atypical erosive osteoarthritis and sjogren's syndrome · annals of the rheumatic diseases,...

Annals of the Rheumatic Diseases, 1986; 45, 281-288

Atypical erosive osteoarthritis and Sjogren'ssyndromeRHONDA SHUCKETT, M LYNN RUSSELL, AND DAFNA D GLADMAN

From the University of Toronto, Rheumatic Diseases Unit, Women's College Hospital, Canada

SUMMARY An unusual, destructive form of erosive hand arthropathy is described in fivepostmenopausal women. Although early clinical and radiological findings were most in keepingwith a diagnosis of erosive osteoarthritis (EOA), hand involvement progressed to a distributionintermediate between EOA and rheumatoid arthritis (RA). Although asymptomatic, all patientshad features of Sjogren's syndrome (SS), including keratoconjunctivitis sicca (KCS) andlymphocytic foci in labial biopsy specimens. These cases, which are clinically unlike either RA or

EOA, may represent a unique arthropathy associated with sicca features.

Key words: inflammatory osteoarthritis, rheumatoid arthritis.

Erosive inflammatory variants of generalisedosteoarthritis have been described by severalauthors, who emphasise differences between theseconditions and rheumatoid arthritis (RA). -7 Sjog-ren's syndrome (SS), although well known to be anextra-articular feature of RA, has not been thoughtto occur in increased frequency in association withosteoarthritis (OA).We have encountered five women, all with sicca

features and two with definite SS, who presentedwith a destructive arthropathy most consistent witherosive osteoarthritis (EOA). After an interval ofseveral years wrist involvement in three cases andsevere proximal interphalangeal joint (PIP) destruc-tion in all raised the possibility of progression toRA. Such atypical cases provoke important ques-tions about the pathogenesis and clinical spectrumof EOA and its relationship to other rheumaticdisorders.

Patients and methods

CLINICAL FEATURESAll five patients were seen over an eight yearinterval in a hospital based rheumatology practice.All were females with a mean age at initialassessment of 68 years. Follow up ranged from oneto 10 years, with a mean of six years.

Accepted for publication 12 Septembcr 1985.Corrcspondcncc to Dr M Lynn Russell, 60 Grosvenor Street,Toronto, Ontario. Canada M5S 1B6.

All patients had a history of asymptomatic Heber-den's nodes for several years before presentationand then developed new symptoms in the distalinterphalangeal (DIP) joints characterised bymarked redness, swelling, pain, and stiffness, fol-lowed by similar PIP joint involvement. No otherjoints were symptomatic initially, and none of thefive had constitutional symptoms.On initial examination all patients showed in-

flammatory changes of DIPs and PIPs characterisedby tenderness and swelling with synovial thickeningor effusions, or both (Fig. 1). Bilateral first carpo-metacarpal (CMC) joint tenderness and squaringdeveloped in all cases. There was a striking lack ofmetacarpophalangeal (MCP), wrist, and foot in-volvement. Decreased range of motion, flexiondeformities, and horizontal subluxations of inter-phalangeal joints were universally present, and onecase developed ankylosis of multiple PIP joints aswell.

After a mean interval of 3-5 years three patientsdeveloped extensor carpi ulnaris (ECU) tenosyno-vitis, and in two of these patients wrist jointinvolvement with swelling and joint line tendernessoccurred. Wrist disease was bilateral in one case andhas remained unilateral in the other. One patientdeveloped bilateral hip disease with radiologicalevidence of superolateral joint space narrowing andwent on to total hip replacement. Two patientsdeveloped knee disease, one necessitating surgicalintervention. The lower limb arthritis in thesepatients was clinically characteristic of degenerative

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282 Shuckett, Russell, Gladman

Fig. 1 Clinical appearance ofcase I on initialexamination. Note Heberden's nodes, tense PIP effusions,and lack ofmetacarpophalangeal (MCP) and wristinvolvement.

rather than inflammatory disease, with minimalpostrest stiffness and significant weight bearingdiscomfort.Morning stiffness was less than 30 minutes in all

cases. None had nodules or other extra-articularmanifestations suggestive of RA, with the exceptionof Sjogren's features. All but one have remainedseronegative throughout their course. None of thecases had nail or skin changes compatible with adiagnosis of psoriasis, and there were no acuteepisodes of joint inflammation suggestive of crystalinduced arthritis.

