AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 137:48–59 (2008)
Investigating the Specificity of Periosteal Reactions
in Pathology Museum Specimens
Darlene A. Weston1,2*
1
Department of Human Evolution, Max Planck Institute for Evolutionary Anthropology, 04103 Leipzig, Germany
2
Institute of Archaeology, University College London, London WC1H 0PY, UK
KEY WORDS periostitis; nonspecific infection; inflammation; paleopathology
ABSTRACT The relationship between periosteal new
bone formation and a number of infectious and metabolic
conditions frequently seen in archeological human skele-
tal remains was investigated by studying human long
bones demonstrating periosteal new bone formation
archived in two London, UK, pathology museums: the
St. George’s Hospital Pathology Museum and the Hunt-
erian Museum. The samples were subjected to macro-
scopic and radiographic analysis to determine if the
characteristics of their periosteal lesions were specific to
the corresponding disease states. The results demon-
strated that no qualitative or quantitative characteristics
of the periosteal reactions emerged that were specific to
Proliferative periosteal reactions, or ‘‘periostitis,’’ as
they are often termed, are a common occurrence in ar-
cheological skeletal remains, being frequently seen on
the long bones, especially the tibiae. This periosteal new
bone formation, occurring as a response to extrinsic or
intrinsic pathological factors, initially has the character-
istic appearance of woven bone, and remodels over time
into lamellar bone. In spite of its ubiquitous nature, very
little investigation of periosteal reactions and how they
relate to specific pathological conditions has occurred.
Bioarcheologists have most commonly interpreted peri-
osteal new bone formation as evidence for nonspecific in-
fectious disease in past populations, with recent syn-
thetic works (Larsen, 1997; Steckel and Rose, 2002)
continuing the trend that was popularized by Cohen and
Armelagos, 1984 influential volume, Paleopathology at
the Origins of Agriculture. Additionally, periosteal new
bone formation also plays a central role in the ‘stress-in-
dicator hypothesis’ (Goodman et al., 1988), within which
periosteal reactions are again deemed to be a sign of in-
fectious disease. This interpretation of periosteal reac-
tions has continued despite a wealth of clinical literature
(e.g. Resnick, 1995; Adler, 2000) indicating multiple
pathological etiologies for proliferative periosteal reac-
tions, and has resulted in generalizations made about
pathogen load models in archaeological populations.
The purpose of this paper is to present the results of
recent research investigating the relationship between
periosteal new bone formation and a number of infec-
tious and metabolic pathological conditions; testing
whether periosteal new bone formation manifests differ-
ently depending on its etiology. To achieve these ends,
macerated dry long bones curated in pathology museums
with records relating to known pathological conditions
were analyzed macroscopically and radiographically. Bio-
archaeology employs biomedical clinical analogy in the
recording and interpretation of the ancient evidence for
C 2008
V WILEY-LISS, INC.
individual disease states. It was established that disease
progression, rather than disease type, was the most im-
portant determinant of periosteal lesion appearance. A
critical analysis of the bioarcheology literature pertain-
ing to the recording and interpretation of periosteal reac-
tions determined that the varied pathogenesis of perios-
teal new bone formation has been largely ignored in
favor of a diagnosis of ‘‘nonspecific infection.’’ Assump-
tions regarding the infectious etiology of periosteal
lesions have become embedded into the bioarcheology lit-
erature potentially skewing the results of skeletal popu-
lation-based paleoepidemiological studies. Am J Phys
Anthropol 137:48–59, 2008. V 2008 Wiley-Liss, Inc.
C
disease, assuming that the same pathological changes in
skeletal remains used in the diagnosis of a clinical
patient can be applied as diagnostic criteria in the inter-
pretation of ancient material (Klepinger, 1983). Thus, in
order to characterize how different pathological condi-
tions manifest periosteal new bone formation, diagnosed
diseased bones exhibiting this feature must be examined.
If the characteristics of the periosteal new bone can be
correlated with a particular pathological condition, it fol-
lows that the techniques could be applied to archeologi-
cal bones, the correlated characteristics could be identi-
fied, and a diagnosis might be made. Pathology muse-
ums are prime repositories of skeletal reference material
of this type, offering specimens with a wide range of
associated pathological conditions and, as such, skeletal
material from two British pathology museums, the
Hunterian Museum at the Royal College of Surgeons of
England and St. George’s Hospital Pathology Museum
were examined.
MECHANISMS OF PERIOSTEAL NEW
BONE PRODUCTION
Periostitis is a poor word for periosteal new bone pro-
duction because by definition it assumes that inflamma-
*Correspondence to: Darlene A. Weston, Department of Human
Evolution, Max Planck Institute for Evolutionary Anthropology,
Deutscher Platz 6, 04103 Leipzig, Germany.
E-mail: weston@eva.mpg.de
Received 2 August 2007; accepted 25 January 2008
DOI 10.1002/ajpa.20839
Published online 8 April 2008 in Wiley InterScience
(www.interscience.wiley.com).
 SPECIFICITY OF PERIOSTEAL REACTIONS IN PATHOLOGY MUSEUM SPECIMENS
tion has occurred (Ragsdale, 1993). However, the mecha-
nisms involved can be much more complex, as almost
anything that breaks, tears, stretches, or even touches
the periosteum (the membrane of connective tissue that
surrounds all bones, except on their articular surfaces)
can stimulate it into initiating bone formation
(Richardson, 2001). The physical elevation of the perios-
teum is often cited as a requirement for the initiation of
periosteal new bone production. Physical elevation may
be present, but it is not a prerequisite for a reaction,
meaning other factors must be operative (Ragsdale,
1993). Likely choices include mechanical adaptation or a
compensation for weakness secondary to underlying
bone resorption, attempts at tumor containment, altered
circulation, and perhaps bone inductive products ema-
nating from tumors (Ragsdale et al., 1981; Ragsdale,
1993).
Lesions that are caused by the elevation of the fibrous
outer layer of the periosteum are formed after the com-
pression and stretching of blood vessels by agents such
