According to Wolff's law, normal or abnormal bone develops the structure most suited to resist forces acting upon it. Bone is constantly being modified in response to physiological and pathological stresses to which exposed. Mass increases in response to vigorous exercise and other stimulae. The degree of change is related to the individual's age at the time of the stress. When affected by any process, physiological or pathological, response can be in seven, limited, ways:
Other than the growth process, alterations associated with degeneration produce more change in the size, shape, and configuration of the skeleton and its individual bones than any single factor. The two major degenerative processes affecting skeletons are modification of articulations (arthritis), and decrease in bone density (osteoporosis). By definition, arthritis is inflammation of a joint; osteoporosis is abnormal rarification of bone due to failure of osteoblasts to lay down bone matrix. Osteoporosis secondary to metabolic disease was discussed in Chapter 5, and degenerative joint disease secondary to trauma was alluded to in Chapter 2 (Accidents and Injuries).
To permit locomotion and manipulation as well as growth, articulations have evolved throughout the skele- ton. Morphologically they are classified:
Synarthroses and amphiarthroses are important primarily for growth, but allow some motion. Diar- throses are variably movable articulations of several types. Degenerative disease affects all types of articulations, but because synovial articulations facilitate movement, any abnormality severely affects the entire individual (314-352). Ham remarked sagely that diseases of joints are probably the greatest single cause of disability encountered by the medical profession today (150-463).
Alterations affecting various joints comprise a large part of the degeneration process. However, the plethora of terms used to designate pathological modification of articulations (atropic, degenerative, hypertropic, osteo-, infectious [septic], inflammatory, neurotropic, rheumatoid [and variants], traumatic) is confusing and interferes with understanding joint disease. In the past atropic, degenerative, hypertropic, and osteo-arthritis were synonyms for joint alterations associated with ageing, as opposed to inflammatory (rheumatoid) arthritis, or change secondary to trauma, infection, or neurotropic factors. To promote uniformity, during the Dry Bones survey abnormality of joints was classified as degenerative joint disease, with elaboration as to site and type.
The pattern of involvement and the cause differ between inflammatory and degenerative joint disease (Fig. 6.2, 6.3), and the antiquity of rheumatoid arthritis has been questioned (294-229). Therefore, comprehension of joint modification in old skeletons required knowledge of joint anatomy (Fig. 6.1) and the active pathological processes.
Degenerative changes in articulations having limited or no mobility entailed calcification of contiguous tissues that ended in fusion.
In synovial joints, modifications involved joint surfaces, bone substance contiguous to the joint, and the capsule and structures surrounding the joint, or all three. Degenerative joint disease began in the articular or supporting cartilages and later involved the remainder of the joint.
Although stimulae for degenerative, traumatic, and infectious changes in joints differ, the pathophysiology and end results are similar. For this reason, degenerative articular disease fits two general catagories, primary (senile, osteoarthritis), and secondary (changes produced by other factors).
Rheumatoid (inflammatory) arthritis begins in the synovial membrane and spreads to the articular surface, leading to typically deformed joints (154-1135;176;219-19;231). Its many variants are common in the general population in this region today, but it is less common in Native Americans. Rheumatoid manifestations are attributed to an autoimmune origin. They usually start in young or middle life, but can remain active into the elderly years. With one possible exception, rheumatoid variants have not been identified in aboriginal skeletons from this area.
Figure 6.3. Hand joints affected by hypertropic and rheumatoid arthritis.
The Present
A search for information relating to the prevalence of diseases affecting elderly North
American and regional Native Americans today showed that very little is known about racial
or geographic distribution of osteoarthritis (294-230). Even less information was found
relating to osteoporosis. Some of the lack of information is explained by reference to the
distribution by age, sex, and race pyramid chart in Figure 6.4. The median age for All
Races U.S. was 28.1 yr., the point in life where degenerative joint disease and bone mass
changes start becomming apparent. The median age for the Indian Aberdeen Area Service Unit
was 16.8 yr.
In 1970 South Dakota vital statistics the median age was 27.4 yr. (White- 28.2, non-White- 17.4); in 1980 it was 28.8 (White- 29.8, Indian- 18.5) (298-5).