All five patients were treated with non-steroidalanti-inflammatory drugs throughout follow up. Inaddition, three patients received chloroquine phos-phate and one penicillamine.

RADIOGRAPHIC FEATURESThe radiographic features of the hands were themost striking and remarkable findings in these

patients. Erosions of DIP and PIP joints werecharacterised by severe central subchondral erosionsleading to a 'gull wing' appearance of the jointspace. In addition, bony overgrowth and lateralsubluxations were dramatic in DIP and PIP joints.On radiological and clinical evaluation the MCPjoints were universally spared through follow up.Hand films of the two most severe cases illustrate

the progressive and destructive nature of thisarthropathy. In case 1 (Fig. 2a) initial x rays showedchanges confined to DIP and PIP joints, with centralerosions and crush deformities. Four years later(Fig. 2b) the disease had advanced markedly, withdramatic increase in severity of erosions of interpha-langeal joints. This was accompanied by evidence ofnew cysts and joint space narrowing of radiocarpaland intercarpal joints. Fullness was present clinicallyand radiographically in the ECU tendons, thoughthe ulnar styloid processes were radiologicallyspared. Erosive dissolution of the first CMC jointswas striking.

Initial radiographs of case 3 again showed strikingcentral IP joint erosions with crush deformity(Fig. 3a), asymmetric radiocarpal and intercarpaljoint space narrowing and cysts, advanced first CMCdisease, and a 'rheumatoid like' erosion at the tip ofthe ulnar styloid. Progression of these changes withultimate fusion of some PIPs is shown in Fig. 3b.

Similar IP erosions were present in the handradiographs of the other cases, though progressionwas not as severe. Moreover, wrist joints were hotaffected, though one additional case had clinicalevidence of ECU tenosynovitis. All patients hadjoint space narrowing and osteophytosis of thefirst MTP joints, without accompanying cysts orerosions. There was no evidence of chondrocalcino-sis or diffuse idiopathic skeletal hyperostosis.

FEATURES OF SJOGREN'S SYNDROMEResults of evaluation for SS are shown in Table 1.None of the five patients had sicca symptoms. Incase 1 direct questioning elicited complaints of milddryness of eyes and, once an association wassuggested, investigation was carried out in the othercases. All had keratoconjunctivitis sicca on the basisof positive Schirmer's test or rose bengal test, orboth. The salivary pool appeared adequate oninspection in all cases, but four of the five hadabnormal parotid scans with delayed uptake andexcretion patterns compatible with SS. Four patientsunderwent lip biopsy, which was performed andgraded according to the method of Chisholm et al.8This grading score is based on the degree oflymphocytic infiltration or the number of lymphocy-tic foci/4 mm2 of gland tissue, or both. A focus isdefined as an aggregate of > 50 lymphocytes, with



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Atypical erosive osteoarthritis and Sjogren's syndrome 283

Fig. 2 (a) Radiologicalappearance ofcase I on initialevaluation. (b) Radiologicalappearance ofcase 1 four yearslater. Notefurther DIP and PIPdestruction and CMC and wristerosions, with sparing ofMCPjoints.

