believed to be a clinically uncommon subset of generalized osteoarthritis (OA)
characterized by a clinical course, which is frequently aggressive - erosive osteoarthritis is a distinct clinical entity from primary generalised nodal osteoarthritis
this condition is also known as inflammatory osteoarthritis
clinical features:
diagnosis based on the radiographic aspects of articular surface erosions
clinical features may lead to a suspicion of EOA. These include:
abrupt onset of pain, swelling, redness, warmth and limited function of IP joints of the hands are commonly found in most patients
throbbing paresthesias of the fingertips, which are often nocturnal
evolution in nodal deformities of distal IP (DIP) and proximal IP (PIP) may be seen to follow a variable course with no significant differences from non-EOA - with the exception of a more accelerated progression for EOA
radiological features:
classic radiological changes of EOA are characterized by a combination of bony proliferation and erosions
characteristic erosions are seen in DIPs and PIPs
most frequent lesions begin at the central portion of the joint in the form of a sharply marginated defect, usually preceded by joint narrowing
joint narrowing and erosions may be seen early in EOA, while only later are margins affected by bone proliferations leading to Heberden's and Bouchard's nodes
diagnosis:
diagnosis of EOA was accepted only for patients meeting American College of Rheumatology clinical criteria of OA of the hand and showing radiographic aspects of articular surface erosions - there is debate as to how many erosions need to occur for a diagnosis of EOA - some suggest that two erosions in two different IPs may be sufficient to be classified as EOA
conditions to be considered in the differential diagnosis include primarily nodal generalized OA, psoriatic arthritis and rheumatoid arthritis
possible to find erosive changes resembling EOA in endocrine diseases, microcrystal-induced diseases, chronic renal diseases, autoimmune diseases and others
laboratory features:
CRP levels are higher in erosive osteoarthritis than in non-erosive osteoarthritis patients. These levels probably reflect the disease activity of erosive osteoarthritis, as suggested by correlations between CRP and joint count at clinical observation and at bone scintigraphy (2)
EOA patients are rheumatoid factor negative and negative for anti-CCP antibodies
management
no definitive therapeutic approach to EOA has been reported
reasonable to assume that in the presence of a symptomatic EOA our therapeutic approach should differ from that used for common, nodal, non-EOA (1)
paracetamol is the drug of first choice in EOA - however this drug is frequently inadequate, and treatment must therefore be shifted toward non-steroidal anti-inflammatory drugs (NSAIDs)
intra-articular injections of corticosteroids may bring some symptomatic relief although there is no demonstration that such therapy may reduce the development of erosions or accelerate their healing
other possible therapeutic measures include:
hydroxychloroquine - there is study evidence for the efficacy of this therapeutic option in EOA
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