In Health Care Needs of American Indians and Alaskan Natives, the leading reasons by system or cause for hospitalization of United States Native Americans over age 65 years were circulatory, respiratory, digestive, accidents-poison-violence (172b-83,84), and nervous system. In individuals 65-74 years, 80% had chronic medical disorders; 45% had disability sufficient to limit activity. Major problems limiting activity in order of frequency were arthritis, orthopedic diseases of the legs and hips, heart disease, and stroke (172b- 85). However, important information relating to the number of individuals now receiving disability related services was not available for use as a measure of future need (172b-85).
The Aberdeen Area Indian Health Office reports frequent hospitalization (males [#1]- 22.3%, females [#2]- 11.07%, overall 13.5%), out-patient visits, and contract services for trauma and residua in all age brackets. Diseases of musculo-skeletal and connective tissue origin ranked #10 (1a-43,45,48;172a;172b-VI- 888=891). No hard data are available concerning the prevalence of arthritis or osteoporosis.
The Past
Shortly after the turn of the century Hrdlicka found "muscular rheumatism and senile
arthritis" to be frequent in southwestern U.S. Indians. He did not mention
osteoporosis by name or symptom (167-191).
In a bibliography of 1483 references relating to health problems of American Indians north of Mexico spanning the interval 1800-1969, Barrow and co-workers listed many reports relating to rheumatoid arthritis and its variants (all of recent date), but only two concerning osteoarthritis. None of these related to the Upper Missouri River Basin. Osteoporosis was not listed by name or symptom (31).
Various joint abnormalities and osteoporosis were not unusual in remnants of Upper Missouri River Basin aborigines (Table 6.2), but their frequency generally was less than what probably exists today, primarily because with short life expectancy most people did not live long enough to develop ageing changes (Ch. 8, Fig. 8.7). Many skeletal collections we examined were small and were not true population samples, limiting the validity of demographic information obtained. However, in a significant number of skeletons of relatively young individuals degenerative changes disproportionate for age were present. This was true especially in the spine, and seemed more prevalent in females. The only obvious explanation was their life-style (agrarian labor, hoeing crops, carrying burdens).
Deteriorative changes in the Crow Creek skeletons are listed in Table 6.3. Fragmentation, dismemberment, and incompleteness precluded assessment of joint and bone mass changes as individual skeletons. In 96 synovial joints degenerative changes were present. Knee (proximal tibia) involvement was most frequent (38/531, 7.1%), followed by jaw (mandible- 8/131, 6.1%), and ankle (tibii- 12/531, 2.3%).
Figure 6.4. From: Charts on Indian Health. 7th ed. DHEW, PHS, HSMHA, IHS, Aberdeen, SD, nd.
Vertebral lipping was in all portions of the, but was most frequent in the lumbar region, with involvement of 432/1694 (25.5%) vertebrae. The lumbar vertebrae we examined represented 69.7% of the total expected in 486+ skeletons (2430, Table 1.3), so by extrapolation the total individuals with lower back disease was greater than the evidence indicated.
During life osteoporosis was characterized by accelerated bone loss and diminished new bone formation (too little bone per volume of tissue, but the mineralized bone to unmineralized matrix ratio was normal) (246-289;307;364). In old bones this was identifiable by light weight, sparce medullary trabeculation, and decreased cortical thickness, most noticeable in ribs, lumbar and thoracic vertebrae, and the tibia and fibula. Vertebral collapse secondary to decreased bone density was in three thoracic vertebrae from two individuals, and three lumbar vertebrae from a single skeleton. Findings in regard to decreased bone density in this skeletal cohort were morefrequent and more pronounced than in other population samples from this region.
Table 6.1. Osteophyte Formation and Porosity
Sully Larson
Osteo- No No
phyte___SNA*__SNA**___%__SNA*__SNA**___%_
Stage
0 28 0 0.0 12 1 7.7
1 45 6 11.8 30 15 33.3
2 26 4 13.3 15 1 6.2
3_________8_____4___33.3___4_____6___60.0
Total 107 14 61 23
Porosity
0 83 9 9.8 36 11 23.4
1 17 4 19.0 15 7 31.8
2 3 1 25.0 8 3 27.3
3_________4_____1___20.0___2_____2___50.0
Total 107 15 61 23
Modified from: Bradtmiller 1984.
