Key Takeaways
- PPID and equine metabolic syndrome (EMS) frequently co-occur, and each raises laminitis risk. In the older horse presenting with joint lameness, this changes the osteoarthritis (OA) treatment calculus.
- Glucocorticoids can worsen insulin dysregulation. The link to laminitis is incompletely understood but clinically relevant, so risk stratification before intra-articular injection is warranted rather than optional.
- Steroid-sparing intra-articular options exist. 2.5% iPAAG (Arthramid) works through synovial membrane integration, not through an anti-inflammatory or glucocorticoid pathway, so it carries no route to glucocorticoid-mediated insulin dysregulation.
- A short, structured pre-treatment assessment supports defensible decisions and protects both the joint and the foot.
The ageing horse with a stiff hock or a positive flexion is a routine presentation. The same horse with a cresty neck, a history of a spring laminitic episode, or a borderline ACTH result is a different clinical problem. The joint still needs managing. The endocrine status just narrowed your options.
This cohort is growing. PPID is the most common endocrine disorder of aged horses, and improved testing means more of these patients are now identified before the classic long coat appears. For the equine practitioner, the question is no longer whether these horses turn up, but how to treat their joints without compounding a metabolic risk. This article sets out a structured clinical approach to OA management in endocrine-compromised horses, including how to select and sequence intra-articular treatment.
Why Does PPID or EMS Complicate OA Management?
Endocrine status changes the risk profile of your treatment, not just the horse. The specific concern is that glucocorticoids, still the default intra-articular anti-inflammatory for many joints, can aggravate insulin dysregulation and, in a predisposed horse, contribute to laminitis.
A brief definitional reset is worth it, because the two conditions are distinct and treatment planning depends on telling them apart. PPID (pituitary pars intermedia dysfunction, formerly equine Cushing’s disease) is an age-related neurodegenerative disorder driven by loss of dopaminergic inhibition of the pars intermedia. It affects roughly one in five horses over the age of 15 (field studies in Australia and Denmark both reported a prevalence of 21.2%). EMS is not a pituitary disease at all. It is a collection of metabolic risk factors with insulin dysregulation as the consistent feature, and it is defined by the increased risk of hyperinsulinaemia-associated laminitis (HAL) that follows.
The two coexist more often than not in the horses that concern us most. Insulin dysregulation is the thread that connects them: it is the central feature of EMS, and it is also present in the subset of PPID horses that go on to laminitis. Hyperinsulinaemia-associated laminitis is detected in approximately 30% of horses with PPID, which is why current endocrinology guidance recommends testing insulin status alongside ACTH in aged horses rather than assuming one result tells you about the other.
The pathway from endocrine disease to a compromised foot is reasonably well characterised. Persistently elevated circulating insulin appears to drive laminitis through inappropriate stimulation of insulin-like growth factor-1 receptors on the lamellar epidermal cells, weakening the lamellar attachment. This is the leading mechanistic theory, and it reframes laminitis in these horses as an endocrine event rather than an inflammatory one. It also explains why anything that pushes insulin higher, including glucocorticoids, is treated with caution in a horse already sitting on that risk.
What Are the Risks of Corticosteroid Use in These Horses
Glucocorticoids can exacerbate insulin dysregulation and, in a horse with PPID or EMS, that raises laminitis risk. The association is incompletely understood, but it is well enough established to warrant risk assessment before intra-articular injection rather than after a problem appears.
Two points keep this proportionate. First, this is not an absolute contraindication. The Equine Endocrinology Group describes the association between glucocorticoid administration and subsequent laminitis as incompletely understood, and epidemiological studies that flag recent corticosteroid use as a laminitis risk factor are largely drawn from systemic or repeated exposure and from animals with existing metabolic dysfunction. Second, the magnitude of risk from a single intra-articular dose in a well-controlled horse is debated and probably low. The clinically important distinction is between a metabolically stable horse and one with active, poorly controlled insulin dysregulation. The calculus is different for each.
That is exactly why a pre-injection assessment matters. Before reaching for a corticosteroid in an older horse, it is reasonable to weigh body condition score and regional adiposity, breed and phenotype, any prior laminitis history, and current insulin status. None of this is onerous, and it converts a blanket worry into a defensible, case-specific decision. It also identifies the horses in which a steroid-sparing option is the more comfortable choice.
What Does a Structured Pre-Treatment Assessment Look Like?
A short clinical checklist reduces risk and supports peer-defensible decision-making. It does not require a full endocrine work-up in every case, but it does require you to know where the horse sits before you inject.