as blood, pus, granulation tissue, neoplasm or trauma
(Bush, 1989). This may result in bleeding beneath the
periosteum, with a subsequent reduced blood supply to
the bone. If this situation is of sufficient duration, the
periosteal bone tissue will die. Amelioration of the blood
vessels will restore osteoblastic activity, producing new
subperiosteal bone that is deposited on the normal corti-
cal bone surface (Jaffe, 1972; Bush, 1989). A row of
refilled Howship’s lacunae forming a reversal line can
usually be seen on the original cortical surface beneath
the newly added bone, testifying to an initial resorptive
phase probably due to active hyperemia (increased blood
flow) (Ragsdale, 1993).
Inflammation vs. infection
Inflammation has an important role to play in the eti-
ology of periosteal new bone production. Although as
previously stated, it is not always present when a perios-
teal reaction arises, it frequently occurs as a general
response to abnormal stimuli such as trauma, neoplastic
disease, or infectious agents (Ortner, 2003), and thus
stimulates periosteal reactions to occur. It is a frequent
practice in studies of archaeological skeletons to attrib-
ute the majority of periosteal lesions to infection,
perhaps due to confusion between the definitions of
inflammation and infection (i.e. Lallo, 1973; Mensforth
et al., 1978; Littleton, 1998). Inflammation is the body’s
vascular response to tissue damage from a variety of
causes, while infection occurs when the body encounters
pathogenic organisms, usually bacteria. Part of the
body’s reaction is to mount an inflammatory response to
neutralize the organism and repair or heal damage.
Although infections are among the most common causes
of the inflammatory response, not all such responses are
caused by infection (Bush, 1989).
The inflammatory process occurs no matter what the
cause of the injury, and is initially acute in nature, last-
ing only a few days. The initial inflammatory response,
termed acute inflammation, follows the same predictable
course: widening of the blood vessels (vasodilatation),
fluid exudation, and phagocyte recruitment. These proc-
esses are all localized at the site of injury and occur
approximately within one hour of the injury occurring
(Mitchinson et al., 1996). If the causative agent persists
(more than about 2 weeks), the inflammatory process
becomes prolonged and is termed chronic inflammation,
49
a more complicated process due to its longer duration,
which allows for a wide variety of patterns of inflamma-
tory mechanisms to come into play. In bone, vasodilata-
tion through hyperemia results in hyperoxia (an increase
in oxygen), which stimulates osteoclast function. Fluid
exudation results in edema, an excess accumulation of
fluid, which causes hypoxia (a decrease in oxygen),
which in turn stimulates osteoblast function. These dif-
fering and sequential oxygen states are crucial in the os-
seous changes of bone inflammation (Roberts and Man-
chester, 1997).
If the inflammatory process is successful, healing
begins. The inflammatory process inevitably results in a
mass of dead tissue and cells, and healing must occur to
replace this matter via the scavenging of dead material,
the regeneration of lost tissue, and repair (Mitchinson
et al., 1996). In bone, scavenging is performed by macro-
phages and osteoclasts. Repair of the bone tissue
involves the formation of granulation tissue, a type of
loose connective tissue abundant in capillary buds, osteo-
blasts, macrophages, and other inflammatory cells. The
granulation tissue creates organization out of a disorgan-
ized mess, and once its job is complete, the tissue
becomes less vascular and less cellular, with the inflam-
matory cells disappearing, the osteoblasts turning into
osteocytes, and the tissue fluid reabsorbing into the
shrinking vasculature. The granulation tissue becomes
the periosteal new bone, initially composed of woven
bone and gradually converted into lamellar bone through
remodeling.
PERIOSTEAL REACTIONS IN PAST STUDIES
The modern clinical literature
The modern clinical literature pertaining to periosteal
new bone production as a whole provides little or no
description of the phenomenon itself. For the most part,
it is merely stated that ‘‘periostitis’’ is present as part of
the manifestations of the clinical disease. There are few
descriptions of specific locations or types of periosteal
reactions, nor are there any gradings of periosteal lesion
severity. Some of these difficulties found within the mod-
ern clinical literature are based on the fact that the ma-
jority of researchers rely on radiographs or other types
of imaging to report on and diagnose the pathological
conditions. Unfortunately, periosteal new bone in its ear-
liest stages does not always appear evident on radio-
graphs and other imaging media and is likely to be over-
looked in autopsies (Kelley, 1989). Regardless, most peri-
osteal reactions are part of the expression of a specific,
identifiable disease process (Ortner, 2003) (see Table 1)
that spans a varied range of conditions, falling under
the categories of trauma, joint, infectious, metabolic, vas-
cular and neoplastic disease.
The bioarcheology literature
Because of its pervasiveness, periosteal new bone pro-
duction is a widely recorded feature of archaeological
skeletons, often being used to assess infectious disease
at the population level. For example, across a sample of
British skeletal populations, prevalence rates for tibial
‘‘periostitis’’ have been recorded as ranging from 5.9% to
8% (Coughlan and Holst, 2000) to 64% (Holst et al.,
2001) (see Table 2). It is often difficult to assess the
number of skeletons with tibial periosteal reactions in
American Journal of Physical Anthropology
50
TABLE 1. Some pathological conditions manifesting periosteal new bone production (after Resnick 1995)
Pathological category
Trauma
Circulatory disorders
Joint disease
Haematological disease
Skeletal dysplasias
Infectious disease
Metabolic disease
Neoplastic disease
D.A. WESTON
Specific conditions
Battered baby syndrome, burns, shin splints
Congenital heart defect, hypertrophic osteoarthropathy, polyarteritis nodosa, venous stasis
Crohn’s disease and primary biliary cirrhosis (as enteropathic arthropathies), psoriatic arthritis,
Reiter’s syndrome, rheumatoid arthritis
Myelofibrosis
Infantile cortical hyperostosis
Bone mycoses, congenital and venereal syphilis, leprosy, osteomyelitis, tropical ulcer,
tuberculosis, yaws
Fluorosis, healing rickets, hypervitaminosis A, renal osteodystrophy, scurvy, thyroid acropachy
Various neoplasms

