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International Journal of Osteoarchaeology, 2025; 0:e3388
https://doi.org/10.1002/oa.3388
International Journal of Osteoarchaeology
RESEARCH ARTICLE
Legg- Calvé- Perthes Disease: Past and Present
RyanFrederick | PaolaPonce
Department of Archaeolog y, PalaeoHub, University of York, Wentworth Way, Heslington York, UK
Correspondence: Ryan Frederick (ryanfrederick2009@hotmail.com)
Received: 19 August 202 4 | Revised: 7 January 2025 | Accepted: 10 January 2025
Funding: This work was supported by BABAO Commercial Grant.
Keywords: femoral head necrosis| LCPD| Legg–Calvé–Perthes disease| osteochondrosis
ABSTRACT
Legg–Calvé–Perthes disease (LCPD) is a rare idiopathic condition that primarily affects the femoral head. It is characterized by
a sudden necrosis, which leads to permanent and irreversible changes of its normal anatomy. Likely due to its rarity and com-
plex etiology, there is a lacuna of its study in archaeological literature. This paper attempts to address this issue by aiming to (1)
gather all known examples of LCPD in the archaeological record worldwide; (2) based on etiological speculation, analyze how
individuals may have developed LCPD in the past; (3) assess how LCPD may have affected these individuals; and (4) how they
may have managed the effects. In this study, a wide range of resources pertaining to archaeology, osteology, paleopathology,
and clinical studies were consulted. The information was extracted from a number of available case studies and osteological site
reports despite data- access difficulties. In the archaeological record, there are 73 reported cases of LCPD affecting individuals,
spanning from the Neolithic to the Postmedieval period, across the globe, with its highest peak in the Late Medieval period.
Modern clinical literature has provided an empirical platform to investigate what may have caused LCPD in the past, though
etiological conjecture continues to prevent any certainty in these extrapolations. The resulting prevalence of the cases of LCPD
are also skewed by issues concerning skeletal preservation and inaccessible data, ultimately affecting its representation and the
evaluation of the disease's laterality and sex preponderance. Nonetheless, physical debilitation caused by LCPD would have varia-
bly inhibited the individuals' mobility, causing pain, compromised quality of life, decline in mental state, and an inability to fully
engage in ambulator y activities. However, coexisting osteological markers suggest methods of managing the disease's symptoms,
such as resorting to an antalgic gait and/or using upper limb apparatus (crutch).
1 | Introduction
This study aims to explore the global distribution of Legg–
Calvé–Perthes disease (LCPD) in the past and assess its poten-
tial etiological factors through the application of modern clinical
interpretations. Furthermore, by analyzing the skeletal changes
of LCPD we may also evaluate how the condition affected indi-
viduals and how they may have attempted to manage its physical
detriments. By drawing upon a large variety of diverse sites from
different periods, a timeline of the disease's known occurrences
was constructed, noting period, location, and historical context.
Consulting modern clinical literature likewise permitted the
creation of a diagram that summarizes the current understand-
ing of its possible pathogenesis.
LCPD is an extensively ill- understood idiopathic orthopedic
affliction of the hip joint that has eluded the field of clinical
pathology since it was first analyzed in the early 20th century
by the respective physicians, Arthur Legg, Jacques Calvé, and
Georg Perthes (Kuo, Wu, Smith, Shih, and Altiok2011). It af-
fects children 14 years of age and under with the highest inci-
dences occurring in those between 5 and 7 years old (Barker and
Hall 1986; Pillai, Atiya, and Costigan2005; Perry etal.2012a).
The condition is generally considered to be a rare disease (Fuchs
© 2025 Joh n Wiley & Sons Ltd.
2 of 17 International Journal of Osteoarchaeology, 2025
etal.2021), with varying annual incidence rates globally, rang-
ing from 1:250,000 in Hong Kong, 1:18,000 in the UK, and
1:3500 on the Faroe Islands (Orphanet: Legg- Calvé- Perthes dis-
ease, Date of access: 9th October 2024). It has been postulated
that this variance in frequency is ancestrally and/or geographi-
cally dependent (Perry2013). However, even on a regional scale
this can vary even more considerably. For instance, with regards
to LCPD in the UK, Wessex, in the south of England, had an an-
nual incidence rate of 5.5:100,000, while Merseyside (Liverpool)
in the north had 11.1:100,000 (Perry2013).
General consensus posits that LCPD represents the obstruction
of the main arterial blood supply to the femoral head initiated by
a form of trauma, leading to bone cell death in the femoral head
(Lauritzen 1975; Inoue etal. 1976; Jensen and Lauritzen1976;
Douglas and Rang 1981; Herring 2011; Berthaume etal.2016;
Pinheiro etal.2018).
Causative links between various agents and the prevalence rate
of LCPD have been explored among global populations. Such
agents include skeletal immaturity and resulting biomechan-
ics (Berthaume et al.2016; Pinheiro et al. 2018), genetic pre-
dispositions: ancestry, endocrinopathies and collagenopathies
(Catterall, Roberts, and Wynne- Davies1971; Rayner, Schwalbe,
and Hall 1986; Ortner 2003; Crofton et al. 2005; Miyamoto
etal.2007; Su etal.2008; Su etal.2010; Perry etal. 2012a; Li
etal.2014; Lindblad etal.2024), socioeconomic effects (Barker,
Dixon, and Taylor1978; Joseph etal.1988; Hall and Barker1989;
Kealey et al. 2000; Pillai, Atiya, and Costigan 2005; Perry
etal.2012b), and pollution exposure to tobacco smoke (García
Mata etal.2000; Gordon etal.2004; Bahmanyar etal.2008) and
to wood smoke (Daniel etal.2012).
The resulting femoral head's necrosis proceeds to under-
mine the bone's microstructures and then deteriorates further
through resorption during the repair process, inducing biome-
chanical weakness and increasing susceptibility to subchondral
fracturing (Herrerín and Garralda2012), which subjects the hip
joint to subluxation, altering directional stressors. In the next
stage, the femoral head will flatten to a variable degree, typi-
cally into a mushroom- like shape, and the acetabulum will at-
tempt to remodel to cater for this change. This morphological
alteration affects the level of femoro- acetabular congruency, and
subsequently, the individual's capacity for mobility. Areas of the
proximal femur af fected include the femoral head, femoral neck,
and greater trochanter. Detriments to the changes in these areas
are dependent on variations of weight- bearing and locomotory
activity. Physiological limitations of the disease report an af-
fected gait and range of motion at differing rates, involving ab-
duction, adduction, f lexion, and rotational movement. The level
of recovery from LCPD is generally defined by how it affects the
individual's quality of life, which is determined by the severity of
morphological changes within the affected areas and the result-
ing congruency of the femoro- acetabular joint (Catterall1971).
With regards to age and sex, LCPD is a pediatric condition ex-
clusively diagnosed in infants and juveniles up to the age of
14, most commonly between ages of four and eight, and av-
eraging at 6 years (Aufderheide and Rodríguez- Martín 1998;
Van Campenhout, Moens, and Fabry 2007; Murray, Holmes,
and Misra 2008). The age of the individual at the beginning
of the disease's onset and its duration is fundamental in in-
fluencing LCPD's various signs, symptoms, and prognoses
(Weinstein2000). The older the individual during the onset of
LCPD yielded the worst outcomes due to the eventual inability
of the femoral head and acetabulum to remodel due to bone mat-
uration, preventing proper rectification of the altered morphol-
ogy (Stulberg, Cooperman, and Wallensten 1981). In contrast,
sex does not appear to hold considerable influence over the se-
verity of the disease but is rather distinct for its male preponder-
ance, averaging 5:1 relative to females (Grauer2019).
Unilateral involvement is the most common presentation of
LCPD cases (c. 80%–90%) while bilateral instances are compar-
atively low (c. 10%–35%) in prevalence, and those with bilateral
LCPD are also predominantly male, though the condition does
not behave differently from unilateral cases regarding progno-
sis (Catterall 1971; Ortner 2003). Furthermore, in these bilat-
eral cases, the onset of LCPD does not occur simultaneously
but rather successfully within an interval range between 2 and
4 years, developing femoral heads that can equally be of the
same group classification or be different entirely, resulting in
prognoses that differ accordingly (Catterall 1971; Aufderheide
and Rodríguez- Martín1998).
1.1 | Paleopathological Diagnosis
In contrast to modern clinicians who have the living individual,
musculature, and radiographs to examine, paleopathologists are
left only with skeletal remains to identify the presence of LCPD.
In addition, differential diagnoses pose a risk due to LCPD's
pathological ambiguity with other diseases, namely, slipped
capital femoral epiphysis (SCFE), developmental dysplasia of
the hip (DDH), and aseptic necrosis, which develop in childhood
and persist throughout adulthood (Aufderheide and Rodríguez-
Martín 1998; Ortner2003; Waldron2009). Other diseases with
the same risk extend to Gaucher's disease, Meyer dysplasia,
multiple epiphyseal dysplasia (MED), spondyloepiphyseal dys-
plasia (SED), coxarthrosis (secondary osteoarthritis), hyperthy-
roidism, and infantile coxa vara (Meyer 1964; Khermosh and
Wientroub 1991; Amirfeyz, Clark, and Gargan 2005; Smrčka
etal.2009; Anthony etal.2015). Despite these difficulties, there
are certa in osteological markers paleopathologists us e to identify
LCPD (Ortner and Putschar1985; Smrčka etal.2009). Arguably,
its most fundamental trait is the deformity of the femoral head
and its recognizable flattening into a mushroom- type shape,
which is caused by compressional fracturing and paucity of
endochondral growth occurring during the onset (Aufderheide
and Rodríguez- Martín 1998; Ortner 2003; Grauer 2019; see
Figures1, 2, 3, and 4). The volume of the femoral head could also
be considered as a marker if it exceeds the space of the acetabular
socket (acetabular coverage) either through coxa magna or con-
siderable flattening (Aufderheide and Rodríguez- Martín 1998;
Waldr on 2009). Circumferential wideness and/or shortness of
the femoral neck are equally key, ref lecting both subchondral
fracturing and loss of endochondral growth for varying lengths
of time (Grauer2019).
However, the physical changes are not limited to just the proxi-
mal femur. A secondary effect of the flattening and widening of
3 of 17
the femoral head is the followi ng deformation of the acetabulum,
which is characterized by the flattening, shallowing, and elon-
gation of the acetabular fossa and lunate surface. These changes
are the result of the bone attempting to remodel to the now de-
formed femoral head (Aufderheide and Rodríguez- Martín1998;
see Figure 2). Changes made to the proximal femur without
noticeable differences to its corresponding acetabulum are in-
dicative of a late onset due to bone maturation preventing the
acetabulum from remodeling.