the grading system as follows: grade 1 =lymphocytesabsent; grade 2=moderate infiltrate; grade 3=onefocus/4 mm2 tissue; grade 4=.more than one focus/4mm2 tissue. In all cases neoplasm, labial glandinfection, local mucosal trauma, and cytotoxic drugtherapy were ruled out. When biopsies were inter-preted duct dilatation, extravascular polymorpho-nuclear leucocytic infiltration, and areas of atrophyadjacent to lymphocytic foci were excluded.8With this scoring system all four biopsy specimens

had at least one lymphocytic focus/4 mm2 tissue, inkeeping with the presence of focal lymphocyticsialadenitis (FLS). Two patients had a score of 4,indicating more than one focus/4 mm2. These twocases fulfilled criteria for the diagnosis of definite SSas defined by the presence of two of the following:(a) KCS signified by a positive Schirmer's test orrose bengal test, or both; (b) labial salivary glandbiopsy specimen with more than one lymphocyticfocus/4 mm2 gland tissue (i.e., focus score > 3); (c)

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Fig. 3 (a) Case 3 at initialpresentation. Asymmetric CMCand wrist involvement is alreadypresent. (b) Case 3 six years later.There is progression ofunilateralwrist disease andfusion ofsomePIPjoints. Again note absence ofMCP disease.

connective tissue disease. The lip biopsy score of 3seen in case 5, although indicating the presence ofFLS, is considered to be a transitional value,suggesting possible SS.10 However, this patient andthe case who did not undergo lip biopsy had KCS,

and the latter had an abnormal parotid scancharacteristic of SS, strengthening the likelihood ofthis diagnosis. The labial biopsy specimen of onepatient, case 4, showed one focus/4 mm2, butconsiderable fibrosis and fatty infiltration of



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Atypical erosive osteoarthritis and Sjogren's syndrome 285

Table 1 Sicca features of cases with erosive OA andSjogren's syndrome

Case Age Sicca* Scan* Lip Bx* Schirmer* R-B*

1 69 ± + >4 ++ ++2 66 ± + 4 ++ +3 68 - + ND ++ +4 74 - + 2-5 ++ -5 74 - N 3 ++ +

*Sicca=symptoms of dry eyes or mouth, or both; Scan=parotidscan; Lip Bx=focus score; Schirmer=Schirmer's test; R-B=rose-bengal test.

surrounding gland tissue rendered a diagnosis ofFLS in this patient uncertain. Thus all four biopsiedpatients fulfilled criteria for definite (or possible) SSon the basis of clinical or pathological glandulardisease, or both. If their arthritis manifestationswere considered to fulfil the third criterion-that ofan associated connective tissue disease-all wouldmeet requirements for a diagnosis of definite SS.

SEROLOGICAL INVESTIGATIONSHaemoglobin, white blood cell count, and plateletcounts were normal in all except case 1, in whom anormocytic anaemia characteristic of chronic diseasedeveloped. The erythrocyte sedimentation rate wasintermittently raised in two patients in relation toflares of inflammatory disease. Serum calcium,phosphorus, and uric acid were within normal limitsin all cases. The relevant serological findings areshown in Table 2, which shows that the patientswere remarkable for their lack of the serologicalreactivity usually associated with RA or SS, or both.Only one patient was rheumatoid factor positive at atitre of 1/640, while the others were persistentlyseronegative. A fluorescent antinuclear antibodytest carried out on HEp2 cells was negative in allcases. Anti-Ro and La antibody tests performed byOuchterlony diffusion (courtesy of Dr Morris Reich-lin, Oklahoma City) showed that anti-La was absentin all cases and anti-Ro was present only in case 1,

the case with rheumatoid factor activity also. Anti-salivary gland antibody tested for by indirect im-munofluorescence with goat antihuman IgG, IgM,and IgA polyvalent antiserum was negative in allpatients. Case 1 developed biochemical hypothy-roidism without thyroid antibodies, and case 2 hadboth antithyroglobulin and antimicrosomal anti-bodies in the absence of clinical thyroid disease.Complete HLA typing showed that case 1, with themost widespread inflammatory disease and the mostactive labial biopsy, was HLA-A1, B8, DR2. Twocases, which were the least rheumatoid like sincethey lacked both wrist and MCP disease, wereHLA-DR4. None was HLA-DR3.

