dish and the monastic way of life

International Journal of OsteoarchaeologyInt. J. Osteoarchaeol. 11: 357–365 (2001)DOI: 10.1002/oa.574

DISH and the Monastic Way of LifeJULIET ROGERSa AND TONY WALDRONb,*a Rheumatology Unit, Bristol Royal Infirmary, Bristol BS2 8HW, UKb Institute of Archaeology, University College London, London WC1H 0PY, UK

ABSTRACT Diffuse idiopathic skeletal hyperostosis (DISH) is a common condition and its prevalenceincreases markedly with age. This paper describes the pathology and aetiology of the condition;DISH seems to be related to obesity and type II diabetes and is probably a multisystem hormonaldisorder. DISH occurs frequently in human skeletal remains, particularly in those recovered frommonastic sites.

Evidence is presented to confirm this association and the causes are discussed. We alsopresent criteria for the diagnosis of DISH in human remains, which we suggest would permit validinter-study comparisons. Copyright © 2001 John Wiley & Sons, Ltd.

Key words: DISH; palaeopathology; diabetes; obesity; monasteries

Introduction

Diffuse idiopathic skeletal hyperostosis (DISH)is a complex disorder characterized by exuber-ant hyperostosis and ankylosis of the spinalcolumn, and calcification or ossification ofextra-spinal entheses and ligaments. Forestier &Rotes-Querol (1950) were the first to compre-hensively describe the condition; they notedthat, in general, it was confined to those beyondmiddle age (the average age of their patientswas 65 years) and that the prevalence increasedconsiderably with age. Forestier extended hisobservations in a much later paper in which themajor pathological and radiological features ofthe condition were described (Forestier &Lagier, 1971).

Changes in the spine are the result of ossifi-cation into the anterior longitudinal ligament(ALL) and other spinal ligaments; although theymay occur in all areas of the spine, they areusually most prominent in the thoracic region(Figure 1). In time, the ossification leads toankylosis of variable numbers of vertebrae, butthe intervertebral disc space and the facet jointsare normal in the absence of other pathology.One of the features of the spinal manifestations

of DISH is that the changes are only found onthe right-hand side of the thoracic region; it isthought that this results from the left-handpresence of the descending aorta, the pulsationof which prevents ossification of the ALL onthat side. Whether or not this is the mechanism,there is good evidence to suggest that thepresence of the aorta is important in preventingossification; such evidence includes the fact thatthose with a right-hand side descending aortawill only have the typical changes associatedwith DISH on the left-hand side (Ciocci, 1987;Revn-Pedersen & Jurik, 1988; Carile et al., 1989).

During the 1970s, Resnick and his colleaguesfirst reported extra-spinal manifestations in pa-tients suffering from what had by then becomeknown as Forestier’s disease (Resnick et al., 1975;Resnick & Niwayama, 1976; Utsinger et al.,1976). Resnick found that extra-spinal liga-ments, especially those in the pelvis, were ossi-fied, and that entheses were ossified in somecases, producing prominent spurs and spiculesof bone. These are particularly noticeable at thesite of insertion of the Achilles tendon and theplantar fascia into the calcaneum, the insertionof the patellar tendon, and the triceps tendoninto the olecranon process (Figure 2). Ossifica-tion may take place also into blood clots follow-ing trauma (Figure 3).* Correspondence to: 31 Maidstone Road, London N11 2TR, UK.

Copyright © 2001 John Wiley & Sons, Ltd. Received 10 April 2000Revised 26 June 2000

Accepted 4 August 2000

J. Rogers and T. Waldron358

Figure 1. Thoracic spine showing typical flowing new boneformation on right-hand side. The disc spaces are preserved.

Figure 2. Extra-spinal new bone formation on patellae andcalcaneum in a case of DISH.