Tables 5 & 6 combined.
SNA- separate neural arch.
* Raw frequency individuals each stage
a osteophyte development.
** Raw frequency individuals with separate
neural arches, divided/development stage.
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Table 6.2. Degenerative Disorders
Site Degenerative Joint Disease Vertebral
Skeletons_____Culture____TMJ__Shoulder__Elbow__Hip__Knee__Ankle___Lipping_____Osteopor
Swan Creek
39WW7 Arik 3 1 1 - - - CTL -
N= 82
Mobridge
39WW1 Arik 1 1 - - - 2 TL Gen
N= 55
Four Bears
39DW2 Arik 2 - 1 - - - CT,CL,CL,T T
N= 41
DeSpeigler
39RO2 Woodland 1 - 2 - 2 1 CL,L,L Mand
N= 50(est)
Ufford
39CL2 Woodland 1 - 1 - 2 - CL,L,T -
N= 40
Double Ditch
32BL18 Mandan? 1 - - - - - TL,TL,TL,TL -
N= 24(est)
ND Hist. Soc.
N = 151* Several - - - - - - L -
Over Coll.
N= 228 Several 7 - 13 6 9 4 L,L,TL,L, Spine,
Gen,CTL,TL Spine,
TL,L,CLS, Mand.,
L,L Sacrum
Misc. Coll.
& Spec. Several - 1 1 - 1 - TL,L,CTL,CT -
_N=_241_______________________________________________________________________________
Total= 912 16 3 19 6 14 7 33 7
* Analysis limited to skull primarily.
C= cervical, T= thoracic, L=lumbar, S= sacrum.
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Bradtmiller evaluated the lower spine in Arikara skeletons from the late 17th century Sully and the early 18th century Larson sites. Separate neural arches (spondylolysis, a deep bilateral structural defect in the neural arches, most commonly the fifth lumbar, that predisposes to spondylolisthesis- see Fig. 6.8 and text) were in 73 Sully males (12.3%) and 47 females (10.6%), and 46 Larson males (28.2%) and 43 females (23.2%).
Osteophyte formation (vertebral lipping) and intervertebral disk joint porosity were considered a result of activity in the development of the separate neural arch trait. Osteophytes, graded according to increasing severity on a scale 1-4, were in 14/121 (11.6%) Sully skeletons and 23/84 (27.4%) Larson skeletons (Table 6.1). Joint porosity was in 15/122 (12.3%) Sully skeletons and 23/84 (27.4%) Larson skeletons (57). For comparison neural arch defects in Crow Creek skeletons are in Tables 7.4, 7.5.
Ericksen evaluated humerus and femur cortical bone loss with age in 134 Arikara skeletons from 11 ar- chaeological sites in northern South Dakota and compared her findings with 142 New Mexico Pueblo skele- tons, and 123 Eskimo skeletons (104). Although archaeological sites were not identified, a few South Dakota skeletons dated to the Extended Coalescent Horizon, 1550-1675 A.D.
Table 6.3. Degenerative Changes In Crow Creek Skeletons
Bones Very
Abnormality________________Counted____Mild____Mild____Moderate____Severe______Total
Degenerative_joint_disease-------------------------------------------------- 96
Jaw temporo- 963/131 -- 5 1 2 16
mandibular
Shoulder- humerus/ 413/521 -- 2 -- -- 4
scapula
Elbow- humerus/ulna 413/244 -- 1 -- -- 2
Wrist- radius/ulna 206/244 -- 1 -- -- 2+
Hip- innominate/ 1133/734 -- 4 -- -- 8
femur
Knee- femur/tibia 734/531 -- 16 2 1 38
Ankle- tibia/fibula 531/299 -- 5 -- 1 12+
Sacro-iliac 396/1133 -- 1 2 -- 6
Pubic symphysis --- -- 2 2 -- 8
Vertebral_lipping----------------------------------------------------------- 550
Cervical 1665 -- 4 16 -- 20
Thoracic 3498 5 20 5 -- 30
Lumbar 1694 56 168 164 44 432
Generalized --- -- 60 12 -- 72
Decreased_bone_mass (osteoporosis)------------------------------------------ 244
Mandible 131 -- -- 1 -- 1
Vertebra- thoracic 3498/1694 3 21 21 -- 45
& lumbar
Vertebra- lumbar 1694 -- 43 16 3 62
Vertebra- collapse
Thoracic 3498 -- 1 2 -- 3
Lumbar (2,3,4) 1694 -- -- 3 -- 3
Tibia & fibula 531/299 -- 12 2 2 32
Radius & ulna 206/244 -- 1 -- -- 2
Ribs --- -- 70 10 -- 80
Femur 734 -- 7 1 -- 8
Humerus 413 -- 7 1 -- 8
Modified from: Zimmerman et_al, 1980, p. 243.