Synovial fluid was aspirated on two occasionseach from the knee and wrist in case 1 and from theknee in case 5. Only small amounts of fluid wereobtained, allowing limited examination. The kneefluid from case 1 was turbid, with increased neut-rophils on smear and no crystals. The wrist aspiratesand that of the knee in case 5 were clear, non-inflammatory fluids with few cells and no crystals.

Synovial tissue was obtained at surgery in threeinstances: bilateral hip replacement in case 1, fusionof the IP joint of the thumb in case 2, and at totalknee replacement in case 3. Pathology in all casesshowed modest synovial cell hyperplasia, with mildsubsynovial increase in vascularity and a scatteredlymphocytic infiltrate. No lymphoid follicles wereseen.

Discussion

Awareness of a polyarticular form of OA of thehands was reflected in the 19th century writings ofHaygarth, Garrod, and Adams.'-13 More detailedclinical descriptions have since followed, and withthese, various terms for this condition have emergedin the literature. These include 'generalised OA''inflammatory OA', and 'erosive OA' (EOA).Generalised osteoarthritis was initially described inthe classic monograph of Kellgren and Moore, inwhich a characteristic distribution of OA with

Table 2 Serological features of cases with erosive osteoarthritis and Sjogren's syndrome

Case RP ANF* Ro* La* Sal* G* HLA-A HLA-B HLA-DR

1 640 0 + 0 0 1 1,3 8,35 1,22 0 0 0 0 0 N 2,- 62,44 2,43 0 0 0 0 0 N 29,31 44,18 1,74 0 0 0 0 0 N 2,24 7,44 4,65 0 0 0 0 0 N 2,11 13,14 7,6

*RF=rheumatoid factor; ANF=antinuclear factor; Ro=anti-Ro antibody; La=anti-La antibody; Sal=antisalivary gland antibody; G=gammaglobulin.



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prominent hand involvement and predilection formiddle aged females was reported. In 1961 Craininitiated the concept of OA of the finger joints withstriking inflammatory features and frequent pro-gression to ankylosis.l Shortly after, Kidd andPeter3 and Peter et al2 coined the term 'erosive OA'to denote characteristic erosive lesions of theinterphalangeal joints. Clearly, the abundantnomenclature for interphalangeal OA can lead toconsiderable confusion. These terms, however,should probably be regarded as descriptions ofvariants of the same disease category.

Several others have added to the list of reports oninflammatory, erosive variants of OA, emphasisingfeatures which help to distinguish this conditionfrom RA.f7 In contrast with RA, inflammatoryerosive OA is characterised by lack of juxta-articular osteoporosis, the presence of prominentDIP joint involvement, and radiological subchon-dral sclerosis and hypertrophic new bone formationat both the DIP and PIP joint. Wrist involvementoccurs in EOA but is generally confined to the radialside of the carpus, with frequent involvement of thetrapezium and adjacent metacarpal and carpalbones. 15

It is noteworthy that Peter et al found thatsynovial pathology in cases of EOA was notqualitatively different from that of RA, with syno-vial lining cell hyperplasia, round cell infiltration,subsynovial fibrosis, and pannus being commonfindings.2 However, others have felt that despitemany similarities, significant differences in thesynovial pathology do exist. 16 Moreover, theradiological findings of central subchondral erosionsand hypertrophic bone reaction in EOA, in contrastwith the peripheral 'pocket' erosions due to pannusin RA, imply critical differences in synovial-cartilage interaction in the two conditions.Although several reports suggest that judicious x

ray interpretation facilitates differentiation betweenEOA and RA, potential for confusion still exists.Moreover, Ehrlich has described progression tofeatures of classical or definite RA in 15% ofpatients with typical inflammatory OA.17 18 'Con-version' to RA was signalled by clinical and radio-logical involvement of joints typical of RA such asMCPs, wrists, and elbows. Three of our cases withwrist or ECU tendon involvement, or both arehighly reminiscent of Ehrlich's experience, thoughnone of our small group developed nodules or MCPsynovitis and only one case was seropositive.The development of disease similar to RA in his