Association with other conditions

DISH has been found in association with manyother conditions, including ossification of theposterior longitudinal ligament (Resnick et al.,1978a), gout (Littlejohn & Hall, 1982),acromegaly (Littlejohn et al., 1986), Paget’s

Epidemiology

The prevalence of DISH shows considerablegeographical and racial variation, although allauthors agree that the condition is more com-mon in men than in women. They also agreethat it is unusual to find it in individuals underthe age of 40 years and that the prevalenceincreases markedly with increasing age(Julkunen et al., 1971, 1975; Utsinger, 1985).The crude prevalence rate in those over 40years of age is estimated to be 3.8% in malesand 2.6% in women (Mata et al., 1997). Theprevalence is greater in whites than in blacks,and seems to be relatively low in Asians andNative Americans, suggesting that genetic fac-tors may be involved in the aetiology of thecondition (Spagnola et al., 1978; Cassim et al.,1990; Weinfeld et al., 1997).

Figure 3. Three left ribs from a case of DISH showing ossifica-tion into a haemorrhage subsequent to fracture.

Copyright © 2001 John Wiley & Sons, Ltd. Int. J. Osteoarchaeol. 11: 357–365 (2001)

DISH and the Monastic Way of Life 359

disease (Morales et al., 1993; Marcelli et al.,1995) and multiple myeloma (Scutellari et al.,1995). Although there is no positive associationbetween DISH and rheumatoid arthritis (Mata etal., 1995), the presence of the former maymodify the radiological features of the latter(Resnick et al., 1978b). An association betweenthe presence of DISH and ankylosing spondyli-tis has been reported in a small number of cases(Troise Rioda & Ferraccioli, 1990; Maertens etal., 1992; Tischler & Yaron, 1992), but no morefrequently than would occur by chance(Moreno et al., 1996). Whether any of theseassociations are the result of a common causalmechanism is unclear; many of the associatedconditions are more common in the elderly andit is likely that most of the associations arecoincidental. The association with late onset(type II) diabetes, which has been causally re-lated to DISH, is discussed below.

DISH and osteoarthritis (OA)

OA is an extremely common condition and, likeDISH, its prevalence increases markedly withage. In the skeleton, OA and DISH are oftenfound together and although there is no sugges-tion that the two are linked aetiologically in anyway, the formation of new bone where OA andDISH co-exist is usually florid and the os-teoarthritic changes would certainly be consid-ered to be hypertrophic.

DISH and bone forming

In a proportion of the population, there seemsto be a tendency to form osteophytes andenthesophytes; we have previously referred tothis as ‘bone forming’ (Rogers & Waldron,1995). In bone forming individuals (bone form-ers), the formation of osteophytes and entheso-phytes is significantly correlated with age andsex (Rogers et al., 1985) and ossification ofextra-spinal ligaments is also more likely tooccur. There is clearly some overlap betweenbone forming and DISH; indeed, DISH may bethe extreme end of the bone forming diathesis.Bone forming may be an exaggerated responseto repeated minimal trauma, but it may also

result in exuberant new bone growth in condi-tions such as OA, similar to what occurs inDISH.

Symptomatology

The general consensus is that DISH, which hasbeen referred to as a ‘state’ rather than a ‘dis-ease’, has little clinical significance (Hutton,1989). Some patients may complain of periph-eral bone or joint pain (Utsinger et al., 1976),but the prevalence of back pain is no greater inthose with DISH than in those without thecondition (Schlapbach et al., 1989). However,patients with DISH complain more of backstiffness and they may have reduced movementof the neck and trunk (Mata et al., 1997).

Before writing off DISH as nothing morethan a minor inconvenience, however, it is im-portant to realize that it may cause serioussymptoms in some patients, usually as the resultof compression of the spinal cord or otherstructures. Thus, it may give rise to cervicalmyelopathy (Goto et al., 1995) or thoracic cordcompression as a result of spinal stenosis(Wilson & Jaspan, 1990), sometimes causingsudden paraplegia requiring urgent treatment bylaminectomy (Johnsson et al., 1983). DISH mayalso cause dysphagia (Eviatar & Harell, 1987)and laryngeal oedema with severe dyspnoeanecessitating emergency tracheotomy (Marks etal., 1998).

