Nodal generalised osteoarthritis is an autoimmune disease

[Pages:4]Annals ofthe Rhewnatic Diseases 1990; 49: 1017-1020

1017

HYPOTHESIS

Ann Rheum Dis: first published as 10.1136/ard.49.12.1017 on 1 December 1990. Downloaded from on November 12, 2023 by guest. Protected by copyright.

Nodal generalised osteoarthritis is an autoimmune disease

Michael Doherty, Martin Pattrick, Richard Powell

Nature of osteoarthritis

ment, 'joint failure'), OA has been increasingly

Osteoarthritis (OA), the commonest abnormality divided into clinically determined subsets.3

to affect synovial joints, has accompanied man Such categorisation has been by distribution of

throughout his evolutionary history, and a joint disease (generalised, pauciarticular, mono-

similar process occurs in other animals that fuse articular'4); predominance of certain radio-

epiphyses in the adult."13 Such prevalence and graphic features ('atrophic', 'hypertrophic'l5);

phylogenetic preservation suggest that OA is a associated crystal deposition (pyrophosphate

process rather than a disease, reflecting the arthropathy,16 apatite associated destructive

response of articular tissues to extrinsic or arthritis'7); and presumed aetiological factors-

intrinsic insult, or both.4 5 The recognised for example, epiphysial dysplasia, Kashin-Beck

synthetic activity of osteoarthritic tissues," the disease. Such subsetting, especially for common

radiographic remodelling and favourable out- forms of OA, has proved problematic because of

cdone seen in many patients with OA,7-9 and the overlap,'6 18 temporal transition from one sub-

prevalence of asymptomatic 'disease'3 10 11 sup- set to another,'6 19 and difficulties in radio-

port the concept of OA as a repair process.4'5 graphic interpretation and crystal identifi-

Like any repair process, OA may succeed or fail cation."'21 Nevertheless, several groups are

when responding to a variety of triggering or generally accepted.3

perpetuating insults (fig 1). The pathogenesis Nodal generalised OA, the best recognised

and variability of OA are poorly understood, subset, is characterised by polyarticular hand

but multiple factors, including genetic, consti- OA (principally interphalangeal and first

tutional, and environmental, are likely to play a carpometacarpal joints), female preponderance,

Unit, Rheumatology City Hospital,

part.3 12 13 Marked variability in the nature and early symptomatic inflammatory component,

chronicity of the insult(s), and host differences and Heberden (with or without Bouchard) node

Nottham NG5 1PB in effective repair response, result in the confus- formation, or both3 14 22: of all OA subsets,

M Doherty

M Pattrick

ing heterogeneity of radiographic and clinical familial tendency is particularly recognised.'3

Department of

Immulology,

maniestations.

Erosive OA is a less common generalised subset sharing many features of NGOA but differing in

Queen's Medical Centre,

having marked subchondral erosive change, a

Notnham R Powell

Correspondence to: Dr Doherty.

Accepted for publication 16 March 1990

The 'subset' ofnodal generalised OA (NGOA) In an attempt to understand OA better and to identify factors initiating and influencing compensation (no symptoms, good outcome) or decompensation (symptoms, functional impair-

more florid and prolonged inflammatory component, and a tendency to intra-articular osseous fusion.3 23 24 Minor subchondral erosions in NGOA, however, are not uncommon and whether erosive OA is a discrete

subset or merely the more severe end of the

NGOA spectrum has been questioned.25 Many

elderly subjects have patchy hand interphalan-

Insults

geal OA or nodes: this may relate to obvious prior trauma, but is often asymptomatic and

apparently sporadic. Although there is no sharp

division between such hand OA and NGOA,

the latter is classically symptomatic in middle

age, presenting as a stuttering-onset 'mono-

arthritis multiplex', is unrelated to obvious

trauma, and affects most if not all rays. At sites

other than the hand, such as the hip, the

tendency to bilateral disease and to diffuse

(concentric/central) rather than focal (supero-

lateral) cartilage loss26 27 further supports the

separation of NGOA as an inflammatory subset

of OA.

Repair

Figure I Representation ofosteoarthritis as a repair process that may compensate orfail in Genetic associations

response to a variety ofinsults.

Surprisingly, despite marked familial predis-

1018

Doherty, Paunch, Powell

Ann Rheum Dis: first published as 10.1136/ard.49.12.1017 on 1 December 1990. Downloaded from on November 12, 2023 by guest. Protected by copyright.

position, few studies have searched for genetic markers in NGOA.'3 Until recently only four

nOobdsaelmagteinoenrasliwsheidcohsesauprptohrrtisautoimne mechanism in

studies had examined the frequencies of HLA Geneic associatons:

antigens, with conflicting results: Lawrence et al reporting increased frequency of HLA-

FeMmHaLZlAe-aA,prlaeBpn8otnidterryapnnce

A1B8,8 Brodsky et al an increase in HLA-B8,29 and two studies finding no associations.30 31 A

Peimnomusal onaet (Horm al inluence on disease expression)

Association with other autoimmune disease

recent large study by Pattrick et al, however, confirmed increased frequency of HLA-AlB8

Sj6gren's syndrome (?erosive osteoarthritis only)

Thyroid disease

Immunological findings

in

synovium

and

cartisge

in 90 unrelated patients with NGOA (relative Increased frequency of rheumatoid factor

risk compared with reference population 2-79;

p ................
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