Secondary signs of LCPD include early onset osteoarthritis
(Wa ldr on 2009) and atrophy and/or increased density (robust-
ness) of the lower limbs. Coxarthrosis is detectable through sev-
eral osteological sig ns including osteophytic lipping surroundi ng
the margins of the femoral epiphysis or within the acetabulum,
epiphyseal eburnation, subchondral pitting, and joint contour
changes. All are consequences of abnormal/repetitive locomo-
tion and the weight- bearing detriments of LCPD (Ortner2003).
Atrophy, or tissue wasting, can also be detected by a visibly re-
duced circumference in the metaphysis and/or diaphysis of the
femur. This is likely due to limb disuse. Robusticity, because of
ill- dependency on the afflicted lower limb, can sometimes be
seen in the contralateral leg elements (femur, tibia, and fibula);
an increase of bone mass has generally been associated with
enduring constant heavy weight or loads, building strength in
a particular area to manage a resulting increase in stress and
strain (Yang et al.2019). The effects of both primary and sec-
ondary signs of LCPD, that paleopathologists are confronted
with, are examined in the archaeological cases of this study. The
methods used to evaluate all available cases of LCPD published
and unpublished literature are explained below.
2 | Materials and Methods
The materials used to carry out this study included all available
published and unpublished case studies and osteological/site re-
ports that found ex amples of LCPD. Books a nd monographs were
also consulted in addition to the raw site data from the Museum
of London Collections (Centre for Human Bioarchaeology).
2.1 | Search Strategy
This search took place until October 2024; any cases recorded
after were not included in this study. Cases of LCPD reported
have most commonly been described as possible occurrences in
site reports due to the ambiguities of the disease's characteristics
and bone preservation. Research platforms (PubMed, Google
Scholar, JSTOR, Science Direct, and Wiley Online Library) were
used to collate all the available paleopathological literature on
LCPD. Sources were searched using keywords such as “circu-
latory diseases,” “coxa plana,” “femoral head necrosis,” “Legg-
Calvé- Perthes' disease,” “osteochondrosis of the hip,” “Perthes
palaeopathology,” “Perthes' disease in archaeology,” “Perthes'
classifications,” and the acronym “LCPD”.
2.2 | Methods to Standardize the Collected Data
For the sake of brevity, all archaeological cases were placed
within standardizations of chronological dating familiar to the
British Isles, i.e., Neolithic (4000 –2600 BC); Bronze Age (2600–
800 BC); Iron Age (800 BC–100 AD); Roman (43–410 AD); Early
Medieval (410–1050 AD); Late Medieval (1050–1550 AD); and
Postmedieval (1550–1900 AD).
In terms of acute symptoms, LCPD is a pediatric condition and
therefore presents with specific diagnostic characteristics that
are only attainable during childhood. The individuals examined
in this study were predominantly adults, and so mostly exhib-
ited the condition in its healed stage. Evaluating the age demo-
graphics of those with LCPD was thereby deemed inappropriate
for this study and was omitted.
FIGUR E | Anterior v iew of left and r ight proximal femur (RLP05,
Context 40207, Museum of London). The right femoral head retains its
spherical shape while the left has flattened into a characteristic mush-
room shape resulting from LCPD. [Colour figure can be viewed at wi-
leyonlinelibrar y.com]
FIGUR E | Posterior view of left and right acetabula (RLP 05,
Context 40207, Museum of London). The left acetabulum is shallower
and wider than its right counterpart with additional osteophytic lipping
(coxarthrosis). [Colour figure can be viewed at wileyonlinelibrary.com]
4 of 17 International Journal of Osteoarchaeology, 2025
Socioeconomic status of individuals was predominantly inferred
by the sources in which they came, where available, which looked
at factors both bioarchaeological (Berger et al. 2017; García-
Moreno, López- Costas, and Dorado Fernández 2022) and an-
thropological (i.e., funerary practices; Booth etal.2010; Connell
etal.2012; Jones2012; Cooper, Heinzle, and Reitmaier2019), or
a mixture of the two (Fuchs etal.2021). Status was standardized
as follows: low, middle, high, and unknown status.
3 | Results
Archaeological cases of LCPD were found in 22 countries world-
wide. The total number of cases reported in the paleopatholog-
ical literature was 73 individuals out of 6999 analyzed, giving a
crude prevalence rate of 1.0% (see Table1). Studies and reports
examined varied in their depth of the description of the disease,
and this was reflected in the following dataset.
The earliest archaeological evidence of LCPD came from a
Neolithic site in Poço Velho, Carcais, Portugal (Antunes-
Ferreira2005), and the most recent from the Realta Correctional
Facility and Asylum cemetery in Switzerland—dating between
1858 and 1917 AD (Cooper, Heinzle, and Reitmaier2019). Most
of the individual cases in this study were adults, just two were
children and four were adolescents.
Regarding sex, 53/73 (72.6%) were male, 9/73 (12.3%) female,
and 11/73 (15.1%) were either unknown sex or were assessed as
indeterminate sex.
Unilateral cases were 60/73 (82.2%), bilateral cases were 6/73
(8.2%), and 7/73 (9.6%) were unknown. Concerning those with
a known side affected, LCPD was present in 35/68 (51.5%) of the
left femur and 37/68 (54.4%) of the right. It was unknown whether
7/73 (9.6%) of individuals were affected either unilaterally or
bilaterally. Overall, 21/73 (28.8%) individuals exhibited positive
signs of coxarthrosis, 14/21 (66.7%) of which were male, 4/21
(19.0%) were female, and 3/21 (14.3%) were of unknown sex.
FIGUR E | Medial v iew of left femoral head af fected by LCPD
(RLP05, Context 40207, Museum of London). [Colour figure can be
viewed at wileyonlinelibrary.com]
FIGUR E | Anterior view of a bilateral case of LCPD affecting both femoral heads (SRP98, Context 27608, Museum of London). [Colour figure
can be viewed at wileyonlinelibrary.com]
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TABLE | Record of sites and individuals with cases and possible cases of LCPD. Key: P†. Case study. R†. Osteological/site report. Child (1–11 years); Adolescent (12–17 years); YA: young adult (18–
25 years); YMA: young middle adult (26–35 years); OMA: old middle adult (36–45 years); MA: mature adult (46 + years). “Adult” description provided when this was the only information given with no
specific age parameters. M—male, I—intermediate, F—female, and U—unknown. L/R—left/right hip. Social status is divided into low, middle, high, and unknown. MoLC, CHB—Museum of London
Collections, Centre for Human Bioarchaeology. ‡—minimum number of individuals. The crude prevalence rate (CPR) was calculated by the number of cases affected by LCPD/total population.
Site Location
Ind iv idual ID/
context No. Age Sex
Hip
affected
Socioeconomic
status CPR References
Neolithic
(c. 4000–2600 BC)
P†. Poço Velho, Carcais, Portugal Femur 233.2444 Adult U — Unknown 1.7%
(2/115)
Antunes- Ferreira(2005)
Femur 233 2445 and
Os coxa 233 2129
Adult U R Unknown
Bronze age
(c. 2600–800 BC)
P†. Northern Caucasus,
Kudachurt cemetery, Russia
Grave 67 YMA–OMA M L Low 0.8% (1/130) Fuchs etal.(2021)
P†. Agizór, Türkiye M4B M L Unknown 5.6% (1/18) Açikkol Yildirim etal.(2003)
P†. Karagündüz, Türkiye K1 Adult M — Unknown (2/- ) Sevim etal.(2002)
K8 Adult M — Unknown
2.7%
(4/148)
Iron age
(c. 800 BC- 100 AD)
P†. Egypt (unknown site) Mummy No. 8 YMA F L Unknow n 1.9% (1/52) Fritsch etal.(2015)
P†. Valle Pega, Ferrara, Italy 92D OMA–MA ?M LUnknown 0.3% (1/300) Manzon etal.(2017)
P†. Shijahe cemetery, China SHSM22 YMA M R Low 2.7% (1/37) Berger etal.(2017)
R†. Westerhausen, Harz, Germany 3oo 4- 3 YMA M R Unknown 4.2% (1/24) Jacobi etal.(2009)
R†. Danebury Hillfort,
Hampshire, England
Deposition 46 YA M L Unknow n 1. 4% (1/70) Hooper(1984)
R†. Melton, East Yorkshire, England SK 4 OMA M L Unknown 2.3% (1/44) Ponce and Holst(2020)
1.1%
(6/52 7)
Roman
(c. 43 –410 A D)
R†. Baldock, Hertfordshire, England SK 469a OMA M R Unknown 3.5% (2/57) Keefe, Challanáin,
and Holst(2015)
SK 563 YMA M R Unknown
R†.Lankhills, Winchester, England SK 109 MA ?M RMiddle 0.2 % (1/451) Booth etal.(2010)
P†. Ampliación del MNAR
cemetery, Mérida, Spain
SK ME249 YA M R Low 0.5% (1/118) García- Moreno, López- Costas,
and Dorado Fernández(2022)
0.6%
(4/626)
(Continues)
6 of 17 International Journal of Osteoarchaeology, 2025
Site Location
Ind iv idual ID/
context No. Age Sex
Hip
affected
Socioeconomic
status CPR References
Early medieval
(c. 410 –1050 A D)
P†. Wadi Halfa, Nubia, Sudan — Adult ?M LUnknown 0.5% (1/218) Armelagos(1969)
P†. Kefevi, Sinop, Türkiye M38 Adult F L Unknown 0.9% (1/118) Çirak and Şarbak(2021)
P†. Lužice, Hodonín
District, Czechia