Aetiology

The aetiology of DISH is by no means certain,but one of the earliest suggestions was that itwas related to obesity (Julkunen et al., 1971) andlate onset (type II) diabetes. DISH was found tobe more common among elderly patients withdiabetes than in normal age-matched controls(Hajkova et al., 1965; Julkunen et al., 1966) and,conversely, diabetes was found in up to 40% ofpatients with DISH (Lesquene et al., 1970; Hen-rard & Benett, 1973); moreover, patients withDISH were found to have marked hyperinsuli-naemia following a glucose challenge (Littlejohn& Smythe, 1981). Later studies have, however,failed to confirm the relationship between



DISH and diabetes (Daragon et al., 1995; Vezy-roglou et al., 1996), but have noted a number ofother metabolic abnormalities, including alter-ations in lipid metabolism and hyperuricaemia(Vezyroglou et al., 1996) and elevated levels ofgrowth hormone (Altomonte et al., 1992; Denkoet al., 1994). The latter considered that theevidence suggests that DISH is a multisystemhormonal disorder, which seems to be the mostreasonable conclusion to date.

Other hypotheses have suggested that DISHmay be related to disorders of vitamin Ametabolism (Pennes et al., 1984; Abiteboul &Arlet, 1985) and to idiopathic hypoparathy-roidism (Lambert & Becker, 1989), or that it isthe result of a vascular disorder (el Miedany etal., 2000) or repeated microtrauma (Pappone etal., 1996).

DISH in palaeopathology

Morphologically, radiologically and epidemio-logically, DISH is similar in both archaeologicaland modern skeletons and ought to presentlittle difficulty in diagnosis to the experiencedbone specialist. The disease has a very ancientlineage, having been described in a skeleton(Shanidar 1) from the middle Palaeolithic(Crubezy & Trinkhaus, 1992). Cases have alsobeen found from the Edo period in Japan(Suzuki et al., 1993), from the Sudan (Arriaza etal., 1993), north Chile (Arriaza, 1993), andthroughout Europe (Rogers et al., 1985; Krameret al., 1990).

In 1985, one of us (TW) suggested, on thebasis of finding an apparently elevated preva-lence of DISH in burials of a group of supposedmonks at Merton Priory, that this might repre-sent a ‘new’ occupational disease (Waldron,1985). The paper appeared in the Christmasissue of the British Medical Journal, which is some-what more light hearted than the issues that

appear during the rest of the year. However, itnevertheless started an investigation which wehave been following up ever since, and we arenow able to present some support for the origi-nal hypothesis that DISH is related to a monas-tic or a high status way of life.

DISH and the monastic life

Since the original observations at Merton Pri-ory, we have been able to examine skeletonsfrom other sites and there are also confirmatoryreports in the literature. Two sites are of partic-ular importance in this regard, namely WellsCathedral and the Royal Mint in London.

Wells CathedralThis site was excavated between 1978 and 1982,and 337 skeletons were recovered in total. Alarge area of the cemetery was given over to theburials of the general population, but skeletonswere also recovered from the 13th century ladychapel and the 16th century Stillington’s chapel;in both cases, the burials in the chapels werethose of priests or lay benefactors. Of the totalnumber, 287 skeletons, 205 of which wereadult, were sufficiently well preserved for exam-ination. The skeletons were examined by JR andthe diagnosis of DISH was made based on thecriteria described elsewhere (Rogers & Waldron,1995). Ninety-three males were definitelypresent in the main cemetery, 15 in the ladychapel and 13 in Stillington’s chapel. The preva-lence of DISH is shown in Table 1; the rate isconsiderably higher in both the lady chapel andStillington’s chapel than in the lay cemetery,and although the difference is not statisticallysignificant (p=0.12) it is, nevertheless, highlysuggestive.

During the time of the excavations at WellsCathedral, the tombs of some the bishops weremoved and the skeletons examined. Among the

Table 1. Prevalence of DISH at Wells Cathedral

Number of males Prevalence (%)Number with DISHSite

693 6.5Lay cemetery15Lady chapel 13.32

23.113 3Stillington’s chapel



skeletons was that of Giso, the last Anglo-Saxonbishop of Wells, and he was found to have all ofthe classic manifestations of DISH (Rogers, un-published observations).