TABLE 2. Prevalence rates for tibial periosteal reactions in a sample of British skeletal populations
% of population
Site Period affected Authors Context
Kempston, Bedfordshire Romano-British (AD 43-410) 25% Boylston and Roberts, 1996 Rural cemetery
Eccles, Kent Anglo-Saxon (AD 410-1066) 22–25% Boocock et al., 1995 Rural cemetery
Towton, North Yorkshire Medieval (AD 1461) 5.9–8% Coughlan and Holst, 2000 Mass battlefield grave
St Helen-on-the-Walls, York Medieval (c. AD 1100-1550) 22.4% Grauer, 1993 Urban cemetery
St Andrew’s Fishergate, York Medieval (c. AD 1200-1538) 23% Stroud and Kemp, 1993 Monastic cemetery
Hospital of St James and Medieval (c. 12th-16th C) 39% Lee, 2001 Hospital cemetery
St Mary Magdalene,
Chichester, West Sussex
Hull Magistrates’ Court, Medieval (c. AD 1300-1450) 64% Holst et al., 2001 Monastic cemetery
Kingston-upon-Hull

published reports and articles due to differences in re-
cording and reporting these types of lesions.
In the bioarcheology literature, periosteal new bone
production is often mentioned as a result of specific in-
fectious disease, such as tuberculosis (e.g. Kelley et al.,
1994; Roberts et al., 1994), the treponematoses (e.g.
Hackett, 1976; Schermer et al., 1994), and leprosy (e.g.
Lewis et al., 1995; Roberts and Manchester, 1997). Occa-
sionally it is mentioned in association with syndromes
such as hypertrophic osteoarthropathy (Fennell and
Trinkaus, 1997), or trauma (Detweiler-Blakely, 1988).
However, it is most frequently discussed as a product of
nonspecific infection (e.g. Pfeiffer and Fairgrieve, 1994;
Larsen, 1997).
When using the term ‘‘nonspecific infection’’ in this
way, it implies that an infection of some sort was visited
upon an individual, its manifestation was a periosteal
reaction, but the exact pathological organism involved
in the infection is unknown. The ‘‘nonspecific infection’’
is thus not an entity unto itself; it is essentially an
abbreviation of ‘‘I don’t know what caused this perios-
teal new bone formation.’’ The majority of bioarcheology
papers offer few precise descriptions as to the location
or type of periosteal lesion present in an archaeological
skeleton. Most papers simply state that ‘‘periostitis’’
was present on the shaft of a tibia or another bone (e.g.
Lallo et al., 1978; Hodges, 1987; Palfi et al., 1992). The
terminology used by bioarcheologists to describe and
classify periosteal reactions has been inconsistent. A
number of researchers have devised classification sys-
tems for use in the analysis and description of perios-
teal new bone production including: Lallo (1973);
Strothers and Metress (1975); Cook (1976); Hackett
(1976); Lallo et al. (1978); Mensforth et al.(1978); Gra-
uer (1993), and Buikstra and Ubelaker (1994), but
unfortunately no recording system has been universally
adopted.
MATERIALS AND METHODS
Pathological specimens from two London, U.K. pathol-
ogy museums, St. George’s Hospital Pathology Museum
and the Hunterian Museum were selected for study. For
inclusion in the research, specimens had to be long
bones exhibiting pathologically induced periosteal new
bone, and had to be modern, pre-antibiotic, macerated,
dry, and unmounted.
St. George’s Hospital Pathology Museum is located
within the Histopathology Department of the hospital’s
medical school. The majority of the selected study speci-
mens had been in the museum’s collections prior to 1866
(Ogle and Holmes, 1866) and were obtained from patient
autopsy (see Table 3). The Hunterian Museum is located
within the Royal College of Surgeons of England and
contains specimens collected by the surgeon and anato-
mist John Hunter (1729–1793), those donated by other
18th and 19th century surgeons and physicians, and the
skeletons of executed felons acquired for anatomical
demonstration (RCSE, 2006). Specimens examined from
the Hunterian Museum are presented in Table 4.
When employing pathology museum specimens in com-
parative research, a number of factors must be taken
into consideration. Pathology museum specimens usually
consist of single bone elements and are displayed as
such. For example, if a researcher wanted to look at os-
seous syphilitic specimens, he/she would find skulls with
caries sicca displayed together in one case, single tibiae
with syphilitic lesions displayed in another, and perhaps
there may be a syphilitic fibula, ulna, or humerus. The
bones of complete individuals, if present, are rarely dis-
played together, prohibiting the viewing of the overall
distribution of skeletal lesions. There appears to be a
general lack of interest in the individual from whence
the pathological specimen came. Age and sex data
regarding the specimen is rarely provided, nor is patient

American Journal of Physical Anthropology

 SPECIFICITY OF PERIOSTEAL REACTIONS IN PATHOLOGY MUSEUM SPECIMENS 51
TABLE 3. St. George’s Pathology Museum study specimens TABLE 5. System for scoring periosteal new bone production
and periosteal vascularization (after Cook, 1976)
Specimen no. Bone(s) Diagnosed condition
Type of woven or lamellar periosteal lesion
98.39C Tibia Chronic osteomyelitis
98.39I Tibia and fibula Osteomyelitis and fracture 1. Normal
98.39K Tibia Ulcer 2. Isolated elevated plaque or plaques covering
98.39L Fibula Chronic periostitis less than one third of the functional/vascular surface
98.39M Tibia Chronic osteomyelitis 3. As above covering one to two thirds of the
98.39N Tibia and fibula Periostitis functional/vascular area
98.39O Tibia and fibula Chronic periostitis 4. Uniform elevation of two thirds or more of the
98.39R Tibia Chronic osteomyelitis area with little increase in diameter
98.39U Femur Chronic osteomyelitis 5. As above with elevation of more than 2–3 mm
98.39X Femur Chronic osteomyelitis Periosteal vascularization
(Brodie’s abscess) 1. Normal
98.56B Femur Rickets 2. Multiple small* striae
98.56C Fibula Rickets 3. Multiple small* foramina
98.56D Tibia and fibula Rickets 4. Multiple large striae
98.372C Tibia Syphilis 5. Multiple large foramina
6. Mixed abnormal vascularization

* Small is defined as pinpoint in diameter (for foramina) or pin-

TABLE 4. Hunterian Museum study specimens point in depth (for striae).

Specimen no. Bone Diagnosed condition

P616, P617, P618, Tibia Acute osteomyelitis ing of the following information: 1) anatomical location(s)
P621, P622, P623
P639 Humerus Necrosis
of the periosteal lesion(s); 2) the size of the periosteal
P644, P645 Femur Necrosis lesion(s) in mm (essentially determining whether a lesion
P649, P650 Tibia Necrosis is focal or diffuse); 3) the type of periosteal lesion(s),
P660, P661, P662, Fibula Necrosis whether consisting of woven bone, lamellar bone or
P663, P664 mixed; 4) the type of woven or lamellar periosteal
P683 Fibula Chronic osteomyelitis lesion(s) based on Cook’s (1976) criteria (see Table 5);
in leg ulcers 5) the type of periosteal vascularization, also based on
P684, P685, P686, P688, Tibia Chronic osteomyelitis Cook’s (1976) criteria (see Table 5); 6) the severity stage
P689, P690, P691 in leg ulcers of the lesion(s) based on Lallo’s (1973) criteria (see
P687 Fibula Chronic osteomyelitis
in leg ulcers
Table 6); and 7) the type of periosteal reaction present
P692, P695, P697 Tibia Osteoplastic periostitis based on Hackett’s (1976) criteria (see Table 7).
P693, P694 Femur Osteoplastic periostitis All measurements were taken with sliding digital cali-
P696 Humerus Osteoplastic periostitis pers and, to compensate for intra-observer error, meas-
P698, P699, P700, Fibula Osteoplastic periostitis urements were repeated three times with the average
P701, P703 measurement recorded. Qualitative characteristic were
P729, P730, P731, Femur Syphilis recorded twice, to see if consistency was maintained.
P732, P745 The exact anatomical location and size of the perios-
P761 Tibia Rickets teal reaction is of great importance as it has been recog-
nized that different diseases have predilections for differ-
ent locations on a bone (Ortner, 2003). To obtain precise
history. Pathology museums tend to specialize in spectac- information regarding lesion location, each bone was di-
ular-looking rare conditions such as congenital oddities vided into seven sections: proximal and distal epiphyses,
or unusual tumors, lacking the representation of a proximal and distal metaphyses, and proximal, middle,
wider-range of skeletal pathology and more commonly and distal thirds of diaphysis, and the locations of the
occurring diseases. Additionally, there is a problem asso- periosteal lesions were identified within these sections.
ciated with the diagnostic certainty of the pathology mu- Periosteal lesions could span various sections, and multi-
seum specimens. The specimens were largely collected ple lesions in discontinuous sections could occur. When
by medical practitioners who did not have modern diag- determining the size of a lesion, it is not the actual nu-
nostic capabilities and as specimens were diagnosed merical measurement that is of concern, but whether the
using the state of the art at the time; many could most lesion is focal or diffuse, with the measurement aiding in
certainly have been misdiagnosed. However, pathology this determination. A focal, clearly defined lesion with
museums are arguably the only sources of pathological distinct boundaries is more likely to be of a nonsystemic
bone specimens from the pre-antibiotic era, a crucial nature, while a diffuse lesion that covers a large area
necessity for comparing data with archaeological skele- and has obscured boundaries is more likely to be sys-
tons. If a biomedical clinical analogy framework is to be temic (Ortner, 2003). Periosteal lesions with distinct
employed, researchers must simply be cautious in their boundaries tend to exhibit a clear division between the
interpretations, as pathology museum specimens are too periosteal new bone and the underlying bone cortex,
precious a resource to ignore. while lesions with indistinct boundaries tend to blend in
with the underlying cortex, making it difficult to deter-
mine where the lesion begins or ends.
Macroscopic analysis The type of periosteal new bone present in the lesion,
whether woven, lamellar, or a mixture of the two types,
Macroscopic analysis of the long bones involved exam- indicates whether the lesion was active, healed or heal-
ining the outer cortical surfaces of the bones and record- ing at the time of death, and thus provides information