G. No. 2 OMA M L Unk nown 0. 8% (1/120) Smrčka etal.(2009)
P†. Brandỷsek Kladno
District, Czechia
No. 9 Adult M L Unknown 2.1% (1/47) Smrčka etal.(2009)
P†. Duratón, Segovia, Spain No. 12 MA M R Unknown 0.3%
(1/3 4 5 +)
Herrerín and Garralda (2012)
R†. St. Tugual's Chapel,
Herm, Guernsey
SK 003 OMA F R Unknow n 2.5% (1/40) De Jersey and Cataroche(2012)
R†. Filton, Bristol, England SK 140 OMA U L Unknown 1.9% (1/52) Caffell and Holst(2005)
P†. Tiszafűred, Hungar y — YMA–OMA M L Unknown (1 /- ) Józsa and Pap (2014)
R†. Westness, Rousay,
Orkney Islands, Scotland
Grave 25 Child U R Unknown 3.5% (1/29) Sellevold(1999)
P†. Olympia, Greece Individual 1 YMA–OMA M L and R Unknown 4.2 % (1/24) Ahlbrecht, Pilz, and Gresky(2024)
P†. Maiorca, Portugal —Adult U U Unknown 4.7% (1/21) Marques and Cunha(1999)
1.0%
(1 0// 9 9 0)
Late medieval
(c. 105 0–15 50 AD)
P†. Dilkaya Mound, Türkiye DK 88 BMD, R48 MA M R Unknown 0.3% (1/319) Şahin(2019)
P†.R†.St Marys Spital,
London, England
23126 YA M L Low 11.3%
(14/12 4‡)
Connell etal.(2012)
24011 YA ?M LLow
27651 ?Adolescent I R Low
30298 YA ?M RLow
31395 YA M R Unknow n
11328 YA ?M LUnknown
12251 OMA ?M RLow
19543 MA I R Low
25009 YMA M L Unknown
(Continues)
TABLE | (Continued)
7 of 17
Site Location
Ind iv idual ID/
context No. Age Sex
Hip
affected
Socioeconomic
status CPR References
25477 YMA ?M LLow
27608 YMA ?M L and R Low
28114 YMA ?M RUnknown
28227 YA M R Low
10110 YA F R Unknown
R†. St. John's Hospital,
Staffordshire, England
SK 197 OMA M L Unknown 2.2% (1/46) Holst and Loeffelmann(2017)
P†. Dominican Friary,
London, England
Context: 30 6 YA M R Unknown 1.8% (1/57) MoLC, CHB
R†. St. James' Abbey,
Northampton, England
SK 3173 OMA M L Unknown 0.7% (2/278) Anderson, Hodgins, and
Andrews(2000a); Anderson,
Hodgins, and Andrews(2000b)
SK 3154 YA ?M RUnknown
R†. Blackfriars' Friary,
Suffolk, England
SK 1892 Adult M L and R Unknown 0.8% (2/250) Mays(1991)
SK 1917 OMA F L Unk nown
P†. St. James and St. Mary
Magdalene, West Sussex, England
UB C- 13 OMA M L and R Unknown (1/- ) Ortner(2003)
P†. Mudéjar de Uceda cemetery,
Guadalajara, Spain
—YMA M L Unknow n (1/- ) Dorado- Fernández etal.(2015)
R†. Lorrha, Co. Tipperarry, Ireland No. 29 YMA M — Unknow n 2.3% (1/44) Bolger, Moloney, and Troy(2012)
R†. Dunbar, East Lothian, Scotland SK 72 YMA–OMA M L and R Unknown 0.8% (1/127) Moloney etal.(2001)
P†. San Nicolao di Pietra
Colice, Liguria, Italy
T34 US2614 SN06 ind. A YMA F L Unknown 25.0 % (1/4) Cesana, Benedictow,
and Bianucci(2017)
R†. Largo da Sé- Praça
dos Mártires, Silves,
Portugal
Burial 23 Adult M L Unknown 0 .5% (1/193) Lopes Dos Santos and
Ramos(2004)
R†. Grasshopper Pueblo,
Arizona, USA
Burial 191 Adolescent M L Unknown 0. 2% (1/390) Hinkes(1983)
R†. Qilakitsoq, Uummannaq
district, Greenland
Mummy 2 Child M — Unknown 12 .5% (1/8) Hansen and Nordkvist(1996);
Bourbou(2005)
P†. St. Agostino, Caravate, Italy T 18 MA M R Unknown 5. 0% (1/20) Fusco, Larentis, and Tesi(2021)
(Continues)
TABLE | (Continued)
8 of 17 International Journal of Osteoarchaeology, 2025
Site Location
Ind iv idual ID/
context No. Age Sex
Hip
affected
Socioeconomic
status CPR References
P†. Paucarcancha Cave, Peru — Adult M L Unknow n (2/- ) MacCurdy(1923),
Rothhammer(1990)
—Adult F R Unknown
1.7%
(32/1860)
Postmedieval
(c. 1 550–19 00 AD)
P†. Santa Maria dos Olivais'
Church, Tomar, Portugal
Context: SMOL- 271 OMA M R Unknown 1. 4% (1/7 3) Curto and Fernandes(2013)
P†. St. Ilija Church. Serbia No. 7 YMA–OMA M L Unknown 0.2% (1/522) Durić etal.(2004)
P†. Patallacta, Peru — YA M — Unknown (1/23‡) MacCurdy(1923),
Rothhammer(1990)
P†. Fairport, Ohio, North America B8.1 YMA F R Unknown 1.6% (1/62) Clark, Bargielski, and
Reich(2020)
P†. Necropolis of Santa
Maria, Sintra, Portugal
Grave 35 Adult U L Unknown 0.8% (1/120) Wasterlain and Umbelino(2014)
P†. Lagos, Algarve, Portugal B No. 2 Adult U R Unknown 9.1% (1/11) Ferreira, Neves, and
Wasterlain(2013)
P†. San Carlos, Mendoza
province, Argentina
Context: 12CA Adolescent U R Unk nown 5.3% (1/19) Ponce and Novellino(2014)
R†. Realta Correctional Facility
and Asylum, Switzerland
g56 YA–Y MA M R Low 1.0 % (1/103) Cooper, Heinzle, and
Reitmaier(2019)
P†. Radom, Poland No. 317/13 OMA M L and R Unknown (1/- ) Myszka etal. (2023)
R†. St. Benet Sherehog,
London, England
Context: 179 Adolescent U R Unknow n 0.4% (1/231) MoLC, CHB
R†. St. Thomas' Hospital,
London, England
Context: 115 MA M L Low 0.5% (1/193) MoLC, CHB
R†. Queens Chapel of the
Savoy, London, England
SK 1090 YA–YMA ?M RUnknown 0.2% (1/609) MoLC, CHB
R†. Royal London Hospital,
London, England
Context: 40207 YMA M L Unknown 0 .2% (1/639) MoLC, CHB
0.4%
(12/2732)
(Continues)
TABLE | (Continued)
9 of 17
4 | Discussion
4.1 | Sex Distribution
Concerning sex, worldwide analysis of known past individuals
with LCPD revealed a demographic aligning with that found
in modern clinical literature (Molloy and MacMahon 1966;
Catterall 1971; Gray, Lowry, and Renwick 1972; Stulberg,
Cooperman, and Wallensten 1981; Wiig et al. 2006; Murray,
Holmes, and Misra2008; Wiig2009), reflecting a distinct male
preponderance (72.6% vs. 12.3%, respectively). There are several
posited theories for this tendency including sex- related activity,
femoral- acetabular anatomy (Lauritzen 1975), and/or earlier
bone maturation in females (Rampal, Clément, and Solla2017).
However, these theories are yet to be proven, leaving the sex dis-
parity seen in LCPD's prevalence rate inexplicable.
4.2 | Unilateral vs. Bilateral
The quantitative comparison between right and left hip afflic-
tion exhibited no marked difference as the right hip was affected
by 54.4% (37/68) and left hip by 51.5% (35/68). Unilateral cases
were predominant (84.5%) relative to bilateral cases (5.6%),
which, like the disparity in sex prevalence, closely aligns with
trends provided by clinical literature (Catterall 1971; Murray,
Holmes, and Misra 2008). However, it was unknown whether
7/73 individuals (9.6%) were affected unilaterally or bilater-
ally. This absence of data in the sources may have been due to
post- depositional variables (i.e., preservation, taphonomy, and
completeness).
4.3 | Etiology
Based on the clinical literature analyzed, LCPD appears to
be a multifaceted, systemic disease. Due to LCPD's etiologi-
cal complexities, a diagram was created to demonstrate the
different pathomechanisms explored in related studies (see
Figure 5) consisting of a variety of agents postulated to con-
tribute to or be associated with LCPD's cause. Environmental
factors and genetic predispositions were fundamental in our
research to provide insights into the possible causes of LCPD
in the past.
4.3.1 | Physical Trauma
Physical trauma (Figure 5) causing an occlusion of the main
blood supply to the femoral epiphysis has been one of many dif-
ferent theories for initiating the onset of LCPD. Except for one
study (Clark, Bargielski, and Reich2020), examining those with
LCPD based on etiological speculation has not been the fore-
front of recent analyses. In Clark, Bargielski, and Reich(2020) it
was attempted to contextualize forms of trauma that could have
caused LCPD in the past, exploring the occupational activities
possibly undertaken by an individual of a late prehistoric Erie
community (17th c. North America). Based on the region's ag-
ricultural dependence, it was posited that their analyzed indi-
vidual, a young girl (B8.1), may have been exposed to repeated
microtrauma from prolonged strenuous activity (digging,
Site Location
Ind iv idual ID/
context No. Age Sex
Hip
affected
Socioeconomic
status CPR References
Undated P†. Chicama Valley, Peru Context: NMNH 265331 Adult ?F RUnknown (1/- ) Ortner(2003)
Total 1.0%
(73/6999)
TABLE | (Continued)
10 of 17 International Journal of Osteoarchaeology, 2025
hoeing, carrying hay, bending, twisting, and lifting) that con-
stantly involved muscles used for hip flexion and extension, in-
creasing the risk of restricting blood flow to the femoral head
(Lauritzen1975).
Addressing the physical activities and/or occupations that chil-
dren would have contributed to in the past is a complex topic
that presents differences across periods and cultures. In past
agrarian and pastoralist societies, child labor was known to
have been common practice (García- Moreno, López- Costas, and
Dorado Fernández2022); children would carry out certain age-
appropriate tasks from as early as 3–5 years old that contribute
to their own subsistence (Nieuwenhuys1994; Röder2018). This
would include domestic and agricultura l activities, such as carr y-
ing messages, fetching and delivering goods, cleaning, crafting,
preparing food, and collecting water (Röder2015; Röder2018),
exposing them to biomechanical injury (Sundström, Mispelaere,
and Bäckström2018). These physical activities could have there-
fore increased the risk of an ischemic episode occurring, and
subsequently the development of LCPD.