The Royal Mint siteThis site, situated north-east of the Tower ofLondon, was originally a Black Death plague piton which the Abbey of St Mary Graces—thelast Cistercian foundation in England—was es-tablished in 1350. The church and chapels ofthe Abbey contained burials of monks and im-portant lay people but, in addition, there was alarge graveyard overlying the Black Deathcemetery which served the general population.The site was first excavated in 1972, then in1983–1984 and, finally, between 1986 and1988. The church and chapels contained 133burials and the lay cemetery contained 301.These skeletons were all examined by TW, andDISH among the males was diagnosed using thesame criteria as for Wells Cathedral cases. Theresults are shown in Table 2, where it may beseen that there were no cases at all in the laycemetery burials but six cases among the maleburials from the church and chapels. This differ-ence is highly significant (p=0.0006).

Combining data from both sitesIf the data from Wells Cathedral and the RoyalMint sites are combined and reanalysed, thedifference in the prevalence of DISH in burialsfrom churches and chapels and in those fromthe lay cemeteries is found to be highly signifi-cant (p=0.001), suggesting that it is highlyunlikely to have arisen by chance.

Evidence from other sitesEvidence to support the relationship betweenDISH and monastic or high status burials is alsoavailable from other sites, both in the UK andelsewhere. Mays (1991) examined burials fromthe site of Blackfriars Priory in Ipswich and

noted that 21 showed bony changes which wereprobably associated with DISH, although onlyten met the previously published criteria(Rogers & Waldron, 1995). The crude preva-lence rate of those aged 40 years or more and inwhom at least three vertebrae were available forstudy was 13.4% (Mays, 1991). It is interestingthat no cases of DISH were found among 51adult skeletons from a 10th–11th century laycemetery on the same site, reflecting the situa-tion at the Royal Mint site.

Evidence for the association is even morestriking at the Basilica of Saint Servaas inMaastricht, where all 27 Canons examined byJanssen & Maat (1999) were found to haveDISH. From the Franciscan friary at Dordrecht,Maat et al. (1998) found a crude prevalence rateof DISH of 19% among burials dating between1275 and 1572, which they interpreted as show-ing that the population buried there enjoyed ahigh status. A late Carolingian skeleton found ina stone coffin, and therefore considered to be ofhigh status, was reported to have DISH byBruintjes (1987), who stated that this was fur-ther confirmation of the association betweenDISH and social status.

What explains the relationship between themonastic life and DISH?

The reason why following the monastic way oflife should lead to DISH is unclear, but thereare some pointers. It is very unlikely that thosewho were predisposed to develop DISH se-lected themselves to become monks; thus, theexplanation must lie in the day-to-day activitieswithin the monastery, and the one which sug-gests itself most strongly relates to the monks’diet.

When first established, monastic orders livedunder an austere regime, taking one meal aday in winter and two from Easter to mid-September. There was a general prohibition

Table 2. Prevalence of DISH at the old Royal Mint site

Site Number of males Prevalence (%)Number with DISH

Lay cemetery 09911.56Church and chapels 52



against eating meat, but in time the monksdeveloped considerable skill in avoiding thesedietary regulations. In one 13th centurymonastery in France, for example, the monkswere only permitted to eat game that had beenhunted. To overcome this prohibition, theysmuggled dogs into the monastery and per-suaded them to chase pigs raised on the farmaround the cloisters, thereby instantly trans-forming meat into game. Sick monks were al-lowed to eat meat and so the monks entered theinfirmary in rotation in order to supplementtheir diet (Henisch, 1977). One author hascommented that, ‘Gluttony was the darling viceof the monasteries’ (Bishop, 1983). Studies ofthe rolls from Westminster Abbey by Harvey(1993) have shown that on an average dayoutside Advent and Lent, the monks had a dailyallowance of 6207 calories; during Advent, theallowance was 5291 calories and during Lent itwas 4870 calories. Of course, the monks did notconsume their entire allowance, some having tobe left for the poor at the gate, for example;however, even assuming that they consumedonly 60% of their allowance, on an average dayoutside Advent and Lent, they would still be leftwith 3723 calories. Chaucer’s monk—that fatand personable priest—liked a ‘fat swan best,and roasted whole’, and the friar among theparty on the road to Canterbury was no strangerto the dining table. His semicope sat upon hisshoulders ‘and the swelling fold about him, likea bell about its mould.’ The master friar in PiersPloughman ate no solid meat but ‘costlier foods,special purees and ragouts.’ He ‘gobbled upcountless different dishes—minced meat andpuddings, tripes and galantines and eggs fried inbutter.’ The variety of the monastic diet wasimpressive; fish was always abundant, as werequantities of game—capons and chicken, ducks,geese, egret and herons, pheasants, partridgeand pigeons, quail, teal and swan are all men-tioned in the account books of the 14th centuryabbot of Westminster. In 1372, this same abbotgave a dinner at which beef, mutton, four smallpigs, five ducks, one swan, six geese, six capon,nine fowl, two woodcock, and a milk creamcheese were served, all washed down with aplentiful supply of wine or ale (Gasquet, 1922).The amount of food offered to the monks at