American Journal of Physical Anthropology

52 D.A. WESTON
TABLE 6. Periosteal lesion severity stages (after Lallo, 1973)

Stage 1 Smooth and undamaged periosteal surface Represents appearance of tibia not yet afflicted
by infection
Stage 2 Longitudinal striations begin to appear in at least Initial stages of disease wherein periosteal damage and
three quarters*, two of which must be continuous destruction is only beginning
up and down
Stage 3 From 1 to 3 noncontinuous quarters with mild pitting
and swelling
Stage 4 At least 4 noncontinuous quarters with moderate
pitting and swelling
Stage 5 At least one local large swelling with moderate pitting From stage 5 onward periosteal damage and destruction
in three quarters becomes more acute
Stage 6 Three or more noncontinuous quarters exhibit swelling; or
two continuous quarters (up and down) exhibit swelling;
or one zone may exhibit swelling and scaling
Stage 7 Heavy pitting in at least one zone (zones may consist of
noncontinuous quarters)
Stage 8 Heavy pitting in at least two continuous quarters Stages 8 and 9 represent extremely heavy periosteal
destruction
Stage 9 Heavy pitting of periosteum over the entire area of three
continuous quarters and part of the fourth

* The bone was divided into four parts, each being defined as a ‘‘quarter’’: proximal epiphysis and metaphysis, proximal diaphysis,
distal diaphysis, distal metaphysis, and epiphysis.

TABLE 7. Types of periosteal reaction (Hackett, 1976)
Normal bone with surface changes
1. Normal bone with plaques
2. Normal bone with fine striation
3. Normal bone with superficial sequestra
4. Nodes/expansions with plaques
5. Finely striate nodes/expansions
6. Coarsely striate and pitted expansions
7. Rugose nodes/expansions–slight changes, mostly nodes
8. Rugose nodes/expansions–moderate changes,
mostly expansions
9. Rugose nodes/expansions–gross changes
Nodes/Expansions with destruction
10. Massive destruction–sequestra and expansions
11. Focal destruction – nodes/expansions with superficial
cavitation
12. Focal destruction – metaphyseal expansion and cavitation
Expansions and deformity
13. Platforms
14. Bowing and expansion
about the state of the underlying disease. Woven bone,
with its characteristic grey color, porous and disorgan-
ized appearance, and sharp unremodeled edges, often
appears to be resting on top of the cortical bone surface
and is indicative of a disease process that was still active
at the time of death. Active lesions may have contributed
to the death of an individual, but may not have neces-
sarily caused it. Lamellar bone, usually the same color
as the surrounding bone, with a more organized appear-
ance and rounded remodeled edges, indicates a healed
lesion, i.e. the person survived. A periosteal reaction con-
sisting of both woven and lamellar bone indicates the
lesion was in the process of healing when the individual
died (Roberts and Manchester, 1997).
Radiographic analysis
Each bone was radiographed using Kodak Industrex
AA400 Ready Pack industrial X-ray film. The St.
George’s specimens were radiographed using a Hewlett-
Packard Faxitron machine, while the Hunterian speci-
mens were radiographed with a Todd Research TR X-ray
inspection cabinet machine. On both machines a tube
voltage of 50 kV was used, electrical current flow was
fixed at 3 mA, film to X-ray source distance was
275 mm, and exposure times varied between 10 s and 1
min and 30 s, depending on the bone element and nature
of the pathology. The resulting radiographs were hand
processed using the standard sequence of developer, stop
bath, fixer, and running water wash.
The radiographs were examined and the following in-
formation recorded: 1) appearance of the cortex (gross,
permeated, geographic, or moth-eaten destruction;
replacement of the cortex by periosteal new bone,
increased and decreased cortical thickness) (Greenfield,
1986); 2) appearance of the endosteal surface (new bone
formation in the medulla and on the endosteal surface,
endosteal destruction, thickening of the endosteum, and
bony bridges linking endosteal surfaces) (ibid.); 3) type
of periosteal reaction (Edeiken et al., 1966; Edeiken,
1981) (see Table 8); 4) location of lesion(s); 5) size of
lesion(s) in mm; and 6) margination of lesion(s) (distinct
or indistinct) (Greenfield, 1986). Most periosteal reac-
tions are easily recognized as opaque grey shadows
occurring alongside the dense, white radiographic
appearance of the cortical bone and often, but not
always, there is a distinct, thin black line that separates
the periosteal reaction from the cortex. All radiograph
measurements were taken with sliding digital calipers.
To compensate for intra-observer error, all measure-
ments were repeated three times with the average mea-
surement recorded, and qualitative characteristics were
recorded twice to see if consistency was maintained. The
majority of clinical papers regarding typologies of perios-
teal reaction are based on the radiographic analysis of
tumors (Edeiken et al., 1966; Edeiken, 1981; Ragsdale
et al., 1981; Ragsdale, 1993; Resnick, 1995), though the
authors state that their devised classifications are also
applicable to periosteal reactions associated with various
types of non-neoplastic diseases.
Statistical analysis of the macroscopic and radio-
graphic results was conducted using one way analysis of

American Journal of Physical Anthropology

 SPECIFICITY OF PERIOSTEAL REACTIONS IN PATHOLOGY MUSEUM SPECIMENS 53
TABLE 8. Radiographic types of periosteal new bone production (Edeiken et al., 1966, Edeiken, 1981)
1 Solid
a Dense undulating Greater than 10 mm thick, with a rough and undulating free edge
b Thin undulating Less than 10 mm thick, with a rough and undulating free edge
c Dense elliptical From 2 mm to 10 mm, thickest in the centre and tapering towards both ends,
usually permeated by osteolytic areas
d Cloaked Several mm thick, irregularly dense, with straight free margin
e Codman’s (tri)angle Small angle formed by ossified raised periosteum and the surface of the bone
2 Interrupted

a Lamellated Multiple thin layers

b Perpendicular New bone growing at right angles to the shaft of the host bone
c Amorphous Often oval or spherical shaped, vary in thickness from millimetres to centimetres

Fig. 1. Box plot comparing macroscopically visible lengths of Fig. 2. Box plot comparing macroscopically visible widths of
periosteal lesions. Transverse line represents median, box is periosteal lesions.
interquartile range, whiskers represent spread, circles represent
outliers, and stars represent extreme outliers.

variance (ANOVA), Tukey’s HSD post hoc test, paired-

samples t Tests, and Wilcoxon signed ranks test in SPSS
version 13.0.
It should be noted that histological analysis of a num-
ber of bones from the St George’s Hospital Pathology
Museum was undertaken using back-scattered electron
scanning electron microscopy (Weston, 2004). The results
of this analysis will be the focus of a subsequent paper
(Weston, in prep).

