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consequential to habitual postural habits (e.g., squatting facets, Poirier's facet, Charles's
facet) (see
Kennedy, 1989
). The third type reflects circumarticular changes in areas of liga-
ment or tendon attachment (e.g., enthesopathies, syndesmoses [
Figure 7.3b, 7.3
c], Osgood-
Schlatter syndrome) (
Kennedy, 1989; Benjamin et al., 2006; DiGangi et al., 2010
). These
have traditionally been labeled musculoskeletal stress markers (MSM) but, more recently,
Robert Jurmain and S
´
bastien Villotte (2010) have advocated a different, less cause-presump-
tive label: entheseal changes (EC), which will be used here.
The primarybioarchaeological value ofDJD, pressure facets, andECchanges is the presump-
tive co-association of these reactive changes with repetitive labor-intensive activitywhich argu-
ably predicts, among other things, subsistence, skilled labor, or sexual division of labor.
Such activities include grain-grinding or nut pounding (use of the quern, mortar and pestle,
mano and metate), burden bearing (tump line, balancing on the head), labor skill (weaver,
blacksmith, archer), and transport (canoe, kayak, rickshaw, horseback). Many activity-specific
stress markers have been identified (
Kennedy, 1989
). However, there are a wide range of extra-
neous factors that affect whether DJD and EC are skeletally expressed. These include trauma/
microtrauma (see Kroman and Symes [Chapter 8], this volume), body size or weight, genetic
predisposition, age, and ergonomically incorrect activity patterns (e.g., heavy lifting with
the spine and not the legs, poor posture). Sometimes joint damage is simply idiopathic
(i.e., no known cause) (
Jurmain, 1999; Weiss, 2003, 2004, 2007; Benjamin et al., 2006
).
Many studies have indeed linked differential prevalence and severity of stress markers
with subsistence change or sexual division of labor (e.g.,
Bridges, 1991; Chapman, 1997; Lai
and Lovell 1992; Molleson, 1994; Hawkey and Merbs, 1995; Robb, 1998; Steen and Lane,
1998; Jurmain, 1990, 1999; Lovell and Dublenko, 1999; Eshed et al., 2004; Fornaciari
et al., 2007; Molnar, 2006, 2011; Villotte et al., 2010; Niinim¨ki, 2011
). However, these
pathologies have had a mixed history of behavior-associated explanatory power primarily
relating to difficulties of quantification (e.g., if it is hypertrophy or damage) and primary
cause (
Stirland, 1998; Wilczak, 1998; Jurmain, 1999; Weiss, 2007; Cardoso and Henderson,
2010
; Jurmain and Villotte, 2010;
Villotte et al., 2010; Jurmain et al., 2012; Weiss et al., 2012
).
It is clear from research conducted thus far that age and body size play a strong role in
prevalence and severity of EC and must be controlled for if differences in activity patterns
within and between skeletal samples are to be diagnosed correctly. As greater analytical
control over the range of causative variables (e.g., age, robusticity) and more precise quan-
tification occurs (e.g.,
Stirland, 1998; Wilczak, 1998; Weiss, 2003; Molleson, 2007
; Jurmain
and Villotte, 2010;
Jurmain et al., 2012; Milella et al., 2012; Niinim
¨
ki, 2012; Weiss et al.,
2012
), more bioarchaeological studies of DJD and EC will be conducted. This is a promising
area for future research.
IDENTIFYING A PATHOLOGY
Experience is the best teacher. This begins with familiarization with the texture and
contours of normal bone. This may sound fundamental but be mindful that postmortem
damage (e.g., root marks, mechanical or chemical exfoliation of the outer cortex, exposure
of cancellous bone) can be mistaken for pathological conditions (
White and Folkens,
2005
:49
e
66 and Marden et al. [Chapter 9], this volume). When in doubt, do not dismiss