Canterbury offended one visiting scholar: noless than 16 dishes, all served with stimulatingsauces and accompanied by beer, ale, claret,new wine, mead and mulberry wine (Bishop,1983). The kitchen refuse from St Alban’sAbbey has revealed the presence of many kindsof fish, hare and rabbit, game birds, roe and reddeer, suckling pigs and young lambs; the monkswere not to be faced with mutton or old cows,which appeared to be the main sources ofprotein for those living outside the abbey walls(D. Serjeantson, pers. comm.).

The evidence seems overwhelming, therefore,that obesity and type II diabetes were likely tobe hazards for those living within the monasterywalls, and it seems probable that this wouldpredispose them to developing DISH. Althoughthe monks would have eaten a good deal of oilyfish and offal, both rich in vitamin A, it doesnot seem likely that this would have been a riskfactor; Harvey (1993) estimated that, at least atWestminster, the average daily intake of vitaminA would have been slightly less than dietaryreference value (611 compared with 700 �g).

Conclusions

The evidence linking the monastic way of lifewith an increased prevalence of DISH seems tous to be compelling, but some caveats must beentered at this point. There is always a ten-dency to interpret observations in line withexpectation and authors may be inclined toover-diagnose DISH in burials from monasticsites, which will, of course, reinforce the rela-tionship. In order to study the prevalence ofDISH in skeletal populations and make validinter-study comparisons, it is important thatcriteria for the diagnosis should be agreed andused by different observers. Noting thatchanges seen in a skeleton are ‘probably’ DISH(Mays, 1991) is not helpful—either they are orthey are not. In other words, either the changesmeet the criteria or they do not. We suggestthat the major criteria for diagnosing DISHshould be as follows:

(i) hyperostosis of the spine, affecting at leastthree vertebrae, with or without ankylosis;



(ii) changes confined to the right-hand side ofthe thoracic vertebrae (except in the rareinstance of situs inversus, when thechanges will be confined to the left-handside); and

(iii) evidence of extra-spinal calcification or os-sification in extra-spinal ligaments and/orentheses.

All three criteria should be met before a diagno-sis of DISH is made. Minor criteria, such aspreservation of the inter-vertebral disc spacesand lack of involvement of the facet joints (inthe absence of other disease), should not beused for diagnostic purposes, but may beconfirmatory.

The use of rigid criteria will almost certainlylead to an under-estimation of the true preva-lence of DISH, but this will not affect thevalidity of between-study comparisons as longas the same diagnostic criteria are used in each.

Finally, we should not fall into the logicaltrap of assuming that because DISH may berelated to the monastic way of life or to a highstatus, the converse is necessarily true. FindingDISH in a skeleton cannot be taken as anindication that the individual was either a monkor of high status.

References

Abiteboul M, Arlet J. 1985. Retinol-related hyperos-tosis. American Journal of Roentgenology 144: 435–436.

Altomonte L, Zoli A, Mirone L, Marchese G, ScolieriP, Barini A, Magaro M. 1992. Growth hormonesecretion in diffuse idiopathic skeletal hyperosto-sis. Annali Italiani di Medicina Interna 7: 30–33.

Arriaza BT. 1993. Seronegative spondylarthropathiesand diffuse idiopathic skeletal hyperostosis in an-cient northern Chile. American Journal of PhysicalAnthropology 91: 263–278.

Arriaza BT, Merbs CF, Rothschild BM. 1993. Diffuseidiopathic skeletal hyperostosis in Meroitic ubiansfrom Semma South, Sudan. American Journal ofPhysical Anthropology 92: 243–248.