RESULTS
Fifty-six bones were examined macroscopically and
radiographically (12 from the St. George’s Hospital Pa-
thology Museum and 44 from the Hunterian Museum)
and the macroscopic characteristics and roentgen fea-
tures of the periosteal lesions were recorded as outlined
above. The bones were grouped together under their re- Fig. 3. Box plot comparing macroscopically visible lesion
areas.
spective pathology museum disease categories: osteomye-
litis, necrosis, leg ulcer, syphilis, rickets, and ‘‘periostitis.’’

Macroscopic analysis
The sizes of the periosteal lesions are of interest
because the more diffuse a lesion is, the more likely it is
to result from a systemic pathological condition. Sys-
temic diseases such as syphilis, seem to have diffuse
lesions that are larger and more widely spread over the
surface of a bone (Chiu and Radolf, 1994). Conversely,
focal lesions such as those seen in leg ulcers are usually
contained, smaller, localized reactions affecting single
bone elements (Lippman and Goldin, 1961). As illus-
trated by Figures 1 and 2, most of the ranges of both the
lengths (parallel to the diaphysis) and widths (perpendic-
ular to the diaphysis) of the lesions in all disease catego-
ries overlapped one another. Statistical analysis of the
macroscopic lesion length determined that there was a

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54 D.A. WESTON
TABLE 9. Frequency of anatomical positions of macroscopically and radiographically visible periosteal lesions
across disease categories
Macroscopically visible Radiographically visible
Anatomical position O* N U S R P O N U S R P
Proximal epiphysis 0.04 0.07 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.03
Proximal epiphysis to proximal metaphysis 0.00 0.00 0.00 0.00 0.00 0.00 0.05 0.00 0.00 0.00 0.00 0.00
Proximal epiphysis to proximal third of diaphysis 0.00 0.07 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00
Proximal epiphysis to mid-shaft 0.00 0.07 0.00 0.00 0.00 0.00 0.19 0.00 0.00 0.00 0.00 0.00
Proximal epiphysis to distal third of diaphysis 0.00 0.00 0.00 0.00 0.00 0.00 0.10 0.00 0.00 0.17 0.00 0.00
Proximal epiphysis to distal metaphysis 0.00 0.00 0.07 0.00 0.00 0.00 0.00 0.06 0.00 0.00 0.00 0.00
Proximal epiphysis to distal epiphysis 0.21 0.00 0.07 0.00 0.00 0.05 0.19 0.06 0.00 0.17 0.00 0.00
Proximal metaphysis 0.00 0.13 0.00 0.00 0.00 0.00 0.05 0.00 0.00 0.17 0.00 0.00
Proximal metaphysis to proximal third of diaphysis 0.04 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.08 0.00 0.06
Proximal metaphysis to mid-shaft 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.22 0.06 0.00 0.20 0.03
Proximal metaphysis to distal third of diaphysis 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.06 0.17 0.08 0.00 0.06
Proximal metaphysis to distal metaphysis 0.08 0.00 0.00 0.13 0.00 0.10 0.19 0.00 0.17 0.33 0.00 0.09
Proximal metaphysis to distal epiphysis 0.04 0.07 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.03
Proximal third of diaphysis 0.04 0.00 0.07 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00
Proximal third of diaphysis to mid-shaft 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.17 0.06 0.00 0.20 0.00
Proximal third of diaphysis to distal third 0.00 0.00 0.14 0.63 0.00 0.35 0.00 0.00 0.00 0.00 0.00 0.13
of diaphysis
Proximal third of diaphysis to distal metaphysis 0.00 0.00 0.00 0.00 0.00 0.10 0.00 0.17 0.22 0.00 0.00 0.13
Proximal third of diaphysis to distal epiphysis 0.00 0.00 0.00 0.00 0.20 0.10 0.00 0.06 0.00 0.00 0.00 0.13
Mid-shaft 0.04 0.13 0.14 0.00 0.80 0.00 0.00 0.00 0.00 0.00 0.20 0.00
Mid-shaft to distal third of diaphysis 0.04 0.00 0.07 0.00 0.00 0.05 0.00 0.00 0.00 0.00 0.00 0.03
Mid-shaft to distal metaphysis 0.00 0.00 0.00 0.00 0.00 0.05 0.05 0.00 0.28 0.00 0.00 0.09
Mid-shaft to distal epiphysis 0.17 0.00 0.07 0.00 0.00 0.00 0.10 0.11 0.00 0.00 0.00 0.13
Distal third of diaphysis 0.04 0.40 0.07 0.00 0.00 0.05 0.05 0.00 0.00 0.00 0.20 0.00
Distal third of diaphysis to distal metaphysis 0.04 0.00 0.00 0.00 0.00 0.00 0.05 0.06 0.00 0.00 0.20 0.00
Distal third of diaphysis to distal epiphysis 0.00 0.00 0.00 0.25 0.00 0.05 0.00 0.06 0.06 0.00 0.00 0.06
Distal metaphysis 0.13 0.00 0.29 0.00 0.00 0.05 0.00 0.00 0.00 0.00 0.00 0.00
Distal metaphysis to distal epiphysis 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00
Distal epiphysis 0.08 0.07 0.00 0.00 0.00 0.05 0.00 0.00 0.00 0.00 0.00 0.00

* O 5 Osteomyelitis, N 5 Necrosis, U 5 Leg Ulcer, S 5 Syphilis, R 5 Rickets, P 5 ‘‘Periostitis’’. (Numbers were rounded to two dec-
imal points).