4.3.2 | Socioeconomic Status
Modern epidemiological studies (Perry et al. 2012a; Perry
etal. 2012b; Perry 2013) have shown a probable link between
individuals of low- to mid- socioeconomic strata (Figure5) and
the development of LCPD. Socioeconomic status is a concept rid-
dled with ambiguity; it differs across cultures and can change
over an individual's lifetime. In general, it attempts to reflect
the role a person holds in their respective, typically hierarchi-
cal, society and usually entails a multitude of direct and indirect
factors that revolve around a standard of living. This can include
diet, income, occupation, education, access to healthcare, and
behavior (social norms). Climate and ecological factors can, in
turn, affect accessibility to each of these aspects. One's social
status can expand or restrict the individual's responsibilities and
capabilities, and influences how the individual perceives others
and how others perceive them. However, attempting to analyze
social status across different time periods on a global scale with-
out making generalizations or bias yields a challenge. Likewise,
compared to living populations, the social status of those in the
past cannot be easily assessed but rather examined and inferred
through anthropological (artifacts and burial practice) and bio-
archaeological (skeletal health and δ13C and δ15N isotope levels)
analysis. This proved difficult for this study. The social status of
the individuals in this study was therefore extracted from their
respective sources. The prevalence of those that could be inter-
preted as having low or possibly low status was 19.2% (14/73),
and those of middle status 1.4% (1/73). None was recorded as
high status. The social status of 79.5% (58/73) of individuals was,
however, either too arbitrary, not apparent or not provided for
FIGUR E | Diagram summarizing studied agents that may cause or possibly increase the risk of developing LCPD by initiating the ischemic ep-
isode. COLA 21—Collagen type 2, alpha 1; IGF- I—insulin- like growth factor- I. [Colour figure can be viewed at wileyonlinelibrary.com]
11 of 17
by the sources in which they were analyzed. The social status
ascribed to these individuals in this study should also be consid-
ered with caution, as such interpretation of past individuals is
tentative and inherently problematic.
Likely influenced by the effects of one's socioeconomic status,
diet, or malnutrition, on the other hand, has also been made
suggestive as a possible contributory agent to LCPD (Figure5;
Burwell 1988; Perry2013). Conditions such as cribra orbitalia
(CO), porotic hyperostosis (PH), Harris lines (HL), and dental
enamel hypoplasia (DEH) have been attested to ref lect nu-
tritional stress during childhood (Goodman and Rose 1991;
Hillson2001; Roberts and Manchester2012), and were therefore
considered in this analysis. However, the crude prevalence of all
these conditions with those with LCPD in this study was rela-
tively low. CO and DEH were the most prevalent of the diseases
in this study (both 8.2%, 6/73), followed by PH (2.7%, 2/73), and
then HL (1.3%, 1/73). Because of such low prevalence, this study
could not address the link between these conditions and LCPD.
This was due to most of the LCPD cases being from isolated in-
stances or contexts where only one or two individuals (with ex-
ception to St. Mary's Spital) were reported. Site prevalence rates
of metabolic diseases were largely absent from population stud-
ies. When the information was available, the attempt to assess
whether LCPD had any connection to a comorbid prevalence of
metabolic diseases indicated that there were not enough cases
of LCPD or enough data pertaining to the prevalence of meta-
bolic diseases from each site to reinforce or disparage this no-
tion. Likewise, while individuals may have suffered with both
LCPD and metabolic diseases, the latter may be a representation
of socioeconomic conditions rather than a direct link to LCPD.
Another socioeconomically related agent found in these studies
was exposure to pollution, namely, smoke (Figure5), and its re-
lation to increased LCPD incidence rates, particularly concern-
ing the effects of firewood- stove smoke from cooking in India
(Daniel etal.2012) and tobacco smoke (García Mata etal.2000;
Gordon etal.2004; Bahmanyar etal.2008). While there is no ev-
idence of direct cause and effect, these correlations may instead
collectively represent detriments of polluted air having a p ossible
inf luence on LCPD development. Notably increased p ollutant ac-
tivity in the past would have most likely begun in the Neolithic,
which saw the introduction and control of agriculture and per-
manent settlements. With structures being built to inhabit and
work in, indoor pollution would have been borne with the fir-
ing of wood to heat and cook. The main fuels for domestic and
craftsmen use during the periods up until the mid- 1800s would
have been exclusively charcoal and timber (Camuffo, Daffara,
and Sghedoni 2000). Wood- burning hearths in homes would
have produced smoke, carbon monoxide, and aldehydes. In 14th
century London, for instance, it was estimated that 40,000 t of
wood and 6000 t of sea- coal were burned annually (Dyer1989).
This may partially ref lect the relatively high prevalence (19.2%,
14/73) of LCPD cases in this study coming from Late Medieval
London's St. Mary's Spital burial site, though this statistic and
interpretation could be (and likely is) skewed by issues linked
to the overall low prevalence of individuals with LCPD in the
archaeological record (see Section4.6). Nonetheless, if pollution
is contributory towards LCPD's etiology, domestic cooking prac-
tices, heating, and occupations that involve the production of
airborne pollutants may hold pertinence to its prevalence.
4.3.3 | Genetic Predispositions
In clinical literature, there have been several case studies
(Miyamoto etal.2007; Su etal.2008; Su etal.2010; Li etal.2014)
that make links between LCPD and collagenopathies concern-
ing issues with collagen synthesis. These are either based on
a COL2A1 (a major structural protein in cartilage) mutation,
which has shown an alteration to the collagen fibril matrix
and the overall structure of articular cartilage; or low levels of
insulin- like growth factor- I (IGF- I), which lowered the rate of
collagen synthesis and increased collagen breakdown. Both con-
ditions represented a compromise with collagen synthesis form-
ing the articulatory cartilage that may or may not contribute to
the development of LCPD. However, a recent study (Lindblad
etal.2024) has suggested that there is no strong correlation be-
tween LCPD and collagenopathies, though it could not provide
definitive answers as no specific collagenopathy could be iden-
tified. Given that the results of these studies are the products
of invivo testing, if collagenopathies such as the COL2A1 mu-
tations or low levels of IGF- I are pertinent to causing LCPD, it
is unknown whether paleopathologists are able to explore this
particular agent any further.
4.4 | Disease Effects and Management
Maintaining balance and locomotion with a defective hip
joint could only have produced a lot of pain, and potentially
altered gait and posture permanently leading to secondary
effects of LCPD, such as coxarthrosis. Clinical studies found
a high prevalence of coxarthrosis development after suffer-
ing from the primary effects of LCPD (Mose1980; Stulberg,
Cooperman, and Wallensten 1981), developing during early
or middle adulthood and, more commonly, in mature adults.
This study found that 28.8% (21/73) of all individuals with
LCPD displayed skeletal changes compatible with coxarthro-
sis. Two severe examples are exhibited in the femoral heads of
Late Medieval individuals SK 3173 and SK 3154. Individual SK
3173's femoral head was locked into its acetabulum due to the
osteological defects caused by severe coxarthrosis, practically
rendering ambulatory activity impossible or considerably dif-
ficult, and SK 3154, while not ankylosed, would have been lim-
ited to 80° flexion (Anderson, Hodgins, and Andrews2000a,
2000b). It would therefore be accurate to assume that these
individuals not only suffered restricted movement (Hansen
and Nordkvist1996; Curto and Fernandes2013) but also con-
siderable pain after childhood (García- Moreno, López- Costas,
and Dorado Fernández 2022) up until their death. However,
for how long they suffered from these effects before perishing
cannot be gauged.
The detection of further degenerative joint disease (DJD), as
mentioned by some of the case studies analyzed (Marques and
Cunha 1999; Bolger, Moloney, and Troy2012; De Jersey and
Cataroche 2012; Curto and Fernandes 2013), could also be
suggestive of LCPD incurring further biomechanical injury.
However, it has also been posited that DJD affecting different
areas of the body may instead represent attempts to circum-
vent the detrimental effects of the disease. The prevalence
of those in this assemblage recorded with other DJD- related
pathologies, in addition to LCPD, was 31.5% (23/73), 87.0%
12 of 17 International Journal of Osteoarchaeology, 2025
(20/23) of which included the coxarthrosis of the afflicted
hip. These individuals were particularly affected in the mid-
upper skeletal regions, namely, the shoulders, humeri, spine,
and also the feet. In addition, increased biomechanical stress
may have also led to the simultaneous buttressing of bone
density within certain skeletal elements. An individual in an-
other study (Holst2010), for instance, suffered with DDH, an
affliction so similar to LCPD in its skeletal changes it poses
the risk of misdiagnosis in palaeopathology. This individual
(SK 15548) also had secondary problems, including the forma-
tion of an artificial hip joint with coxarthrosis, inflammation,
atrophy, and osteoarthritis of the spine, with the addition of
distinctly robust upper limbs. This occurrence of robust arms
combined with evident DJD in the shoulders, hip, and right
hand led analysts to posit these changes as being the result
of using a crutch to aid mobility and alleviate pain in daily
life (Holst 2010; Buckberry et al. 2014). This was also sug-
gested for individuals No. 12 and SK ME249 (Herrerín and
Garralda 2012; García- Moreno, López- Costas, and Dorado
Ferná ndez 2022) and, based on the similar pathological cir-
cumstance, could extend to individual 25477 from St Mary's
Spital (Connell etal.2012). Individual No. 12 appeared to have
a strong right humerus based on their robust muscular at-
tachments, indicating frequent use of the right arm (Herrerín
and Garralda 2012). Individual 25477 from St Marys Spital
also exhibited a robust right humerus as well as trauma to
the right clavicle. Individual No. 12 showed increased ro-
busticity in their contralateral femur and tibia (Herrerín and
Garralda2012), suggesting a thickening of bone due to addi-
tional weight- bearing/locomotory stressors transferring from
the afflicted limb. With or without the aid of a crutch, areas
affected by DJD or increased robusticity of bone will likely
have resulted from a restricted (Hinkes1983) or antalgic gait,
a natural consequence of LCPD to a considerably varying de-
gree. The nature of this gait would depend on the severity of
morphological change, joint congruency, level of pain, and ca-
pacit y for mobility.
On the other hand, atrophy of aff licted limbs, of both lower
limb bones (Anderson, Hodgins, and Andrews 2000a, 2000b;
Herrerín and Garralda 2012; Walker 2012; Keefe, Challanáin,
and Holst2015) and musculature (Ratliff1967), was also found
to be secondary to LCPD. Five individuals (No. 12, SK 469a and
3514, and ctxt. 23126 and 306; see Table1) were recorded to have
had atrophy affecting the proximal femur with LCPD in this
assemblage, which totaled 6.8% (5/73), with 60% (3/5) of those
having additional atrophy in their corresponding tibia. These
findings also paralleled with individual 25477 from the afore-
mentioned study (Holst 2010), who similarly exhibited atrophy
in their afflicted limb. Atrophy of bone and musculature may
indicate disuse of the affected limb (Yang etal.2019), likely due
to the secondary effects of LCPD causing discomfort, pain, and/
or general prevention of movement. Crutch use and increased
dependency on the contralateral lower limbs would have only
amplified the disuse of the afflicted leg.
4.5 | Place in Society
Whether the individual had the aid of apparatus for mobility,
a caregiver, or neither, the inability to physically function to
a degree that would be otherwise normative could have made
them a liability, or at least feel like one, particularly when
families often operated as socioeconomic units (Röder 2015;
Röder 2018; Sundström, Mispelaere, and Bäckström 2018).