Bishop M. 1983. The Pelican Book of the Middle Ages.Penguin: Harmondsworth.

Bruintjes TJD. 1987. Diffuse idiopathic skeletal hy-perostosis (DISH). A 10th century AD case fromthe St Servaas church at Maastricht. Bone 1: 23–28.

Carile L, Verdone F, Aiello A, Buongusto G. 1989.Diffuse idiopathic skeletal hyperostosis and situsviscerum inversus. Journal of Rheumatology 16:1120–1122.

Cassim B, Mody GM, Rubin RL. 1990. The preva-lence of diffuse idiopathic skeletal hyperostosis inAfrican blacks. British Journal of Rheumatology 29:131–132.

Ciocci A. 1987. Diffuse idiopathic skeletal hyperos-tosis (DISH) and situs viscerum inversus. Report ofa single case. Clinical and Experimental Rheumatology5: 159–160.

Crubezy E, Trinkhaus E. 1992. Shanidar 1: a case ofhyperostotic disease (DISH) in the middle pale-olithic. American Journal of Physical Anthropology 89:411–420.

Daragon A, Mejjad O, Czernichow P, Louvel JP,Vittecoq O, Durr A, Le Loet X. 1995. Vertebralhyperostosis and diabetes mellitus: a case-controlstudy. Annals of the Rheumatic Diseases 54: 375–378.

Denko CW, Boja B, Moskowitz RW. 1994. Growthpromoting peptides in osteoarthritis and diffuseidiopathic skeletal hyperostosis—insulin, insulin-like growth factor-1, growth hormone. Journal ofRheumatology 21: 1725–1730.

el Miedany YM, Wassif G, el Baddini M. 2000.Diffuse idiopathic skeletal hyperostosis (DISH): isit of vascular aetiology? Clinical and ExperimentalRheumatology 18: 193–200.

Eviatar E, Harell M. 1987. Diffuse idiopathic skeletalhyperostosis with dysphagia (a review). Journal ofLaryngology and Otology 101: 627–632.

Forestier J, Rotes-Querol J. 1950. Senile ankylosinghyperostosis of the spine. Annals of the RheumaticDiseases 9: 321–330.

Forestier J, Lagier R. 1971. Ankylosing hyperostosisof the spine. Clinical Orthopaedics and Related Research74: 65–83.

Gasquet F. 1922. Monastic Life in the Middle Ages. G.Bell: London.

Goto S, Tanno T, Moriya H. 1995. Cervical myelo-pathy caused by pseudarthrosis between the atlasand axis associated with diffuse idiopathic skeletalhyperostosis. Spine 20: 2572–2575.

Hajkova Z, Streda A, Skrha F. 1965. Hyperostoticspondylosis and diabetes mellitus. Annals of theRheumatic Diseases 24: 536–543.

Harvey B. 1993. Living and Dying in England 1100–1540. The Monastic Experience. Clarendon Press:Oxford.

Henisch BA. 1977. Fast and Feast. Food in MedievalSociety. University of Pennsylvania Press: London.

Henrard JC, Benett PH. 1973. Etude epidemi-ologique de I’hyperostose vertebrale. Enquete dans



une population adulte d’Indiens d’Amerique. RevRhum Mal Osteoartic 40: 581–591.

Hutton C. 1989. DISH. . . a state not a disease?British Journal of Rheumatology 28: 277–278.

Janssen HAM, Maat GJR. 1999. Canons buried in the‘Stiftskapel’ of the Saint Servaas Basilica at Maastricht AD

1070–1521. A palaeopathological study, Barge’s Anthro-pologica No 5. Barge’s Anthropologia: Leiden.

Johnsson KE, Petersson H, Wollheim FA, SavelandH. 1983. Diffuse idiopathic skeletal hyperostosis(DISH) causing spinal stenosis and sudden para-plegia. Journal of Rheumatology 10: 784–789.

Julkunen H, Karava R, Viljanen V. 1966. Hyperosto-sis of the spine in diabetes mellitus andacromegaly. Diabetologia 28: 123–126.