significant difference in lesion length between the dis-
ease categories resulting from the greater lengths of the
syphilitic lesions when compared to those of the necrotic,
ulcerous, and rachitic lesions (P \ 0.05). There were no
statistical differences seen among the lesion widths (P \
0.90, ANOVA). Periosteal lesion area was plotted (see
Fig. 3), demonstrating that there were no statistically
significant differences in the overall sizes of the perios-
teal lesions between the disease categories (P \ 0.20,
ANOVA). Aside from one outlier point, the necrotic bone
specimens have the most focal lesions. This relates well
to the clinical literature, which indicates that necrotic
episodes in bone are usually localized events (Adler,
2000). Identifying the percentage area of the bone
affected, rather than the actual physical dimensions of
the periosteal lesion, may better enable the comparison
of lesion size amongst different bones.
The location of the periosteal lesion on the bone is im-
portant, as different diseases have characteristic lesion
distributions (Ortner, 2003). Each bone specimen was di-
vided into seven sections, and the locations of the perios-
teal lesions were identified within and across these
sections (see Table 9). Osteomyelitis affected all of the
segments of the bones, with the entire bone being
affected the most frequently (21%). Necrosis most com-
monly affected the distal third of the diaphysis (40%),
among other areas. Leg ulcers were most commonly seen
affecting the distal metaphysis (29%), but other areas
were also affected. Syphilitic periosteal lesions were
most frequently seen affecting the bone shaft (63%) and
avoiding the proximal epiphysis. Periosteal lesions in
rickets overwhelmingly occurred in the midshaft area
(80%). Finally, periosteal lesions in ‘‘periostitis’’ were
seen primarily in the shaft (35%), although other areas
were also affected.
Lesion types, whether consisting of woven bone, lamel-
lar bone, or a mixture of the two, as previously stated
provide information about the unhealed/healing/healed
nature of the underlying disease. Lesion type did not
show any specific patterning distinguishing the various
disease categories, as most of the lesions in the six dis-
ease categories were of the mixed variety (see Table 10).
This indicates that lesion type is related to the progres-
sive healing of the disease, rather than its nature. Simi-
larly, no patterns emerged with regard to the type of
periosteal vascularization present among the lesions, as
most of the bones in all disease categories had lesions exhib-
iting mixed vascularization, a combination of large and
small striae and large and small foramina (see Table 10).
The application of Lallo’s (1973) lesion severity stages
was of little utility (see Tables 6 and 11) as most of the
lesions in all disease categories exhibited stage 9 sever-
ity. This was most likely due to the inherent bias in the
specimens themselves, as many had been selected for
inclusion in the museums’ collections due to the severity
of their lesions. The use of Hackett’s (1976) criteria for
categorizing bone lesions (see Tables 7 and 12) yielded
similar results, with none of the pathological conditions
being characterized exclusively by one or multiple bony
traits.

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 SPECIFICITY OF PERIOSTEAL REACTIONS IN PATHOLOGY MUSEUM SPECIMENS 55
TABLE 10. Frequency of lesion types and vascularization across disease categories
Lesion type Vascularization
Woven Lamellar Mixed Normal Sm. Striae Sm. Foramina Lg. Foramina Mixed
O 0.08 0.15 0.78 0.00 0.07 0.07 0.14 0.71
N 0.18 0.27 0.55 0.09 0.00 0.18 0.09 0.64
U 0.22 0.00 0.78 0.00 0.00 0.00 0.00 1.00
S 0.40 0.20 0.40 0.00 0.40 0.20 0.00 0.40
R 0.00 0.00 1.00 0.40 0.20 0.00 0.00 0.40
P 0.00 0.24 0.77 0.00 0.00 0.06 0.00 0.94

TABLE 11. Frequency of lesion severity stages across disease because most of the radiographs were taken to illustrate
categories (after Lallo, 1973) the bones in the medio-lateral axis only.
Stages of lesion severity*
No relationship was seen between the different radio-
graphic categories of periosteal new bone production (as
1 2 3 4 5 6 7 8 9 described by Edeiken et al., 1966; Edeiken, 1981) and
O 0.00 0.00 0.08 0.00 0.08 0.00 0.00 0.23 0.62 specific pathological conditions (see Table 13), as most of
N 0.00 0.09 0.09 0.00 0.00 0.09 0.18 0.09 0.45 the disease categories had thin undulating periosteal
U 0.00 0.00 0.11 0.00 0.22 0.11 0.33 0.00 0.23 reactions. The margins of the periosteal lesions were
S 0.00 0.50 0.00 0.00 0.00 0.00 0.00 0.00 0.50 investigated as this indicates the rate of lesion growth
R 0.40 0.20 0.00 0.00 0.00 0.00 0.40 0.00 0.00 (Ragsdale et al., 1981), with radiographically indistinct
P 0.00 0.00 0.00 0.06 0.06 0.29 0.06 0.00 0.53
margins implying a faster growth rate (Greenfield,
* See Table 6 for descriptions of severity stages. 1986). Bones with osteomyelitis, leg ulcers, syphilis, and
rickets most often had periosteal lesions with indistinct
margins, while the margins of the necrotic bones’ perios-
Radiographic analysis teal lesions were most often distinct. The ‘‘periostitis’’
bones had almost equal incidences of distinct and indis-
The lengths and thicknesses of the periosteal lesions tinct periosteal lesions (see Table 14).
seen in the radiographs were plotted in Figures 4 and 5. The analysis of the state of the underlying bone corti-
Both the radiographic lengths and thicknesses of the ces indicated that there were no cortical characteristics
lesions in all disease categories appeared to overlap each that were specific to particular pathological conditions
other in range, but statistical analyses determined that (see Table 15). When examining the radiographic charac-
there were some significant differences across disease cat- teristics of the endosteal surfaces, it was difficult to
egories. For lesion length, differences resulted from the distinguish new bone formation from the effects of med-
smaller lengths of the rachitic lesions when compared to ullary destruction. Histological analysis of the endosteal
those of the ulcerous, and ‘‘periostitis’’ lesions (P \ 0.05). surface may help to distinguish between these two proc-
For lesion thickness, differences resulted from the smaller esses. The only distinctive endosteal feature involved the
thicknesses of the rachitic lesions when compared to those rachitic bone specimens, which had bridges of bone link-
of the osteomyelitic lesions (P \ 0.02). The radiological ing opposite endosteal surfaces. These bony bridges,
dimensions of periosteal lesions are associated with dis- occurring primarily in the diaphysis and in the area of
ease progression. This is especially true of lesion thick- the greatest bone curvature, appear to have been acting
ness, as the more chronic a lesion is, the thicker it will be as struts, supporting the bone in its unnaturally bent
(Dannels and Nashel, 1983; Resnick, 1995). state (see Table 16).
Similar to the macroscopic analysis, no patterns It was only possible to make direct comparisons of the
emerged with regard to the locations of the radiographi- macroscopic and radiographic results with regard to the
cally visible periosteal new bone production across the lengths and positions of the periosteal lesions. There was
various disease categories (see Table 9). The osteomyeli- a great deal of variation between the average lengths of
tis specimens were most often affected on the entire the periosteal lesions seen macroscopically and radio-
bone, from the proximal epiphysis to the mid-shaft, and graphically across the various disease categories (see
from metaphysis to metaphysis (all 19%), the necrotic Figures 1 and 4). Neither the average radiographic
specimens on the proximal metaphysis to the mid-shaft lengths nor the average macroscopic lengths were sys-
area (22%), the leg ulcer specimens from the midshaft to tematically greater - this was dependent on the disease
the distal metaphysis (28%), and the syphilitic speci- category. The syphilitic bones showed the most signifi-
mens from the proximal metaphysis to the distal meta- cant difference between macroscopic and radiographic
physis (33%). The rachitic specimens were affected lesion length (P \ 0.02), with the macroscopic lengths
equally at midshaft, the distal third of the diaphysis, being longer. Significant differences were also seen
from the proximal metaphysis to midshaft, from the among the ulcerous bones (P \ 0.05). The greatest
proximal third of the diaphysis to midshaft, and from amount of congruence occurred among the necrotic
the distal third of the diaphysis to the distal metaphysis bones, where the radiographic lengths were only slightly
(all 20%). Lastly, the ‘‘periostitis’’ specimens were most longer (P \ 0.75). No significant differences were seen
often affected on the bone shaft, from the proximal third among the rachitic (P \ 0.75), osteomyelitic (P \ 0.25),
of the diaphysis to the distal metaphysis, and from the or the bones labeled ‘‘periostitis’’ (P \ 0.10). One might
proximal third of the diaphysis to the distal epiphysis, expect the lesions to be longer on the radiographs, as it
and from the mid-shaft to the distal epiphysis (all 13%). is frequently difficult to discern the margins of the
It was not possible to investigate patterns of orientation lesions when analyzing the bones macroscopically, but