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Most were from the Post-Contact Coalescent Horizon, 1675-1845 A.D. Skeletons with pathology other than osteoarthritis or trauma were excluded from her study. Specimens were divided into young (18-25 yr.), middle aged (30-49), and old (50 and above). Individuals 25-30 years of age were excluded so early developing changes were more evident. Except for Pueblo and Arikara males, few individuals were over 40 yr.
Medial-lateral cortical bone thickness was assayed with radiographs and measured directly in bone plugs from set locations on each bone. To equalize different size and body build, three indices were used to compare maximum bone length with relative cortical thickness: femur medial-lateral, femur anterior, and humerus medial-lateral.
Most statistically sigificant population differences were in the femoral medial-lateral cortex (Fig. 6.5). The greatest differences were between the Eskimo and Pueblo skeletons, except in aged, where Eskimo females and Arikara of both sexes had pronounced cortical bone loss. Arikara males gained cortical bone between youth and middle age, but lost more than other males thereafter. Female rate of cortical loss was consistently greater than in males, but small Eskimo and Arikara female sample sizes clouded the validity of statistics.
In Ericksen's opinion, environmental factors, nutrition and the level of physical activity, are important determinants of the pattern and amount of age-related loss in the femoral medial-lateral cortex.
Sex differences were evident in the anterior femoral cortex by middle age, especially in females (Fig. 6.5). Arikara male skeletons also showed definite difference between young and old. Except in Eskimo males, cortex loss began between youth and middle age and was steady thereafter. Patterns of humeral medial-lateral involution were similar to the anterior femoral cortex (Fig. 6.5). Beginning in youth there was steady decline in humeral cortical thickness in all groups that was statistically significant between all age levels in Eskimo and Pueblo females, and from middle age on in all but Eskimo males. Through out, female humeral cortical loss was higher, the loss being at least twice that in males. The sex difference was statistically significant in middle-aged Eskimos and Arikara, and for all groups in old age. No differences in humeral cortices were attributable to race or environmental factors, such as physical activity or nutrition, that varied considerably between cultures represented. Ericksen concluded that the greater rate of aging bone loss in females is a universal fact of life and not dependent upon factors such as pregnancy and lactation.
Joint disease in regional skeletons varied considerably as to the seriousness of the residua. Many times there was little indication of the cause for the pathology, or the degenerative disease was in isolated specimens. This complicated assignment to specific disease categories, but with a few exceptions articulation modifications could be classified as primary (degenerative) and secondary (traumatic, septic, neurotropic) joint disease. Nine examples of pathology that directly or indirectly affected joints secondary to trauma are presented in Chapter 2. Articulation findings are reported here according to the type of joint affected by disease.
SYNARTHRODIAL Disease.
Figure 6.6. 32DB8 Double Ditch Site, ND (Hart River Phase, 1675-1780 A.D. Mandan adult female.
The manubrium and xyphoid processes were fused to the sternal body and the medial ends of the first costal cartilages were calcified and fused to the manubrium (Fig. 6.6). Sternal attachments of the 3-7th costal cartilages were accentuated. Moderately severe generalized degenerative disease involved the entire spine, but there was no other abnormality.
The manubrium usually does not fuse with the sternum's body until late in life, while the xyphoid and body fuse about age 40 (198-116). Several other specimens with fused sternal pieces and accentuated costo-chondral articulations have been seen, but the severity of modification in this skeleton was more than usual. This finding could represent changes related to previous trauma to the thoracic cage anteriorly. Changes such as these accompany ageing, and may be a part of ankylosing spondylitis (discussed later).