Developments of further biomechanical complications such as
secondary DJD (i.e., coxarthrosis) in later life could only have
exacerbated such situations. Although we cannot evaluate the
psyche of the deceased, having a limited capacity to physically
participate in society could have had a profound effect on
the individual's mental well- being (McKenzie, Murphy, and
Watt 2022). For instance, chronic pain, restriction of move-
ment, and being unable to carry out physical functions could
have all led the individual to feel self- burdening (Cassileth
et al. 1984; Moussavi et al. 2007). The variation in severity
of LCPD's effects would also determine the extent to which
ambulatory activity is possible and the level of care that would
be required to function. However, the role of someone who is
disabled, their quality of life and place in society is not limited
nor defined by what they cannot do. How these individuals
functioned and how they were received by their respective
cultures is multifaceted, varying across time and geography.
In some cultures, those with disabilities have been outright
ostracized, outcasted, tolerated, or treated like an economic
liability, while in others they have been revered, provided
with a respected status and/or were allowed to participate to
their fullest capacity (Munyi 2012). Within these contexts,
individuals with limited physical capacity such as those af-
fected by LCPD could have faced either of these difficulties.
On the basis of the latter possibilities, whether living a more
sedentary life or not, or anything in between, individuals
could still contribute to their household and/or community,
both practically: housekeeping, cooking, cleaning, crafting, or
taking care of children or the elderly (Groce and Zola 1993),
and verbally, such as emotional support or administration.
Attesting to their value in society is the survival from child-
hood, when the disease is active, well into adulthood, which
applies to almost all of the individuals in this study, implying
social integration rather than ostracism (Fuchs etal.2021) in
the contexts from which they derive.
4.6 | Study Limitations
4.6.1 | Missing Data
Overall, this study encountered a low presence of global LCPD
cases reported in the archaeological literature. This was likely
due to a variety of intrinsic and extrinsic factors that influence
the level of preservation of individuals in the archaeological re-
cord. These include taphonomy, burial practices (cremation),
destruction, and/or disturbance of human remains, which are
all important contributors that represent a profound issue with
paleoepidemiology. Seven of the sources with cases of LCPD in
this study were not able to or did not provide data on overall
prevalence of individuals at their respective sites. The overall
prevalence of cases of LCPD yielded is, therefore, more than
likely smaller than what it should be, making it increasingly dif-
ficult to interpret the reality of the once- living (Waldron2007).
Due to these issues of skeletal preservation, a more comprehen-
sive analysis of the sex demographic and laterality of LCPD was
additionally problematic.
13 of 17
Inaccessible gray literature is also plausibly responsible for this
low representation of global cases of LCPD, and sources that
were consulted possessed considerable disparities in contextual
and pathological details. Osteological and site reports were both
largely descriptive, and case studies of LCPD focused on the dis-
ease in isolation, excluding the possible inference of other pa-
thologies present and wider cultural contexts.
4.6.2 | Differential Diagnosis
Clinical guidance of pathological diagnoses can only assist so
much in the analysis of human skeletal remains. While clini-
cians use radiography to identify the most acute symptoms of
LCPD during the condition's active phase in childhood, paleo-
pathologists have only osteological markers to identify LCPD.
These markers will vary in their presence and are affected by
the conditions of the bone; for LCPD, this will rely on the level
of preservation of the proximal femur (greater trochanter and
epiphysis) and the acetabulum. In addition, pathological am-
biguities are a fundamental issue that can lead to differential
diagnoses, preventing the conclusive diagnosis of LCPD. For
these reasons, cases that were conclusive and those deemed
differential/possible cases of LCPD were documented with-
out distinction. It was not within the remit of the authors to
challenge the diagnoses of LCPD derived from the sources
examined.
4.6.3 | Modern Bias
The archaeological cases in this study represent the natural
history of untreated LCPD (Ahlbrecht, Pilz, and Gresky2024).
Today, treatment is prescribed when early onset signs appear,
meaning that modern experiences of the condition will differ
invariably to those in the past. Although the clinical litera-
ture provided a wide breadth for speculation, the interpretive
quality of individuals analyzed was, therefore, restricted by
current clinical conjecture and the bias effects of medical
intervention. Although it can be problematic to provide in-
terpretations despite the limitations of using a paleopatho-
logical approach, this study applied clinical knowledge to
past realities to attempt to understand the nature of LCPD.
Extrapolating clinical data to the past is ubiquitous for paleo-
pathologists (Grauer2019) and has not inhibited other paleo-
pathological studies from contextualizing other individuals
who have also suffered from LCPD and other diseases in
the past (Herrerín and Garralda 2012; Buckberry etal.2014;
McKenzie, Murphy, and Watt2022).
4.6.4 | Etiology
Furthermore, a part of the objectives of this study was to exam-
ine the clinical analyses into LCPD's etiology and unravel pos-
sible causes in the past based on this data. This proved difficult
due to the extent of clinical analyses that LCPD has undergone,
where connections are only hypothetical, typically involving
other pathological causes that also have an obscure or uncertain
pathogenesis.
Analysis of socioeconomic status exhibited a strong correlation
with those of low–mid socioeconomic strata and heightened
LCPD incidence and prevalence rates in modern epidemiol-
ogy (Perry etal.2012b; Perry2013). However, this study found
that determining the socioeconomic status of the individuals
was largely problematic. Conceptual ambiguity of social status,
intra- period and intra- regional differences, and gaps in liter-
ature (burial, site typology, and other pathological data) were
fundamental issues that posed a challenge to study the role of
socioeconomic status in relation to LCPD. As a result, the so-
cial status of most of the individuals in this study could not be
assessed.
The link of LCPD's etiology and ancestr y (Perry etal.2012a) also
limited the capacity to provide a paleopathological interpreta-
tion. The presumption of the ancestry and geographic origin of
the individuals in this study, based on their place of burial, was
found to be inappropriate, as the place of burial does not nec-
essarily reflect the individual's place of origin. Occurrences of
transmigration and periodic introgression in the past meant that
providing an exact provenance for the cases reported was not
possible. Resolution to this issue would have required ancient
DNA analysis, which was outside the scope of this study.
LCPD's complicated and inconclusive etiology has meant that
the interpretations made in this study are considerably specu-
lative. Extrapolating clinical expertise, especially when it con-
cerns a disease with a complex pathogenesis (with possible
links to other pathologies with equally uncertain etiologies), to
archaeological contexts has posed considerable challenges that
palaeopathology cannot easily overcome.
5 | Conclusion
Archaeological cases of LCPD totaled 73 in this study, predomi-
nantly from England. Cases unaccounted for are almost certain.
There is an explicit negligence of rare diseases such as LCPD
in paleopathological studies, and by extension, the archaeo-
logical record. Further interdisciplinary research and collabo-
ration are required for LCPD's further clinical exploration and
acknowledgment among other archaeological sites and regions.
Gray literature in osteological and site reports is considerably re-
sponsible for this lacuna in literature. In addition to this missing
information, true prevalence is prohibited by extrinsic and in-
trinsic factors pertaining to the issues borne by palaeoepidemi-
ology and the archaeological record. Its skeletal manifestations
are also both various and diagnostically ambiguous. However, it
is LCPD's etiological complexity that has ultimately allayed the
prospects of its contextualization in the past.
Despite offering no firm conclusions, modern clinical literature
has yielded a multiplicity of speculations as to LCPD's etiology.
These various hypotheses can allow us to navigate different so-
cial, economic, biological, and environmental aspects in pursuit
of etiological links of LCPD in the past.
Characteristics of LCPD and the differing levels of their severity
have also implicated the physical lives that sufferers may have
led, how they may have physically and/or mentally experienced
14 of 17 International Journal of Osteoarchaeology, 2025
the disease, and how their respective societies and cultures may
have cared for them, if they did at all. Analysis of the affliction's
osteological secondary effects further provided evidence for
speculation as to how they may have even personally managed
its symptoms.
Overall, while employing a speculative approach, this study
has shown that there is promise for future analysis of LCPD.
Following new, more holistic methods of research and synthesis
of interdisciplinary data is required, utilizing clinical studies,
paleopathological approaches and ethnographical information
where possible.
Acknowledgments
The authors would like to thank the BABAO (British Association for
Biological A nthropolog y and Osteoarchaeolog y) commercial g rants that
allowed us to spend time analyzing cases of LCPD from the Museum of
London. Special thank s are given to Jelena Bekvalak, curator of Human
Osteology at the Centre for Human Bioarchaeology at the Museum of
London, UK for help and support during our work at the Museum of
London, UK, and for her assistance in accessing data that would have
been otherwise difficult to obtain.
Conflicts of Interest
The authors declare no conflicts of interest.
References
Açikkol Yildirim, A., H. Yilmaz, İ. Baykara, and S. Şahin. 2003.
“Kütahya Ağızören İskeletlerinin Paleoantropolojik Analizi ve Tunç
çağı Anadolu Halkları Arasındaki Yeri.” Antropoloji 17: 1–26. ht tps: //
doi. org/ 10. 1501/ antro_ 00000 00211 .
Ahlbrecht, Y., O. Pilz, and J. Gresky. 2024. “Testing the Digital Atlas
of Ancient Rare Diseases (DAARD) Using a New Case of Legg- Calvé-
Perthes Disease From Early Byzantine (500- 700 CE) Olympia, Greece.”
International Journal of Paleopathology 46: 62–73. https:// doi. org/ 10.
1016/j. ijpp. 2024. 07. 002.
Amirfeyz, R., C. Clark, and M. Gargan. 2005. “Spondyloepiphyseal
Dysplasia.” Current Orthopaedics 19, no. 4: 309–313. https:// doi. org/ 10.
1016/j. cuor. 20 05. 06. 0 07.
Anderson, T., I. Hodgins, and J. Andrews. 2000a. “The Human Skeletal
Material From St. James' Abbey, Northampton (Express Lifts): Part 1:
The Text.” (Unpublished Report, Northampton Archaeology/MOLA
Northampton).
Anderson, T., I. Hodgins, and J. Andrews. 2000b. “The Human Skeletal
Material From St. James' Abbey, Northampton (Express Lifts): Part
3: The Skeletons.” (Unpublished Report, Northampton Archaeology/
MOLA Northampton).
Anthony, S., R. Munk, W. Skakun, and M. Masini. 2015. “Multiple
Epiphyseal Dy splasia.” Journal of the Amer ican Academy of Ort hopaedic
Surgeons 23, no. 3: 164–172. https:// doi. org/ 10. 5435/ JAAOS - D- 13-
00173 .