Assess the following before intra-articular treatment in a horse with, or suspected of, PPID or EMS:
- Endocrine status. Basal ACTH for PPID, interpreted against a seasonally adjusted reference range, since ACTH rises physiologically in autumn. Add insulin testing (resting insulin, or an oral sugar test where resting values are equivocal) to characterise insulin dysregulation. Horses over 10 to 15 years warrant testing even without overt signs.
- Laminitis history and current laminar health. Previous episodes, hoof rings, and any current digital pulse or lameness localised to the feet.
- Body condition and fat distribution. Overall BCS plus regional adiposity: cresty neck, supraorbital fat, tail-head deposits.
- PPID control. Current pergolide dose, response, and whether the horse is stable or drifting. An uncontrolled PPID horse is a different risk than a well-managed one on effective therapy.
Documenting these four points takes minutes and gives you a written basis for whichever treatment you select.
What Intra-Articular Treatment Options Are Available for These Cases?
Steroid-sparing intra-articular options exist, and 2.5% iPAAG is one that clinicians specifically report using in horses with metabolic disease. The intent is not to abandon corticosteroids, but to have a defensible alternative for the horse in which they give you pause.
The intra-articular landscape, in brief:
- Corticosteroids. Potent, fast-acting anti-inflammatory relief with a well-established role. The limitation in this cohort is metabolic, not efficacy.
- Hyaluronic acid. Viscosupplementation with an anti-inflammatory contribution, generally shorter acting and often used as an adjunct.
- Orthobiologics (for example PRP, autologous conditioned serum). Autologous products that modulate the inflammatory environment. Evidence and cost vary, and preparation is more involved.
- 2.5% iPAAG (Arthramid). A non-resorbable polyacrylamide hydrogel that integrates into the synovial membrane and works through a mechanical, structural mode of action rather than a pharmacological anti-inflammatory one.
The mechanism is what makes iPAAG relevant here. After injection, 2.5% iPAAG integrates into the synovial sub-intima, a process shown histologically to be established by around day 14, through a combination of vessel in-growth and water exchange, and it persists in the joint long term. Biomechanical work indicates this restores more normal synovial membrane elasticity, which is described as the primary mode of action. Transcriptomic studies show it also modulates local synovial immune signalling, but the point for the metabolic horse is what it does not do: it does not rely on a systemic anti-inflammatory or glucocorticoid pathway. There is therefore no mechanistic route by which it would drive the glucocorticoid-mediated insulin dysregulation that makes steroids a concern in these patients.
Durability supports the case for a horse you would rather not re-medicate repeatedly. In a multicentre prospective study, 82.5% of horses were non-lame at 24 months after a single injection, with the effect sustained across the two-year follow-up. For an older patient whose OA you expect to manage for years, a single intra-articular treatment with a multi-year analgesic effect reduces the number of times you need to enter the joint at all.
How Does Arthramid Fit Within the Treatment Protocol for These Cases?
Arthramid is not a replacement for full OA and endocrine management. It is the intra-articular component of a multimodal plan that lets you address the joint without adding to the horse’s metabolic burden.
In practice, that means it sits alongside, not instead of, the rest of the protocol. The PPID horse should remain on effective pergolide, with the dose reviewed and the horse stable before elective joint treatment. Dietary management to restrict non-structural carbohydrate continues, as does appropriate farriery and a considered return to controlled exercise. Arthramid handles the intra-articular pain and joint function piece within that framework. Case selection follows the assessment above: the strongest candidates are horses with a confirmed OA diagnosis, localised on intra-articular analgesia with or without imaging, in which you want durable joint support and have reason to limit corticosteroid exposure.
The wider signal is reassuring. 2.5% iPAAG has been used in more than 300,000 horses worldwide, long-term retrospective data in Thoroughbred practice support a low adverse event rate over years of use, and a small study of concurrent iPAAG and betamethasone in healthy horses reported good tolerability, which is relevant where a short-term anti-inflammatory bridge is genuinely needed. Preclinical osteochondral models also point to disease-modifying activity, consistent with a treatment that acts on the joint environment rather than masking pain alone.
For the endocrine-compromised horse, that combination, durable joint support with no route to glucocorticoid-mediated metabolic risk, is what makes it a clinically defensible choice.
Access the clinical resources.
Treatment guides, case-selection material, and the equine white paper covering mechanism of action, clinical safety, and putting 2.5% iPAAG into practice are available for veterinarians at arthramid.com/nz/equine-vets/.