Julkunen H, Heinonen OP, Pyorala K. 1971. Hyper-ostosis of the spine in an adult population. Annalsof the Rheumatic Diseases 30: 605–612.

Julkunen H, Heinonen OP, Knekt P, Maatela J.1975. The epidemiology of hyperostosis of thespine together with its symptoms and related mor-tality in a general population. Scandinavian Journalof Rheumatology 4: 23–27.

Kramer Ch, Lagier R, Baud CA. 1990. Thoracicspinal hyperostosis in an early mediaeval skeleton.Scandinavian Journal of Rheumatology 19: 163–166.

Lambert RG, Becker EJ. 1989. Diffuse skeletal hyper-ostosis in idiopathic hypoparathyroidism. ClinicalRadiology 40: 212–215.

Lesquene M, Cassan P, Nallet J, Ryckewaert A, deSeze S. 1970. Hyperostose vertebral et diabetesucre. Revue du Rheumatologie et des Maladies Osteoartic-ulaires 37: 281–286.

Littlejohn GO, Hall S. 1982. Diffuse idiopathicskeletal hyperostosis and new bone formation ingouty subjects. A radiologic study. RheumatologyInternational 2: 83–86.

Littlejohn GO, Smythe HA. 1981. Marked hyperin-sulinemia after glucose challenge in patients withdiffuse idiopathic skeletal hyperostosis. Journal ofRheumatology 8: 965–968.

Littlejohn GO, Hall S, Brand CA, Davidson A. 1986.New bone formation in acromegaly: pathogeneticimplications for diffuse idiopathic skeletal hyper-ostosis. Clinical and Experimental Rheumatology 4: 99–104.

Maat GJR, Mastwijk RW, Sarfatij H. 1998. Een fysischanthropologisch onderzoek van begravenen bij het Minder-broedersklooster te Dordricht, circa 1275–1572 AD.ROB: Amersfoort.

Maertens M, Mielants H, Verstraete K, Veys EM.1992. Simultaneous occurrence of diffuse idio-pathic skeletal hyperostosis and ankylosingspondylitis in the same patient. Journal of Rheuma-tology 19: 1978–1983.

Marcelli C, Yates AJ, Barjon MA, Pansard E, Angel-loz-Pessey L, Simon L. 1995. Pagetic vertebralankylosis and diffuse idiopathic skeletal hyperosto-sis. Spine 15: 454–459.

Marks B, Schober E, Swoboda H. 1998. Diffuseidiopathic skeletal hyperostosis causing obstruct-ing laryngeal edema. European Archives of Otorhinolar-yngology 255: 256–258.

Mata S, Wolfe F, Joseph L, Esdaile JM. 1995. Ab-sence of an association of rheumatoid arthritis anddiffuse idiopathic skeletal hyperostosis: a case-control study. Journal of Rheumatology 22: 2062–2064.

Mata S, Fortin PR, Fitzcharles MA, Starr MR, JosephL, Watts CS, Gore B, Rosenberg E, Chem RK,Esdaile JM. 1997. A controlled study of diffuseidiopathic skeletal hyperostosis. Clinical featuresand functional status. Medicine (Baltimore) 76: 104–117.

Mays S. 1991. The Medieval Burials from the BlackfriarsFriary, School Street, Ipswich, Suffolk. Ancient MonumentsLaboratory Report 16/91. English Heritage: London.

Morales AA, Valdazo P, Corres J, Talbot JR, Perez F,Baylink DJ. 1993. Coexistence of Paget’s bonedisease and diffuse idiopathic skeletal hyperostosisin males. Clinical and Experimental Rheumatology 11:361–365.

Moreno AC, Gonzalez ML, Duffin M, Lopez-LongoFJ, Carreno L, Forrester DM. 1996. Simultaneousoccurrence of diffuse idiopathic skeletal hyperos-tosis and ankylosing spondylitis. Revue RhumatologieEnglish Edition 63: 292–295.

Pappone N, Di Girolamo C, Del Puente A, Scarpa R,Oriente P. 1996. Diffuse idiopathic skeletal hyper-ostosis (DISH): a retrospective analysis. ClinicalRheumatology 15: 121–124.