American Journal of Physical Anthropology

56 D.A. WESTON
TABLE 12. Frequency of lesion categorization across disease categories (after Hackett, 1976)
Lesion categorization*
1 2 3 4 5 6 7 8 9 10 11 12 13
O 0.08 0.00 0.08 0.00 0.00 0.00 0.08 0.08 0.00 0.54 0.15 0.00 0.00
N 0.09 0.00 0.00 0.18 0.00 0.00 0.00 0.00 0.00 0.27 0.36 0.09 0.00
U 0.00 0.00 0.22 0.00 0.00 0.00 0.00 0.00 0.22 0.11 0.00 0.00 0.44
S 0.00 0.40 0.00 0.00 0.00 0.40 0.00 0.00 0.00 0.00 0.20 0.00 0.00
R 0.33 0.67 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00
P 0.06 0.18 0.00 0.00 0.06 0.18 0.18 0.06 0.29 0.00 0.00 0.00 0.00

* See Table 7 for descriptions of lesion categories.

Fig. 4. Box plot comparing radiographically visible lengths Fig. 5. Box plot comparing radiographically visible thick-
of periosteal lesions. nesses of periosteal lesions.

surprisingly this was not always the case. The positions
of the periosteal lesions seen macroscopically or radio-
graphically often differed, with the greatest degree of
congruence occurring amongst the bones labeled ‘‘perios-
titis’’ and the least amongst the ulcerous and necrotic
bones (see Table 9). However, when these differences
were tested statistically, no significant differences were
seen (P \ 0.75 [O]; P \ 0.50 [N]; P \ 0.90 [U]; P \ 0.50
[S]; P \ 0.75, P \ 0.10 [P].
DISCUSSION AND CONCLUSIONS
So why was it so difficult to find macroscopic and radi-
ographic traits of periosteal new bone that were patho-
gnomonic of the pathological conditions seen in the
pathology museum specimens? It appears that this lack
of identifying traits is due to the way in which bone and
the periosteum responds pathologically. It is not the dis-
ease that determines how these tissues respond, it is the
tissues themselves. Pathological periosteal new bone is
formed as a type of healing mechanism, whether as a
response to inflammation, mechanical adaptation/com-
pensation due to osteolysis, tumor containment, or
altered circulation (Ragsdale et al., 1981; Ragsdale,
1993), and it appears that the agent that initiates the
periosteal reaction is largely irrelevant. Additionally, the
presence of co-occurring diseases and an individual’s
age, sex, ethnicity, and immune and nutritional status
will influence how a disease manifests itself skeletally
(Roberts and Manchester, 1997).
The clinical and bioarcheology literature and the path-
ological bones studied in the course of this research do
not suggest that periosteal new bone formation at any
location is uniquely diagnostic of any one pathological
condition. Nor are the size, shape and form of periosteal
new bone formation, as seen by the macroscopic exami-
nation of the bone surface or by radiography, uniquely
diagnostic of any pathological condition. Many pathologi-
cal conditions may cause periosteal new bone formation
with no means of clearly diagnosing its etiology, and con-
versely, these same pathological conditions may be pres-
ent without periosteal new bone formation occurring.
The radiographic analyses of the pathology museum
bones emphasized the importance that radiography plays
in the analysis of periosteal new bone. If the goal of an
analysis is to provide an accurate record of the amount
periosteal new bone formation in a skeletal population,
practical implications aside, it is essential that all bones
be radiographed. As demonstrated by the comparison of
macroscopically recorded and radiographically recorded
periosteal lesions lengths, there were great differences
between the macroscopic and radiographic observations.
Many periosteal lesions, particularly those that are
healed, are difficult to differentiate from normal compact
bone, and only become truly visible in radiographs. The
population prevalence of periosteal reactions may have
been underestimated in most archaeological skeletal pop-
ulations due to a lack of thorough radiographic investi-
gation. It is unfortunate that systematic radiographic
analysis is prohibitively expensive, as this is compromis-
ing the acquisition of important data.
The analysis highlighted the importance of analyzing
complete skeletons when studying periosteal new bone
formation in burial assemblages, as the examination of

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 SPECIFICITY OF PERIOSTEAL REACTIONS IN PATHOLOGY MUSEUM SPECIMENS 57
TABLE 13. Frequency of radiographic characteristics of periosteal new bone production across disease categories
(after Edeiken et al., 1966; Edeiken, 1981)
Cloaking Lamellated Lamellated
Dense Dense Thin Codman’s 1 thin 1 dense 1 thin Perpendicular 1
Cloaking undulating elliptical undulating Lamellated angle undulating elliptical undulating thin undulating
O 0.14 0.09 0.14 0.18 0.27 0.00 0.00 0.00 0.18 0.00
N 0.10 0.00 0.10 0.62 0.00 0.00 0.00 0.00 0.19 0.00
U 0.17 0.05 0.00 0.44 0.06 0.00 0.00 0.05 0.22 0.00
S 0.00 0.00 0.00 1.00 0.00 0.00 0.00 0.00 0.00 0.00
R 0.00 0.00 0.00 1.00 0.00 0.00 0.00 0.00 0.00 0.00
P 0.03 0.03 0.09 0.70 0.03 0.03 0.06 0.00 0.00 0.03