Antunes- Ferreira, N. 2005. Paleobiologia de Grupos Populacionais
do Neolítico Final/Calcolítico do Poço Velho (Cascais). Trabalhos de
Arqueologia 40. Lisboa: Instituto Português de Arqueologia.
Armelagos, G. 1969. “Disease in Ancient Nubia.” Science 163, no. 3864:
255–259. https:// doi. org/ 10. 1126/ scien ce. 163. 3864. 255.
Aufderheide, A., and C. Rodríguez- Martín. 1998. The Cambridge
Encyclopaedia of Human Palaeopathology. Cambridge: Cambridge
University Press.
Bahmanyar, S., S. Montogomery, R. Weiss, and A. Ekbom. 2008.
“Material Smoking During Pregnancy, Other Prenatal and Perinatal
Factors, and the Risk of Legg- Calvé- Perthes Disease.” Pediatrics 122,
no. 2: e459–e464. https:// doi. org/ 10. 1542/ peds. 2008- 0307.
Barker, D., E. Dixon, and J. Taylor. 1978. “Perthes Disease of the Hip
in Three Regions of England.” Journal of Bone and Joint Surgery 60- B:
478–480. https:// doi. org/ 10. 1302/ 0301- 620X. 60B4. 711792.
Barker, D., and A. Hall. 1986. “ The Epidemiology of Perthes' Disease.”
Clinical Orthopaedics 209: 89–94.
Berger, E., L. Chen, Z. Sun, and Z. Sun. 2017. “A Probable Case of Legg-
Calvé- Perthes Disease in Warring States- Era China.” International
Journal of Paleopatholog y 16: 27–30. https:// doi. org/ 10. 1016/j. ijpp. 2016.
11. 001.
Berthaume, M., D. Perry, C. Dobson, U. Witzel, N. Clarke, and M.
Fagan. 2016. “Skeletal Immaturity, Rostral Sparing, and Disparate
Hip Morphologies as Biomechanical Causes for Legg- Calvé- Perthes'
Disease.” Clinical Anatomy 29: 759–772. https:// doi. org/ 10. 1002/ ca.
22690 .
Bolger, T., C. Moloney, and C. Troy. 2012. “Archaeological Excavations
at Lorrha, Co. Tipperary.” Journal of Irish Archaeology 21: 113–137.
Booth, P., A. Simmonds, A. Boyle, S. Clough, H. Cool, and D. Poore.
2010. “T he Late Roman Cemetery at L ankhills , Winchester: Excavat ions
2000- 2005.” (Unpublished report, Oxford Archaeology Monograph No.
10).
Bourbou, C. 2 005. “Too Smal l to Be Noticed? Children Mumm ies Reveal
Their Stories.” Journal of Biological Research 1, no. 80: 208–211. ht tps: //
doi. org/ 10. 4081/ jbr. 2 005. 10186 .
Buckberry, J., J. Montgomery, J. Towers, etal. 2014. “Finding Vikings in
the Danelaw.” Oxford Journal of Archaeolog y 33, no. 4: 413–434. https ://
doi. org/ 10. 1111/ ojoa. 12045 .
Burwell, R. 1988. “Perthes’ Disease: Growth and Aetiology.” Archives
of Disease in Childhood 63: 140 8–1412. https:// doi. org/ 10. 1136/ adc. 63.
11. 14 08.
Caffell, A. and M. Holst. 2005. “Osteological Analysis, Filton, Bristol.”
(Unpublished Osteological Report, York Osteoarchaeology No. 2205).
Camuffo, D., C. Daffara, and M. Sghedoni. 2000. “Archaeometry of Air
Pollution: Urban Emission in Italy During the 17th Cent ury.” Journal
of Archaeological Science 27: 685–690. https:// doi. org/ 10. 1006/ jasc.
1999. 0483.
Cassileth, B., E. Lusk, T. Strouse, et al. 1984. “Psychosocial Status in
Chronic Illness: A Comparative Analysis of Six Diagnostic Groups.”
New England Jour nal of Medicine 311, no. 8: 506–511. https:// doi. org/ 10.
1056/ NEJM1 984 08 23311 0805.
Catterall, A. 1971. “ The Natural History of Perthes' Disease.” Journal
of Bone and Joint Surgery 53: 37–53. https:// doi. org/ 10. 1302/ 0301- 620X.
53B1. 37.
Catterall, A., G. Roberts, and R. Wynne- Davies. 1971. “Association of
Perthes' Disease With Congenital Anomalies of Genitourinary Tract
and Inguinal Region.” Lancet 297: 996–997. https:// doi. org/ 10. 1016/
s0140 - 6736(71) 91389 - 4.
Cesana, D., O. J. Benedictow, and R. Bianucci. 2017. “The Origin and
Early Spread of the Black Death in Italy: First Ev idence of Plague Victims
From 14th- Century Liguria (Northern Italy).” Journal of Anthropological
Sciences 125, no. 1: 15–24. https:// doi. org/ 10. 1537/ ase. 161011.
Çirak, A., and A. Şarbak. 2021. “Antik Anadolu'da Nadir Bir Patoloji:
Legg- Calvé- Perthes Hastalığı.” Antropoloji 42: 49–58. https:// doi. org/
10. 33613/ antro poloj iderg isi. 936560.
Clark, M., R. Bargielski, and D. Reich. 2020. “Adult Paleopathology as
an Indicator of Childhood Social Roles: A Case Study of Perthes Disease
in a Native Ohio Female.” International Journal of Osteoarchaeology 30,
no. 1: 24–32. https:// doi. org/ 10. 1002/ oa. 2826.
15 of 17
Connell, B., A. Jones, R. Redfern, and D. Walker. 2012. A
Bioarchaeologi cal Study of Medieval Burials on the Site of St Mary Spital:
Excavations at Spitalfields Market, London E1, 1991–2007. London:
Museum of London Archaeology.
Cooper, C., B. Heinzle, and T. Reitmaier. 2019. “Evidence of Infectious
Disease, Trauma, Disability and Deficiency in Skeletons From the
19th/20th Century Correctional Facility and Asylum «Realta» in Cazis,
Switzerland.” PLoS ONE 14, no. 5: 1–42. https:// doi. org/ 10. 1371/ journ
al. pone. 0216483.
Crofton, P., C. Macfarlane, B. Wardhaugh, etal. 2005. “Children With
Acute Perthes' Disease Have Asymmetrical Lower Leg Growth and
Abnormal Collagen Turnover.” Acta Orthopaedica 76, no. 6: 841–847.
https:// doi. org/ 10. 1080/ 17453 67051 0045462.
Curto, A., and T. Fernandes. 2013. “A Possible Case of Legg- Calvé-
Perthes' Disease in an Adult Male From Medieval/Modern Tomar,
Portugal.” In Proceedings of the X I Congreso Nacional de Paleopatología:
Andorra la Vella, edited by A. Malgosa, A. Isidro, P. Ibáñez- Gimeno,
and y. G. Prats- Muñoz, 231–240. Universitat Autònoma de Barcelona,
Spain: Vetera Corpora Morbo Afflicta.
Daniel, A., H. Shah, A. Kamath, V. Guddettu, and B. Joseph. 2012.
“Environmental Tobacco and Wood Smoke Increase the Risk of Legg-
Calvé- Perthes Disease.” Clinical Orthopaedics and Related Research
470: 2369–2375. https:// doi. org/ 10. 1007/ s1199 9- 011- 2180 - 8.
De Jersey, P., and J. Cataroche. 2012. “Excavation at St Tugual's Chapel,
Herm, 2011.” La Societe Guernesiaise 27, no. 2: 381–431.
Dorado- Fernández, E., I. Ramírez- González, L. Parro- González, etal.
2015. Posible Enfermedad de Perthes en un Individuo del Cementerio
Mudéjar de Uceda (Guadalajara). Proceedings of the XIII Congreso
Nacional de Paleopatología, 313–316. Sevilla, Spain: Écija.
Douglas , G., and M. Rang. 1981. “ The Role of Trauma in t he Pathogenesis
of the Osteochondroses.” Clinical Orthopaedics and Related Research
158: 28–32.
Durić, M., Z. Rakocević, M. Bumbasirević, A. Lesić, and J. Kelecev ić.
200 4. “Two Cases of Joint Disease in Post- Med ieval Church C emetery of
St. Ilija.” Collegium Anthropologicum 28, no. Suppl. 2: 273–282.
Dyer, C. 1989. Standards of Living in the Middle Ages: Social Change in
England c. 1200–1520. Cambridge: Cambridge University Press.
Ferreira, M., M. Neves, and S. Wasterlain. 2013. “Lagos Leprosarium
(Portugal): Evidence of Disease.” Journal of Archaeological Science 40:
2298–2307. https:// doi. org/ 10. 1016/j. jas. 2012. 12. 039.
Fritsch, K ., H. Hamoud, A. Al lam, etal. 2015. “The Or thopedic Diseases
of Ancient Egypt.” Anatomical Record 298: 1036–1046. https:// doi. org/
10. 1002/ ar. 23136 .
Fuchs, K., B. Atabiev, F. Witzmann, and J. Gresky. 2021. “Towards a
Definition of Ancient Rare Diseases (ARD): Presenting a Complex
Case of Probable Legg- Calvé- Perthes Disease From the North
Caucasian Bronze Age (2200- 1650 cal BCE).” International Journal of
Paleopathology 32: 61–73. https:// doi. org/ 10. 1016/j. ijpp. 2020. 11. 0 04.
Fusco, R., O. Larentis, and C. Tesi. 2021. “Paleopathological Evidence of
Legg- Calvé- Perthes Disease From the Medieval Cemetery of St. Agostino
in Caravate, Northwestern Italy.” Medicina Historica 5, no. 3: 1–5.
García Mat a, S., E. Arda naz Alcua, H. O vejero, and A. Martínez Gr ande.
2000. “Legg- Calvé- Perthes Disease and Passive Smoking.” Journal of
Pediatric Orthopaedics 20: 326–330.
García- Moreno, C., O. López- Costas, and E. Dorado Fernández. 2022.
“Un Caso de Enfermedad de Legg- Calvé- Perthes en la Necrópolis
Romana- Tardoantigua de la Ampliación del MNAR (Mérida, España).”
Revista Española de Antropología Física 46: 18–28.
Goodman, A., and J. Rose. 1991. “Dental Enamel Hypoplasias as
Indicators of Nutritional Status.” In Advances in Dental Anthropolog y,
edited by M. Kelly and C. Larsen, 279–293. New York: Wiley- Liss.
Gordon, J., P. Schoenecker, J. Osland, M. Dobbs, D. Szymanski, and S.
Luhman n. 2004. “ Smoking and Socio - Economic Stat us in the Etiology and
Severit y of Legg- Calvé- Per thes Disease.” Journal of Ped iatric Orthop aedics
B- 13: 367–370. https:// doi. org/ 10. 1097/ 01202 412- 20041 1000- 00003 .
