pain quickly.

It is important to note due to limited evidence of beneficial effect, and some quality and safety concerns, other nutritional joint supplements did not receive unanimous support. Similarly, due to lack of unanimous support, experts classify additional analgesics, such as amantadine, gabapentin, and cannabinoids, as secondary treatments for moderate and severe cases (stages 3 and 4) of OA, after instituting a core treatment protocol.

Osteoarthritis can be a painful condition for dogs of all ages, but the good news is it can be managed. Luckily, early intervention with proven effective treatments can help dogs with OA live their best life.

Brandy Cichocki, DVM, MS, DACVS-SA, is a consulting veterinarian for Elanco Animal Health, who is passionate about improving the lives of veterinary patients, particularly, alleviating their pain. Prior to joining Elanco, Dr. Cichocki worked in a variety of clinical settings, including academia, as a faculty member, and in private practice as a staff surgeon and business owner. She is also an active member in the American College of Veterinary Surgeons (ACVS).

Reference

  1. Lascelles, Duncan. “Joint Pain in Pet Dogs and Cats.” International Association for the Study of Pain (IASP) Fact Sheet, no. 9, 2016.
  2. Cachon T, Frykman O, Innes JF, et al. Face validity of a proposed tool for staging canine osteoarthritis: Canine Osteoarthritis Staging Tool. Vet J. 2018;235:1-8. doi: 10.1016/j.tvjl.2018.02.017.
  3. Fox SM, Millis D. Osteoarthritis: The disease. Multimodal management of canine osteoarthritis. Boca Raton, FL: Manson Publishing Ltd; 2010:24.
  4. Enomoto, M., et al. 2022. NCSU CVM Research Forum. Osteoarthritis Staging Tool (COAST). Vet J. 2018; 235: 1-8.
  5. Gruen ME, Lascelles BD, Colleran E, et al. 2022 AAHA Pain Management Guidelines for Dogs and Cats. J Am Anim Hosp Assoc. 2022;58:55-76.
  6. Attur M, Al-Mussawir HE, Patel J, et al. Prostaglandin E2 exerts catabolic effects in osteoarthritis cartilage: Evidence for signaling via the EP4 receptor. J Immunol. 2008;181:5082-8.
  7. Jang Y, Kim M, Hwang SW. Molecular mechanisms underlying the actions of arachidonic acid-derived prostaglandins on peripheral nociception. J Neuroinflammation. 2020;17(1):1-27.
  8. Scanzello CR, Goldring SR. The role of synovitis in osteoarthritis pathogenesis. Bone. 2012;51(2): 249-57.
  9. Adapted from Clinician’s Forum, Expert views from a roundtable on osteoarthritis and pain management: A paradigm shift for canine osteoarthritis. November 2021.
  10. Cachon T, Frykman O, Innes JF, et al. COAST Development Group international consensus guidelines for the treatment of canine osteoarthritis. Front Vet Sci. 2023;10:1-23. doi:10.3389/fvets.2023.1137888
  11. Mosley C, Edwards T, Romano L, et al. Proposed Canadian Consensus Guidelines on Osteoarthritis Treatment Based on OA-COAST Stages 1–4. Frontiers in Veterinary Science. 2022 Apr 26; 9:830098.
  12. Enomoto M, Mantyh PW, Murrell J, Innes JF, Lascelles BD. Anti-nerve growth factor monoclonal antibodies for the control of pain in dogs and cats. Vet Rec. 2019;184(1):23. doi:10.1136/vr.104590
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