Pennes DR, Ellis CN, Madison KD, Voorhees JJ,Martel W. 1984. Early skeletal hyperostosis sec-ondary to 13-cis-retinoic acid. American Journal ofEarly Roentgenology 141: 979–983.

Resnick D, Niwayama G. 1976. Radiographic andpathologic features of spinal involvement in dif-fuse idiopathic skeletal hyperostosis (DISH). Diag-nostic Radiology 119: 559–568.

Resnick R, Shaul SR, Robins JM. 1975. Diffuse idio-pathic skeletal hyperostosis (DISH): Forestier’sdisease with extraspinal manifestations. DiagnosticRadiology 115: 513–524.

Resnick D, Curd J, Shapiro RF, Wiesner KB. 1978a.Radiographic abnormalities of rheumatoid arthritisin patients with diffuse idiopathic skeletal hyper-ostosis. Arthritis and Rheumatism 21: 1–5.

Resnick D, Guerra J, Robinson CA, Vint VC. 1978b.Association of diffuse idiopathic hyperostosis(DISH) and calcification and ossification of the



posterior longitudinal ligament. American Journal ofRoentgenology 131: 1049–1053.

Revn-Pedersen P, Jurik AG. 1988. Diffuse idiopathicskeletal hyperostosis in a patient with right-sidedaorta. Rontgenblatter 41: 495–496.

Rogers J, Waldron T. 1995. A Field Guide to JointDiseases in Archaeology. John Wiley and Sons:Chichester.

Rogers J, Watt I, Dieppe P. 1985. Palaeopathologyof spinal osteophytosis, vertebral ankylosis, anky-losing spondylitis, and vertebral hyperostosis. An-nals of the Rheumatic Diseases 44: 113–120.

Schlapbach P, Beyeler C, Gerber NJ, van der LinderS, Burgi U, Fuchs WA, Ehrengruber H. 1989.Diffuse idiopathic skeletal hyperostosis (DISH) ofthe spine: a cause of back pain? A controlledstudy. British Journal of Rheumatology 28: 299–303.

Scutellari PN, Orzincola C, Castaldi G. 1995. Asso-ciation between diffuse idiopathic skeletal hyper-ostosis and multiple myeloma. Skeletal Radiology 24:489–492.

Spagnola AM, Bennett PH, Teraski PI. 1978. Verte-bral ankylosing hyperostosis (Forestier’s disease)and HLA antigens in Pima Indians. Arthritis andRheumatism 21: 467–472.

Suzuki T, Fujita H, Narasaki S, Kondon O, AdachiK. 1993. A study of skeletal remains with diffuseidiopathic skeletal hyperostosis (DISH) from theEdo period, Japan. Anthropological Science 101: 273–290.

Tischler M, Yaron M. 1992. Two cases of diffuseidiopathic skeletal hyperostosis and ankylosingspondylitis. British Journal of Rheumatology 31: 569–571.

Troise Rioda W, Ferraccioli GF. 1990. DISH andankylosing spondylitis. Case report and review ofthe literature. Clinical and Experimental Rheumatology8: 591–593.

Utsinger P. 1985. Diffuse idiopathic skeletal hyper-ostosis. Clinics in the Rheumatic Diseases 11: 325–351.

Utsinger P, Resnick D, Shapiro R. 1976. Diffuseskeletal abnormalities in Forestier disease. Archivesof Internal Medicine 136: 763–768.

Vezyroglou G, Mitropoulos A, Kyriazis N, Anto-niadis C. 1996. A metabolic syndrome in diffuseidiopathic skeletal hyperostosis: a controlledstudy. Journal of Rheumatology 23: 672–676.

Waldron T. 1985. DISH at Merton Priory: evidencefor a ‘new’ occupational disease? British MedicalJournal 291: 1762–1763.

Weinfeld RM, Olson PN, Maki DD, Griffiths HJ.1997. The prevalence of diffuse idiopathic skeletalhyperostosis (DISH) in two large American Mid-west metropolitan hospital populations. Skeletal Ra-diology 26: 222–225.

Wilson FM, Jaspan T. 1990. Thoracic spinal cordcompression caused by diffuse idiopathic skeletalhyperostosis (DISH). Clinical Radiology 42: 133–135.


dish and the monastic way of life

Documents