Grauer, A. 2019. “Circulatory, Reticuloendothelial, and Hematopoietic
Disorders.” In Ortner's Identification of Pathological Conditions in
Human Skeletal Remains, edited by J. Buikstra, 491–529. San Diego:
Academic Press.
Gray, I., R. Lowry, and D. Renwick. 1972. “Incidence and Genetics of
Legg- Perthes Dis ease (Osteochondritis Defor mans) in British Columbia:
Evidence of Polygenic Determination.” Journal of Medical Genetics 9:
197–202. https:// doi. org/ 10. 1136/ jmg.9. 2. 197.
Groce, N., and I. Zola. 1993. “Multiculturalism, Chronic Illness, and
Disability.” Pediatrics 91, no. 5 Pt 2: 1048–1055.
Hall, A., and D. Barker. 1989. “Perthes' Disease in Yorkshire.” Journal
of Bone and Joint Surgery 71- B: 229–233. https:// doi. org/ 10. 1302/ 0301-
620X. 71B2. 2925740.
Hansen, J. H., and J. Nordkvist. 1996. “The Mummy Find From
Qilakitsoq in Northwest Greenland.” In Human Mummies: a Global
Survey of Their Status and the Techniques of Conservation, edited by
K. Spindler, H. Wilfing, E. Rastbichler- Zissernig, D. zur Nedden, and
H. Nothdurfter, 107–121. Vienna: Springer The Mummy Find From
Qilakitsoq in Northwest Greenland.
Herrerín, J., and M. Garralda. 2012. “Legg- Calvé- Perthes Disease
and Unifocal Eosinophilic Granuloma in a Visigoth From Duratón
Necropolis (Segovia, Spain).” International Journal of Osteoarchaeology
22: 86–97. https:// doi. org/ 10. 1002/ oa. 1189.
Herring, J. 2011. “Legg- Calvé- Perthes Disease at 100: A Review of
Evidence- Based Treatment.” Journal of Pediatric Or thopaedics 32, no. 2:
S137–S140. https:// doi. org/ 10. 1097/ BPO. 0b013 e3182 23b52d.
Hillson, S. 2001. “Recording Dental Caries in Archaeological Human
Remains.” International Journal of Osteoarchaeology 11: 249–289.
https:// doi. org/ 10. 1002/ oa. 538.
Hinkes, M. J. 1983. Skeletal Evidence of Stress in Subadults: Trying to
Come of Age at Grasshopper Pueblo (Arizona). Tuscon: University of
Arizona PhD thesis.
Holst, M. 2010. “Ost eological Ana lysis, Coppergate , York.” (Unpublished
Osteological Report, York Osteoarchaeology No. 1110).
Holst, M. and T. Loeffelmann. 2017. “Osteological Analysis, St. John's
Hospital, Birmingham Road, Lichfield, Staffordshire.” (Unpublished
Osteological Report, York Osteoarchaeology No. 1316).
Hooper, B. 1984. “Anatomical Considerations.” In Danebur y: An Iron
Age Hillfort in Hampshire. Vol. 2: The Excavations 1969- 1978: The
Finds, edited by B. Cuncliffe, 463–474. London: Council for British
Archaeology.
Inoue, A., M. Freeman, B. Vernon- Roberts, and S. Mizuno. 1976. “The
Pathogenesis of Perthes' Disease.” Journal of Bone and Joint Surgery 58-
B: 446 –453. https:// doi. org/ 10. 1302/ 0301- 620X. 58B4. 101803.
Jacobi, F., J. Pape, V. Dresely, and K. Alt. 2009. “Sonderbestattungen
der Vorrömischen Eisenzeit im Nordharzvorland? Ergebnisse der
Anthropologischen Bearbeitung der Skelettfunde der Fundstelle III von
Westerhausen, Lkr. Ha rz.” Jahresschrift für Mitteldeutsche Vorgeschichte
91, no. 2007: 293–328.
Jensen, O., and J. Lauritzen. 1976. “Legg- Calvé- Perthes' Disease:
Morphological Studies in Two Cases Examined at Necropsy.” Journal
of Bone and Joint Surgery 58- B, no. 3: 332–338. https:// doi. org/ 10. 1302/
0301- 620X. 58B3. 956251.
Jones, A. 2012. “Defining Catastrophe: Mass Burial at St Mary Spital.”
In A. Bioarchaeological Study of Medieval Burials on the Site of St Mary
Spital, edited by B. Connell, A. Jones, R. Redfern, and D. Walker, 217–
231. London: Lavenham Press.
16 of 17 International Journal of Osteoarchaeology, 2025
Joseph, B., V. Checko, B. Rao, and A. Hall. 1988. “The Epidemiology of
Perthes' Disease in South India.” International Journal of Epidemiolog y
17, no. 3: 603– 607. https:// doi. org/ 10. 1093/ ije/ 17.3. 603.
Józsa, L., and I. Pap. 2014. “Legg- Calvè- Perthes kór Középkori Leleten.”
Magyar Traumatológia 57: 127–132. https:// doi. org/ 10. 21755/ MTO.
2014. 057. 0203. 006.
Kealey, W., A. Moore, S. Cook, and A. Cosgrove. 20 00. “Deprivation,
Urbanisation a nd Perthes' Disease in Nor thern Ireland.” Journal of Bone
and Joint Surger y 82- B: 167–171. https:// doi. org/ 10. 1302/ 0301- 620X.
82B2. 0820167.
Keefe, K., M. Challanáin, and M. Holst. 2015. “Osteological Analysis,
Land to the Rear of California, Baldock, Hertfordshire.” (Unpublished
Osteological Report, York Osteoarchaeology No. 0515).
Khermosh, O., and S. Wientroub. 1991. “Dysplasia Epiphysealis
Capitoris Femoris. Meyer's Dysplasia.” Journal of Bone and Joint
Surger y (Br it i sh) 73, no. 4: 621–625. https:// doi. org/ 10. 1302/ 0301- 620X.
73B4. 1906473.
Kuo, K., K. Wu, P. Smith, S.- F. Shih, and H. A ltiok. 2011. “Cla ssifications
of Legg- Calvé- Perthes Disease.” Pediatric Orthopaedics 31, no. 2: 168–
173. https:// doi. org/ 10. 1097/ BPO. 0b013 e3182 23b50e.
Lauritzen, J. 1975. “Legg- Calvé- Per thes Disease: A Comparative Study.”
Acta Orthopaedica Scandinavica 46: 1–137. https:// doi. org/ 10. 3109/ ort.
1975. 46. suppl - 159. 01.
Li, N., J. Yu, X. Cao, et al. 2014. “A Novel p. Gly630Ser Mutation of
COL2A1 i n a Chinese Family With P resentations of Legg- Calvé- Perthes
Disease or Avascular Necrosis of the Femoral Head.” PLoS ONE 9, no. 6:
1–6. https:// doi. org/ 10. 1371/ journ al. pone. 0100505.
Lindblad, M., M. Bladh, H. Björnsson- Hallgren, G. Sydsjö, and T.
Johansson. 2024. “No Correlation to Collagen Synthesis Disorders in
Patients With Perthes's Disease: A Nationwide Swedish Register Study
of 3488 Patients.” BMC Musculoskeletal Disorders 25, no. 1: 42. ht tps ://
doi. org/ 10. 1186/ s1289 1- 023- 07161 - 8.
Lopes Dos Santos, C., and S. Ramos. 2004. “Resultados Preliminares
da Intervençao Antropológica no Largo da Sé e Praça dos Mártires.” In
Enfermeda d, Muerte y Cult ura en las Socied ades del Pasado: Imp ortancia
de la Contextualización en los Estudios Paleopatológicos: Proceedings
of the VIII Congreso Nacional de Paleopatología, edited by F. J. Barca
Durán and J. Jiménez Ávila, 424–432. Spain: Cáceres.
MacCurdy, G. 1923. “Human Skeletal Remains From the Highlands
of Peru.” American Journal of Physical Anthropolog y 6, no. 3: 218–329.
https:// doi. org/ 10. 1002/ ajpa. 13300 60302 .
Manzon, V., Z. Ferrante, M. Giganti, and E. Gualdi- Russo. 2 017. “On the
Antiquity of LeggCalvé- Perthes Disease: Skeletal Evidence in Iron Age
Italy.” Homo 68, no. 1: 10–17. https:// doi. org/ 10. 1016/j. jchb. 2016. 11. 002.
Marques, A., and E. Cunha. 1999. “A Paleopathological Evidence
of Perthes Disease.” In Proceedings of the V Congreso Nacional de
Paleopatología, edited by J. A. Sánchez Sánchez, 1–3. Alcalá La Real:
Asociación Española de Paleopatología y Ayuntamiento de Alcalá la
Real, Spain.
Mays, S. 19 91. “Part I: The Medieva l Burials From the Bl ackfriars F riary,
School Street, Ipswich, Suffolk (Excavated 1983–85).” (Unpublished
Report, Ancient Monuments Laboratory, Report 16/91 (Parts I and II)).
McKenzie, C., E. Murphy, and I. Watt. 2022. “Considering Care: A
Traumatic Obturator Fracture Dislocation of the Hip in a Middle-
Aged Man From Gaelic Medieval Ballyhanna, Co. Donegal, Ireland.”
International Journal of Palaeopathology 38: 115–122. https:// doi. org/
10. 1016/j. ijpp. 2 022. 07. 0 03.
Meyer, J. 1964. “Dysplasia Epiphysealis Capitis Femoris: A Clinical-
Radiological Syndrome and Its Relationship to Legg- Calvé- Perthes
Disease.” Acta Orthopaedica 34, no. 1–3: 183–197. https:// doi. org/ 10.
3109/ 17453 67640 8989316 .
Miyamoto, Y., T. Matsuda, H. Kitoh, etal. 2007. “A Recurrent Mutation
in Type II Collagen Gene Causes Legg- Calvé- Perthes Disease in a
Japanese Family.” Human Genetics 121: 625–629. https:// doi. org/ 10.
1007/ s0043 9- 007- 0354- y.
Molloy, M., and B. MacMa hon. 1966. “Incidence of Legg - Perthes Disea se
(Osteochondritis Deformans).” New England Journal of Medicine 275:
988–990. https:// doi. org/ 10. 1056/ NE JM1 96611 03275 1804.
Moloney, C., M. Hastie, T. Holden, J. Roberts, J. Franklin, and D.