cases led Ehrlich to speculate on the relationshipbetween EOA and RA and to suggest that theformer condition may represent a disease 'interface'between RA and benign OA.'8 19 As Ehrlich

pointed out cases that begin with inflammatory orerosive OA are distinct from the 'engrafted RA'described in the German literature, which refers tothe concurrence of non-inflammatory Heberden'sand Bouchard's nodes with RA.20 In view of theknown high prevalence of benign Heberden's nodesin middle aged females, and the not infrequentoccurrence of RA in this population, coexistence ofthe two conditions would not be surprising. How-ever, inflammatory, erosive variants of hand OA arefar less prevalent than Heberden's nodes and areestimated to affect approximately 1% of females inthe age range at risk. Concurrence of EOA and RAwould therefore not be expected to be frequent.

In keeping with Ehrlich's series our experienceindicates a subset of patients with joint diseasecompatible with a diagnosis of inflammatory, ero-sive OA but with eventual appearance of rheuma-toid like features in the involved joints. This conceptis further supported by a recent report byUtsinger.On the other hand, McCarty's emphasis on DIP

involvement in RA as assessed by joint tendernessraises the issue of rheumatoid disease as the solediagnosis in such cases.22 Thus it could be proposedthat these women have an unusual localised form ofRA with prominent DIP involvement, sparing moreclassic rheumatoid sites and lacking serologicalreactivity. This possibility seems unlikely in ourcases, though case 1 was seropositive and developedwrist disease. The others, in most respects similar tocase 1, look clinically and radiologically distinctfrom RA.

Apart from RA it is probable that few otherarthritides would present like our cases. Despiteabsence of skin or nail lesions, psoriatic arthritis(PSA) must be considered. PSA is known to occurwithout psoriasis, and the distribution of jointdisease can be similar to that of OA. Erosive OAand PSA are similar in their predilection for DIPjoints, lack of juxta-articular osteoporosis, andpotential for ankylosis, and even main en lorgnettedeformity.23 However, key radiological differencesbetween the two conditions have been described.24The central subchrondral IP erosions seen in ourcases conform more to the 'gull wing' pattern ofEOA rather than the peripheral 'mouse ear' lesionsmore typical of PSA. Clearly, a diagnosis of PSAcould only be, at best, speculative in the absence ofskin or nail lesions.

Calcium pyrophosphate dihydrate (CPPD) de-position disease is known to lead to osteoarthriticinvolvement of atypical sites, including MCP andradiocarpal joints.2927 This generally, but not in-variably, occurs in the context of chondrocalcinosisor documented crystal induced synovitis, or both,



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Atypical

neither of which were found in our cases. Thus it isunlikely that CPPD arthopathy is present in ourcases.

In addition to their unusual arthropathy all of ourcases had features of Sjogren's syndrome. Of thefour patients who underwent lip biopsy, two haddefinite SS pathologically, and the other two hadlymphocytic foci of a degree representing a tran-sitional value. The remaining unbiopsied patienthad both a positive parotid scan and keratocon-junctivitis sicca.The incidence of SS is not known to be increased

in patients with OA, though this has not beenevaluated in a controlled fashion. In one postmor-tem study of lip biopsy specimens only one of 10patients with OA had focal lymphocytic sialadenitis,and that of non-diagnostic grade.28 Two otherstudies report an increased incidence of sicca symp-toms in OA, sometimes associated with otherautoimmune manifestations.29-" However, lipbiopsies were not performed, and a diagnosis of SSis therefore uncertain. Sicca features alone in theabsence of glandular infiltrates would be expected tobe common among elderly females.