TABLE 14. Frequency of distinct or indistinct periosteal lesion
margins across disease categories
Distinct Indistinct
O 0.31 0.69
N 0.78 0.22
U 0.22 0.78
S 0.00 1.00
R 0.00 1.00
P 0.56 0.44
isolated bone elements may present a false impression of
the nature of periosteal new bone formation throughout
a skeleton. The varied results of the nature of the perios-
teal reactions seen in individual bones was illustrative of
this point and suggests that studies that derive preva-
lence rates for ‘‘nonspecific infections’’ based on the pres-
ence of periosteal reactions on individual bones may lead
to an overestimation of the prevalence of infectious dis-
ease in a population, as individual bones with periosteal
lesions could have been subject to trauma, localized
ulceration, hypertrophic osteoarthropathy, or other non-
infectious conditions, for which differential diagnoses
may be ascertained with a complete skeleton. The perios-
teal reactions seen in individual bones should not be
diagnosed in isolation from the rest of the skeleton.
From the specimens described in this research, it is
clear that the term ‘‘periostitis’’ is fraught with difficul-
ties. In many practitioners’ minds, the term ‘‘periostitis,’’
or inflammation of the periosteum, is synonymous with
the term ‘‘nonspecific infection.’’ This is patently untrue,
and may be derived from confusion between the terms
‘‘inflammation’’ and ‘‘infection.’’ A bone that exhibits
periosteal new bone production did not necessarily come
from an individual whose body was invaded by a patho-
genic organism, nor does it even necessarily involve
inflammation (Ragsdale, 1993; Ortner, 2003) as, to reit-
erate, periosteal new bone production can result from
almost anything that breaks, tears, stretches, or even
touches the periosteum (Richardson, 2001). The list of
pathological conditions that can manifest periosteal new
bone production is long, but in spite of this, researchers
repeatedly equate ‘‘periostitis’’ with infection.
The problems associated with the equation of perios-
teal new bone formation with infection are compounded
by the coupling of ‘‘periostitis’’ with ‘‘nonspecific infec-
tion.’’ Powell (1988) stated the problem eloquently when
she wrote that: ‘‘. . . reporting the prevalence of infectious
response or ‘‘periostitis’’ in general terms deliberately
ignore[s] an aspect of population health of major signifi-
cance: the influence of specific infectious diseases upon
levels of morbidity and mortality.’’ By routinely recording
periosteal new bone formation as ‘‘nonspecific infection,’’
researchers could be potentially overlooking the effects
of specific infectious diseases, such as the treponemato-
ses or leprosy.
No standardized, universally accepted terminology has
been devised to describe the various manifestations of
periosteal new bone production seen in archaeological
skeletons. Most bioarcheologists use a number of termi-
nologies, not clearly defined, which makes comparisons
between research results difficult. In published papers
and reports, precise descriptions of the location, or type,
of periosteal lesion present are usually lacking. Most
simply state that ‘‘periostitis’’ was present. The terminol-
ogy is extremely inconsistent between researchers, and
some use the qualifiers ‘‘mild,’’ ‘‘moderate,’’ and ‘‘severe’’
without defining what these terms mean. As previously
mentioned, a number of researchers have attempted to
devise strategies for scoring periosteal reactions in skele-
tal remains and all these methods have their strengths
and weaknesses, but most importantly they are all lack-
ing a consistency of use in the bioarcheology community.
There has not been a method that has gained universal
acceptance as a recording standard, but Hackett’s (1976)
system for classifying periosteal lesions as they relate to
the treponematoses appears to have been the most suc-
cessful (Elting and Starna, 1984; Reichs, 1989; Lewis,
1994; Schermer et al., 1994).
It does not help that bioarcheological research involv-
ing periosteal reactions has been hampered by the lack
of interest in the topic by clinicians. This was a problem
as far back as 1817 when Crampton complained that
‘‘inflammation of the periosteum . . . [had not] been
noticed in any systemic work . . .’’ (Crampton, 1817, p.
331). The trend has continued into the modern era, with
medical texts still bereft of information. The majority of
the clinical categorizations and descriptions of periosteal
new bone formation are based almost entirely on the radi-
ological appearances of periosteal reactions associated
with neoplastic disease, a condition that is not a common
occurrence in archaeologically derived skeletal material.
Clinicians rarely examine periosteal reactions as they
appear directly on bone, and pathologists often overlook
them during autopsy, unless specifically seeking them.
Periosteal new bone formation is generally considered a
sign of a disease—a sign that does not require any treat-
ment. Moreover, because it does not require treatment, it
is not worthy of significant study. This is unfortunate for
bioarcheologists because it leaves them with few clinical
models that can be applied to ancient skeletal material.
In this respect, bioarchaeology has to generate its own
models for how periosteal reactions relate to various dis-
ease states, for it is only the bioarcheologists who truly
see how periosteal reactions manifest themselves in dry
bone specimens. For example, how are clinicians supposed
to qualify and quantify periosteal reactions, when in their
initial manifestation, periosteal new bone formation is not
visible radiologically (Shopfner, 1966).

American Journal of Physical Anthropology

58 D.A. WESTON
TABLE 15. Frequency of radiographic cortical characteristics across disease categories
Permeated
Replacement destruction Permeated
Gross by periosteal Permeated Geographic Moth eaten 1 moth eaten destruction
Normal destruction new bone Thickened Thinned destruction destruction destruction destruction 1 thickening
O 0.09 0.13 0.35 0.00 0.04 0.30 0.00 0.00 0.09 0.00
N 0.00 0.19 0.06 0.06 0.13 0.00 0.13 0.06 0.00 0.00
U 0.14 0.07 0.00 0.29 0.07 0.43 0.00 0.00 0.00 0.00
S 0.00 0.11 0.00 0.56 0.11 0.11 0.00 0.00 0.00 0.11
R 0.00 0.00 0.00 0.50 0.00 0.30 0.00 0.00 0.00 0.20
P 0.13 0.00 0.04 0.21 0.00 0.46 0.00 0.00 0.00 0.17

TABLE 16. Frequency of radiographic endosteal characteristics across disease categories

New bone on 1
New bone Destruction of New bone on Thickening of Bridges of destruction of
Normal in medulla endosteal surface Solid medulla endosteal surface endosteum bone endosteal surface
O 0.15 0.46 0.07 0.00 0.15 0.07 0.00 0.07
N 0.56 0.11 0.11 0.11 0.11 0.00 0.00 0.00
U 0.89 0.11 0.00 0.00 0.00 0.00 0.00 0.00
S 0.33 0.00 0.17 0.17 0.00 0.33 0.00 0.00
R 0.20 0.20 0.00 0.00 0.00 0.00 0.60 0.00
P 0.75 0.19 0.00 0.00 0.00 0.06 0.00 0.00

CONCLUSIONS sity College London, Prof. George Maat, Leiden Univer-

It was not possible to link definite qualitative or quan-
titative characteristics of the periosteal reactions to indi-
vidual disease states. The macroscopic analysis indicated
lesion size, type, vascularization, and severity was not
specific, and there was overlap in the bone regions that
were affected by periosteal reactions. The syphilitic
lesions tended to be more diffuse, but this difference was
not significant when compared across all disease states.
The radiographic analysis determined that lesion size,
type, margination, and cortical and endosteal character-
istics were not specific to individual disease categories,
and as before, there was overlap in the bone regions
affected. There was a tendency for the radiographic
appearance of the rachitic lesions to be short and thin,
but again these differences were not significant when
compared across all the disease types.
These results indicate that periosteal reactions should
be interpreted with extreme caution, as lesion character-
istics overlap across disease categories. The etiology of
the periosteal reaction appears have to minimal influ-
ence over its macroscopic and radiological appearance
due to the prescribed pathological response of bone tis-
sue. Bioarcheologists should be particularly careful when
attempting to impose diagnoses on periosteal lesions
from incomplete skeletons, as this may result in false
extrapolation and misinterpretation, presenting a false
impression of the types of periosteal reactions occurring
throughout the body and potentially leading to the mis-
calculation of disease frequencies in populations, in par-
ticular, overestimating the amount of infectious disease.
ACKNOWLEDGMENTS
Thanks to Prof. Carolyn Finlayson and Mr. Paul
Bates, St George’s Hospital Medical School, the Presi-
dent and Council of the Royal College of Surgeons of
England, Mr. Martin Cooke and Ms. Jane Pickering,
Hunterian Museum, for allowing and facilitating access
to their museums’ collections. Thanks to Prof. Simon
Hillson, Prof. Louise Scheuer, Dr. Tony Waldron, Univer-
sity, Dr. Philipp Gunz, Max Planck Institute for Evolu-
tionary Anthropology, the Journal editor and associate
editor, and the three anonymous reviewers for their
helpful comments.
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