In dogs, IMPA is a common noninfectious idiopathic accumulation of inflammatory immune complexes within the synovial membrane of affected joints.1,2 Clinical signs are associated with pathological changes in the affected joints and frequently include signs of pain or stiffness, joint effusion, and lameness.3,4 Affected dogs may also be febrile with anorexia and lethargy.3,4 Up to 25% of dogs with IMPA do not have joint effusion or lameness, and instead are examined because of signs of vague systemic illness.3,4 The most commonly affected joints are the carpal, tarsal, stifle, and elbow joints.3,5–7 By definition, dogs with IMPA have multiple affected joints, although grossly evident clinical abnormalities may be limited to only 1 joint during initial physical examination of dogs in the early stages of the disease. A definitive diagnosis of IMPA is made on the basis of the detection of characteristic abnormalities during cytologic and radiographic evaluation of multiple joints.5,8–11
Immune-mediated polyarthritis typically results in nonerosive lesions; IMPA-associated erosive lesions and bone destruction are rare. The term canine rheumatoid arthritis has been used to describe erosive IMPA,12,13 but the latter term will be used exclusively in the present report. Risk factors and the underlying mechanism for the development of erosive IMPA have yet to be elucidated. Dogs with erosive IMPA may develop joint instability subsequent to damage or destruction of the soft tissue structures that support affected joints.12,13 Compared with dogs with nonerosive IMPA, dogs with erosive IMPA are less responsive to treatment, have a poorer prognosis, and often require lifelong treatment with high doses of immunosuppressive drugs with or without joint arthrodesis.12–15
Immune-mediated polyarthritis is typically diagnosed on the basis of cytologic evaluation of synovial fluid samples obtained by arthrocentesis from multiple joints.16 Dogs with IMPA frequently have multiple joints in which the synovial fluid protein concentration is > 3.0 g/dL (reference range, 1.5 to 3.0 g/dL) and TNCC is ≥ 3,000 cells/μL (reference range, 0 to 2,900 cells/mL).11,16 Synovial fluid samples with > 12% nondegenerate PMNLs are supportive of inflammatory arthritis.4,17 When an adequate volume of synovial fluid cannot be obtained for a complete analysis, evaluation of a direct smear can be used to estimate the TNCC.18 Evaluation of radiographic images of joints can be useful for determining which joints are affected and whether bone lysis is present in those joints.4 Additional diagnostic testing modalities such as bacterial culture may be indicated to rule out infectious causes of polyarthritis. Clinical information about erosive IMPA is limited. Therefore, the purpose of the study reported here was to evaluate the clinical features and pathological joint changes in dogs with erosive IMPA at initial examination and during subsequent immunosuppressive therapy.
The authors thank Dr. Karen Young and Ms. Zhengling Hao for technical assistance.
Cranial cruciate ligament rupture
Total nucleated cell count
1. Colopy SA, Baker TA, Muir P. Efficacy of leflunomide for treatment of immune-mediated polyarthritis in dogs: 14 cases (2006–2008). J Am Vet Med Assoc 2010; 236:312–318.
2. Johnson KC, Mackin A. Canine immune-mediated polyarthritis. Part 1: pathophysiology. J Am Anim Hosp Assoc 2012; 48:12–17.
3. Chabanne L, Fournel C, Monestier M, et al. Canine systemic lupus erythematosus: part I: clinical and biological aspects. Compend Contin Educ Pract Vet 1999; 21:135–141.
4. Rondeau MP, Walton RM, Bissett S, et al. Suppurative, nonseptic polyarthropathy in dogs. J Vet Intern Med 2005; 19:654–662.
5. Jacques D, Cauzinille L, Bouvy B, et al. A retrospective study of 40 dogs with polyarthritis. Vet Surg 2002; 31:428–434.
6. Clements DN, Gear RN, Tattersall J, et al. Type I immune-mediated polyarthritis in dogs: 39 cases (1997–2002). J Am Vet Med Assoc 2004; 224:1323–1327.
7. Stull JW, Evason M, Carr AP, et al. Canine immune-mediated polyarthritis: clinical and laboratory findings in 83 cases in western Canada (1991–2001). Can Vet J 2008; 49:1195–1203.