Henderson. 2001. “New Evidence for the Origins and Evolution of
Dunbar: Excavations at the Captain's Cabin, Castle Park, Dunbar, East
Lothian.” Proceedings of the Society of Antiquaries of Scotland 131: 283–
317. https:// doi. org/ 10. 9750/ PSAS. 131. 283. 317.
Mose, K. 1980. “Methods of Measuring in Legg- Calvé- Perthes Disease
With Special Regard to Prognosis.” Clinical Orthopaedics and Related
Research 150: 103–10 9.
Moussavi, S., S. Chatterji, E. Verdes, A. Tandon, V. Patel, and B. Ustun.
2007. “Depression, Chronic Diseases, and Decrements in Health:
Results From the World Health Surveys.” Lancet 370, no. 9590: 851–858.
https:// doi. org/ 10. 1016/ S0140 - 6736(07) 61415 - 9.
Munyi, C. 2 012. “Past and Present Perc eptions of Disability: A H istorical
Perspective.” Disability Studies Quarterly 32, no. 2. https:// doi. org/ 10.
18061/ dsq. v32i2. 3197.
Murray, J., E. Holmes, and R. Misra. 2008. A- Z of Musculoskeletal and
Trauma Radiology. Cambridge: Cambridge University Press.
Myszka, A., H. Mańkowska- Pliszka, E. Rzeźnicka, A. Dąbkowska, and
J. Tomczyk. 2023. “Case St udy of Legg- Calvé - Perthes Disease in Radom
(Poland, 18th–19th Century) With Literature Review.” Anthropological
Review 86, no. 1: 23–26. https:// doi. org/ 10. 18778/ 1898- 6773. 86.1. 03.
Nieuwenhuys, O. 1994. Children's Lifeworlds: Gender, Welfare and
Labour in the Developing World. London: Routledge.
Ortner, D. 2003. Identif ication of Pathological Conditions in Human
Skeletal Remains. Second ed. San Diego: Academic Press.
Ortner, D., and W. Putschar. 1985. Identification of Pathological
Conditions in Human Skeletal Remains. Washington, DC: Smithsonian
Institution Press.
Perry, D. 2013. “Unravelling the Enigma of Perthes Disease.” Annals of
the Royal College of Surgeons of England 95: 311–316. https:// doi. org/ 10.
1308/ 00358 8413X 13629 96004 6192.
Perry, D., C. Bruce, D. Pope, P. Dangerfield, M. Platt, and A. Hall. 2 012b.
“Perthes' Disease of the Hip: Socioeconomic Inequalities and the Urban
Environment.” Archives of Disease in Childhood 97: 1053–1057. ht tps: //
doi. org/ 10. 1136/ archd ischi ld- 2012- 302143.
Perry, D., D. Machin, D. Pope, et al. 2012a. “Racial and Geographic
Factors in the Incidence of Legg- Calvé- Perthes' Disease: A Systematic
Review.” American Journal of Epidemiology 175, no. 3: 159–166. ht t ps://
doi. org/ 10. 1093/ aje/ kwr293.
Pillai, A., S. Atiya, and P. Costigan. 2005. “The Incidence of Perthes'
Disease in Southwest Scotland.” Journal of Bone and Joint Surgery [Br]
87: 1531–1535. https:// doi. org/ 10. 1302/ 0301- 620X. 87B11. 16744 .
Pinheiro, M., C. Dobson, D. Perry, and M. Fagan. 2018. “New Insights
Into the Biomechanics of Legg- Calvé- Perthes Disease: The Role of
Epiphyseal Skeletal Maturity in Vascular Obstruction.” Bone and Joint
Research 1: 148–156. https:// doi. org/ 10. 1302/ 2046- 3758. 72. BJR- 2017-
0191. R1.
Ponce, P. and M. Holst. 202 0. “Osteological A nalysis, Melton, E ast Riding
of Yorkshire.” (Unpublished osteological report, York Osteoarchaeology
No. 1020).
Ponce, P., and P. Novellino. 2014. “A Palaeopathological Example of
Legg- Calvé- Perthes Disease From Argentina.” International Journal of
Paleopathology 6: 30–33. https:// doi. org/ 10. 1016/j. ijpp. 2014. 03. 0 04.
17 of 17
Rampal, V., J.- L. Clément, and F. Solla. 2017. “Legg- Calvé- Perthes
Disease: Classifications and Prognostic Factors.” Clinical Cases in
Mineral and Bone Metabolism 14, no. 1: 74–82. https:// doi. org/ 10. 11138/
ccmbm/ 2017. 14.1. 074.
Ratliff, A. 1967. “Osteochondrontritis Dissecans Following Legg- Calvé-
Perthes' Disease.” Journal of Bone and Joint Surger y 49- B, no. 1: 108–
111. https:// doi. org/ 10. 1302/ 0301- 620X. 44B3. 562.
Rayner, P., S. Schwalbe, a nd D. Hall. 1986. “An Asses sment of Endocrine
Function in Boys With Perthes' Disease.” Clinical Orthopaedics and
Related Research 209: 124–128.
Roberts, C., and K. Manchester. 2012. The Archaeology of Disease. 3rd
ed. Stroud: History Press.
Röder, B. 2015. “Kinderarbeit Heute: Perspektiven Fur Die Ur- und
Frühgeschichte.” In With the Collaboration of R. Masanz, Levenswelten
von Kindern und Frauen in der Vormoderne. Archäologische und
Anthropolohische Froschungen in Memoriam Brigitte Lohrke. PAST—
Paläowissenschaftliche Studien 4, edited by R. Korey, 275–298. Berlin:
Curach Bhán.
Röder, B. 2018. “Prehistoric Households and Childhood: Growing up
in a Daily Routine.” In The Oxford Handbook of the Archaeology of
Childhood, edited by S. Crawford, D.Hadley and G.Shepherd. Oxford:
Elsevier Academic Press.
Rothhammer, F. 1990. “Ethnogenesis and Affinities to Other South
America n Aboriginal Popul ations.” In The Aymara. Strat egies in Human
Adaptation to a Rigorous Environment. Studies in Human Biology 2, ed-
ited by W. Schull and F. Rothhammer, 20 3–210. Netherlands, Dordrecht:
Springer.
Şahin, S. 2019. “Dilkaya (Orta Çağ) İnsanlarının Sağlık Yapısı.”
Antropoloji 37: 50–71. https:// doi. org/ 10. 33613/ antro poloj iderg isi.
5172 17.
Sellevold, B. 1999. “Picts and Vikings at Westness. Anthropological
Investigations of the Skeletal Material From the Cemetery at Westness,
Rousay, Orkney Islands.” NIKU Scientif ic Report 10: 1– 62.
Sevim, A., C. Pehlevan, A. Açikkol, H. Yilmaz, and E. Güleç. 2002.
“Karagündüz Erken Demir Çağı İskeletleri.” Arkeometri Sonuçları
Toplantısı 17: 49–57.
Smrčka, V., I. Marik, M. Svenssonova, and J. Likovsky. 2009. “Legg-
Calvé- Perthes Disease in Czech Archaeological Material.” Clinical
Orthopaedics and Related Research 467, no. 1: 293–297. https:// doi. org/
10. 1007/ s1199 9 - 00 8- 0527- 6.
Stulberg, S., D. Cooperman, and R. Wallensten. 1981. “The Natural
History of Legg- Calvé- Perthes Disease.” Journal of Bone and Joint
Surgery 63- A, no. 7: 1095–1108.
Su, P., R. Li, S. Liu, etal. 20 08. “Age at Onset- Dependent Presentations
of Premature Hip Osteoarthritis, Avascular Necrosis of the Femoral
Head, or Legg- Calvé- Perthes Disease in a Single Family, Consequent
Upon a p.Gly1170Ser Mutation of COL2A1.” Arthritis & Rheumatism 58,
no. 6: 1701–1706. https:// doi. org/ 10. 1002/ art. 23491 .
Su, P., L. Zhang, Y. Peng, A. Liang, K. Du, and D. Huang. 2010. “A
Histological and Ultrastructural Study of Femoral Head Cartilage in
a New Type II Collagenopathy.” International Orthopaedics 34, no. 8:
1333–1339. https:// doi. org/ 10. 1007/ s0 026 4- 010 - 0985 - 9.
Sundström, A., J. Mispelaere, and Y. Bäckström. 2018. “Above and
Below the Surface: Environment, Work, Death, and Upbringing in
Sixteenth- to Seventeenth Century Sweden.” In The Oxford Handbook
of the Archaeology of Childhood, edited by S. Crawford, D. Hadley, and
Shepherd. Oxford: Elsevier Academic Press.
Van Campenhout, A., P.Moens,and G.Fabry. 2007. “Reliability of Serial
Bone Scintigraphy Classification According to Conway in Legg- Calvé-
Perthes Disease.” Acta Orthopaedica Belgica 73, no. 2: 196–199.
Waldron, T. 2007. Palaeoepidemiology: The Epidemiology of Human
Remains. California: Left Coast Press.
Waldron, T. 2009. Palaeopathology. Cambridge: Cambridge University
Press.
Walker, D. 2012. Disease in London, 1st- 19th Centuries, An Illustrated
Guide to Diagnosis, 56. London: Museum of London Archaeology
(Mola) Monograph.
Wasterlain, S., and C. Umbelino. 2014. “Legg- Calvé- Perthes Disease
and Slipped Femoral Capital Epiphysis in the Skeletal Remains of the
Mediaeval Necropolis of Santa Maria (Sintra, Portugal).” Cadernos do
GEEvH 2, no. 2: 27–39.
Weinstein, S. 2000. “Long- Term Follow- Up of Pediatric Orthopaedic
Conditions. Natural Histor y and Outcomes of Treatment.” Journal of
Bone and Joint Surgery 82A, no. 7: 980–990. https:// doi. org/ 10. 2106/
00004 623- 20000 7000- 00010 .
Wiig, O. 2009. “Perthes' Disease in Norway. A Prospective Study on 425
Pat ients.” Thesis. Acta Orthopaedica 80, no. 333: 1–44. https:// doi. org/
10. 1080/ 17453 69 061 00 46594.
Wiig, O., T. Terjesen, S . Svenni ngsen, and S. L ie. 200 6. “T he Epidemiology
and Aetiology of Perthes' Disease in Norway: A Nationwide Study of
425 Patients.” Journal of Bone and Joint Surgery [Br] 88- B: 1217–1223.
https:// doi. org/ 10. 1302/ 0301- 620X. 88B9. 17400 .
Yang, H., X. Xu, W. Bullock, and R. Main. 2019. “Adaptive Changes in
Micromechanical Environments of Cancellous and Cortical Bone in
Response to in Vivo Loading and Disuse.” Journal of Biomechanics 89:
85–94. https:// doi. org/ 10. 1016/j. jbiom ech. 2019. 04. 021.