Articular manifestations of primary SS, althoughill defined, are not like those seen in our patients. Arecent study addressing this issue found a highprevalence of joint involvement, which tended to bepolyarticular, symmetrical, and intermittent, with amild degree of synovitis.3' Wrist and MCP involve-ment were common, but the chronic synovitis anderosive disease as encountered in our group werenot found.Our cases, although comprising a small group, are

surprisingly inactive serologically for either primaryor secondary SS. Negative rheumatoid factor isparticularly unusual in SS occurring with RA, andthe presence of anti-Ro in only one case is less thanthat usually encountered in primary SS32-35 and maybe related to the presence in the same patient ofrheumatoid factor. No case had antisalivary anti-bodies, which one would expect in 20-30% of casesof SS with RA.36Our cases provoke several questions about the

nature of erosive OA and suggest a greater thanexpected association with Sjogren's syndrome. Theymay represent a subset of patients having EOA withan autoimmune background. The presence of HLA-DR4 in two patients and HLA-A1/B8 in anothermay be relevant in this regard.While it remains useful for the sake of consistency

in nosology and classification to regard EOA as aseparate entity, our experience suggests that at leasta subgroup with atypical features exists. Whetherthis indeed represents a particularly destructiveform of EOA, a disease interface with RA, or a

erosive osteoarthritis and Sjogren's syndrome 287

distinct arthropathy is at present unclear. Furtherstudy of such patients, with close attention toclinical, immunological, and pathological features,should help answer these questions.

We are grateful to Dr M Reichlin for performing the anti-Ro andLa determinations, to Dr A Katz for the antisalivary antibodydeterminations, and to Mrs J Clapp for preparation of themanuscript.

References

1 Crain D C. Interphalangeal osteoarthritis. JAMA 1961; 175:1049-53.

2 Peter J B, Pearson C M, Marmor L. Erosive osteoarthritis ofthe hands. Arthritis Rheum 1966; 9: 365-88.

3 Kidd K L, Peter J B. Erosive osteoarthritis. Radiology 1965; 86:640-7.

4 McEwen C. Osteoarthritis of the finger joints with ankylosis.Arthritis Rheum 1968; 11: 734-44.

5 Smukler N M, Edeiken J, Giuliano V J. Ankylosis inosteoarthritis of the finger joints. Radiology 1971; 100: 525-30.

6 Utsinger P D, Resnick D, Shapiro R F, Wiesner K B.Roentgenologic, immunologic and therapeutic study of erosive(inflammatory) osteoarthritis. Arch Intern Med 1978; 138:693-7.

7 Ehrlich G E. Inflammatory osteoarthritis-I. The clinicalsyndrome. J Chron Dis 1972; 25: 317-28.

8 Chisholm D M, Mason D K. Labial salivary gland biopsy inSjogren's disease. J Clin Pathol 1968; 21: 656-60.

9 Waterhouse J P, Doniach I. Post-mortem prevalence of focallymphocytic adenitis of the submandibular salivary gland. JPathol Bacteriol 1966; 91: 5344.

10 Daniels T E. Labial salivary gland biopsy in Sjogren's syn-drome. Arthritis Rheum 1984; 27: 147-56.

11 Haygarth J. A clinical history of diseases. London: Crutwell,1805: 105.

12 Garrod A B. A treatise on rheumatism and rheumatoid arthritis.2nd ed. London: Churchill, 1873: 503-7.

13 Adams R. A treatise on rheumatic gout. 2nd ed. London:Churchill, 1873: 2-5.

14 Kellgren J H, Moore R. Generalised osteoarthritis and Heber-den's nodes. Br Med J 1952; i: 181-7.

15 Greenway G, Resnick D, Weisman M, Mink J H. Carpalinvolvement in inflammatory (erosive) osteoarthritis. J CanAssoc Radiol 1979; 30: 95-8.

16 Katona G. Osteoarthritis-an inflammatory disease? Int JTissue React 1984: 6: 453-61.

17 Ehrlich G E. Inflammatory osteoarthritis-II. The superim-position of rheumatoid arthritis. J Chron Dis 1972; 25: 635-43.