8. Bennett D. Immune-based non-erosive inflammatory joint disease of the dog. 1. Canine systemic lupus erythematosus. J Small Anim Pract 1987; 28:871–889.
9. Bennett D, Kelly F. Immune-based non-erosive inflammatory joint disease of the dog. 2. Polyarthritis/polymyositis syndrome. J Small Anim Pract 1987; 28:891–908.
10. Bennett D. Immune-based non-erosive inflammatory joint disease of the dog. 3. Canine idiopathic polyarthritis. J Small Anim Pract 1987; 28:909–928.
11. MacWilliams PS, Friedrichs KR. Laboratory evaluation and interpretation of synovial fluid. Vet Clin North Am Small Anim Pract 2003; 33:153–178.
12. Bennett, D. Immune-based erosive inflammatory joint disease of the dog: canine rheumatoid arthritis. 1. Clinical, radiological, and laboratory investigations. J Small Anim Pract 1987; 28:779–797.
13. Bennett, D. Immune-based erosive inflammatory joint disease of the dog: canine rheumatoid arthritis. 2. Pathological investigations. J Small Anim Pract 1987; 28:799–819.
15. Ralphs SC, Beale BS, Whitney WO, et al. Idiopathic erosive polyarthritis in six dogs (description of the disease and treatment with bilateral pancarpal arthrodesis). Vet Comp Orthop Traumatol 2000; 13:191–196.
16. Johnson KC, Mackin A. Canine immune-mediated polyarthritis: Part 2: diagnosis and treatment. J Am Anim Hosp Assoc 2012; 48:71–82.
17. Chabanne L, Fournel C, Rigal D, et al. Canine systemic lupus erythematosus. Part II: diagnosis and treatment. Compend Contin Educ Pract Vet 1999; 21:402–410.
18. Dusick A, Young KM, Muir P. Relationship between automated total nucleated cell count and enumeration of cells on direct smears of canine synovial fluid. Vet J 2014; 202:550–554.
19. Parker HG, Shearin AL, Ostrander EA. Man's best friend becomes biology's best in show: genome analyses in the domestic dog. Annu Rev Genet 2010; 44:309–336.
20. Ollier WER, Kennedy LJ, Thomson W, et al. Dog MHC alleles containing the human RA shared epitope confer susceptibility to canine rheumatoid arthritis. Immunogenetics 2001; 53:669–673.
21. Bell SC, Carter SD, May C, et al. Antibodies to heat shock proteins in dogs with rheumatoid arthritis and systemic lupus erythematosus. Br Vet J 1995; 151:271–279.
23. Farr M, Scott DL, Constable TJ, et al. Thrombocytosis of active rheumatoid disease. Ann Rheum Dis 1983; 42:545–549.
24. Boilard E, Blanco P, Nigrovic PA. Platelets: active players in the pathogenesis of arthritis and SLE. Nat Rev Rheumatol 2012; 8:534–542.
26. Smee NM, Harkin KR, Wilkerson MJ. Measurement of serum antinuclear antibody titer in dogs with and without systemic lupus erythematosis: 120 cases (1997–2005). J Am Vet Med Assoc 2007; 230:1180–1183.
27. Chabanne L, Fournel C, Faure JR, et al. IgM and IgA rheumatoid factors in canine polyarthritis. Vet Immunol Immunopathol 1993; 39:365–379.
28. Foster JD, Sample S, Kohler R, et al. Serum biomarkers of clinical and cytological response in dogs with idiopathic immune-mediated polyarthropathy. J Vet Intern Med 2014; 28:905–911.
30. Bleedorn JA, Greuel EN, Manley PA, et al. Synovitis in dogs with stable stifle joints and incipient cranial cruciate ligament rupture: a cross-sectional study. Vet Surg 2011; 40:531–543.
31. Erne JB, Goring RL, Kennedy FA, et al. Prevalence of lymphoplasmacytic synovitis in dogs with naturally occurring cranial cruciate ligament rupture. J Am Vet Med Assoc 2009; 253:386–390.
32. Muir P, Schwartz Z, Malek S, et al. Contralateral cruciate survival in dogs with unilateral non-contact cranial cruciate ligament rupture. PLoS One 2011; 6:e25331.