18 Ehrlich G E. Osteoarthritis beginning with inflammation-definitions and correlations. JAMA 1975; 232: 157-9.

19 Ehrlich G E. Introduction: Of syndromes and interfaces. In:Ehrlich G E, ed. Oculocutaneous manifestations of rheumaticdiseases. Basel, Switzerland: Karger. 1973: 1-12.

20 Boni A. In: Boni A. Schoen R, Meihike R, eds. DieProgredient Chronische Polyarthritis, Klinik der RheumatischenErkrankugen. Berlin: Springer, 1970: 156.

21 Utsinger P D, Resnick D D, McLaughlin G E, Moidel R A.Inflammatory osteoarthritis: a presenting manifestation of atleast 4 arthritides [Abstractl. Arthritis Rheum 1983: 26 (suppl):S19.

22 McCarty D J, Gatter R A. A study of distal interphalangealjoint tenderness in RA. Arthritis Rheum 1966; 9: 325-36.

23 Swezey R L, Alexander S J. Erosive osteoarthritis and the mainen lorgnette deformity (opera glass hand). Arch Intern Med1971; 128: 269-72.

24 Martel W. Stuck K J, Dworin A M, Hylland R G. Erosive



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Ann R

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osteoarthritis and psoriatic arthritis: A radiologic comparison in

the hand, wrist and foot. AJR 1980; 134: 125-35.25 Resnick D, Niwayama G. Georgen T G, et al. Clinical.

radiographic and pathologic abnormalities in CPPD. Radiologs1977; 122: 1-15.

26 Gerster JC, Vischer T L, Fallet G H. Destructive arthropathy in

osteoarthritis with articular chondrocalcinosis. J Rheumatol1975; 2: 265-9.

27 Resnick D, Utsinger P D. The wrist arthropathy of 'pseudo-gout' occurring with and without chondrocalcinosis. Radiology1974; 113: 633-41.

28 Whaley K, Chisholm D M, Downie W W, Dick W C,Williamson J. Lymphocytic sialadenitis in the buccal mucosa inSjogren's disease, rheumatoid arthritis and other arthritides-aclinical and laboratory study. Acta Rheumatol Scand 1968; 14:298-308.

29 Strickland R W, Tesar J T, Berne B H, et al. The prevalence ofSjogren's syndrome and associated rheumatic diseases in an

elderly population. Arthritis Rheum 1984; 27: S45.30 Singleton P T, Cevvantes A G. Sicca complex and erosive

osteoarthritis: immunologic implications of a new osteoarthritissubset. Arthritis Rheum 1983; 26: S191.

31 Castro-Poltinieri A, Alarcon-Segovia. D. Articular manifes-tations of primary Sjogren's syndrome. J Rheumatol 1983: 10:485-8.

32 Alspaugh M A, Talal N. Tan E M. Differentiation andcharacterization of autoantibodies and their antigens in Sjog-ren's syndrome. Arthritis Rheum 1976; 19: 216-22.

33 Martinez-Lavin M. Vaughan J H. Tan E M. Autoatntibodicsand the spectrum of Sj-ogren's syndromc. Anti Initern Med 1979:91: 185-90.

34 Elkon K B. Ghasari A E. Hughes G R. Moutsopoulos H M.Autoantibodies in sicca syndromc (primarv Sjogrcn's syn-drome). Ann Rheum Dis 1984; 43: 24-5.

35 Alexander E L. Provost T T. Ro (SSA) and La (SSB)antibodies. Springer Semin Immnunopathol 1981: 4: 253-73.

36 Macsween R N. Goudie R B. Anderson J R. et al. Occurrenceof antibody to salivary duct epithelium in Sjo6grcn's discasc.rhcumatoid arthritis, and othcr arthritidcs: a clinical andlaboratorv study. Antn Rlieutn Dio 1967: 26: 402- 11.



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