AMPHIARTHRODIAL Disease.
Figure 6.7. 39BF11 Crow Creek. Proto-Arikara adult female.
The cervical spine from an early 14th century woman has anterior lipping, narrowing of the intervertebral spaces, and remodeled vertebral bodies (Fig. 6.7). Decreased vertebral body bone mass was a significant contributing factor.
Throughout the Upper Missouri Basin degenerative changes were frequent findings in amphiarthroses, most prominent in vertebrae (Tables 6.1,6.2, 6.3). Some accompanied aging but in relatively young individuals, physical activity during life was the more likely cause.
The sequence of events in primary vertebral degenerative disease began with breakdown of the inter- vertebral discs followed by stretching of paraspinal ligaments. As the result, bone spurs formed (lipping), primarily on anterior and lateral vertebral body margins (304;307-260), most often in the lumbar and cervical regions.
Secondary vertebral degenerative disease, the result of prolonged stress on the lower spine of an adult male with developmental anomaly complicated by non-reduced hip dislocation (Fig. 2.13) is demonstrated graphically in (Fig. 6.8).
Figure 6.8. 39SL4 Sully Site. Arikara male 40 yr.
Vertebrae T-11 through L-5 show extensive osteophytosis. There is anterior lipping to the point of fusion (F) of L-2 and 3 anteriorly, and partial fusion (P) of L-1 and 2, and L-3 and 4. The posterior neural arches of L-5 and S-1 are separate (S) (spondylolysis) and the vertebral bodies of L-1 anteriorly and L-4 posteriorly are collapsed (C). The findings are from shearing stress upon the pelvis and lumbo-sacral spine during a long period of time.
Spondylolisthesis, (anterior displacement of one vertebra over another) of the L-5 body over the sacrum was an important part of the total process. When spondylolysis is present, during exercise altered lower back dynamics cause unusual pressures upon intervertebral discs, vertebrae, and regional ligaments, resulting in disability and painful lower back. As the disease progressed vertebral alignment was altered, stimulating compensatory osteoanagenesis.
DIARTHRODIAL JOINT Disease.
Primary degenerative (atropic, hypertropic, osteo-,) diarthrodial joint arthritis involved articular cartilage and contiguous bone. The cartilages (Fig. 6.1) became softened or fragmented, broke down, and dissolved. When cartilage eroded, underlying bone was exposed. After the protective buffer disappeared, contiguous bone became sclerotic (eburnated). Cystic change in the injured bone often accompanied the process along with modification of tissues at the joint's periphery, forming osteophytic spurs.
Figure 6.9. 39UN1 Arbor Hill, Over Collection #3355. Woodland female 50+ yr.
The articular surface (arrow) of an edentulous mandible's head was worn flat and underlying bone was densely eburnated (sclerotic) (Fig. 6.9). Multiple micro-cysts were in the mandibular neck sub-condylar area. Tooth sockets were extensively remodeled; the body of the mandible was severely osteoporotic. No other skeletal components were available. The severity of condyle attrition and loss of bone mass suggests the process affecting the jaw joint existed for a long time, probably for many years. Unusual chewing motions as part of masticatory efforts to "gum" food after tooth loss early in life, offer an excellent explanation for the extreme condylar attrition. However, despite defective masticatory apparatus, the individual had survived for a longtime.
Figure 6.10. 39BF11 Crow Creek Proto-Arikara.
Figure 6.11. 39BF11 Crow Creek. Proto-Arikara male adult.
During adult life this woman's facial support structures were remodeled as part of dental attrition. Tooth wear brought on by the consistency and quality of diet, food processing techniques, and the probable high carbohydrate content, caused the teeth to deteriorate. Ultimately all were lost. Alterations in the facial skeleton accompanying dental wear were translated into temporo-mandibular joint derangement, followed by joint remodeling, and ended in modification of the articulating surfaces. Additional contributory factors to this woman's dental problem include the possibility of malocclusion, malnutrition, the effect of pregnancy and lactation upon the teeth, and use of teeth and jaws as tools.
Figure 6.12. 39BF11 Crow Creek. Proto-Arikara male adult.
The anterior portion of the left head is undergoing degenerative change in an almost completely edentulous adult mandible (Fig. 6.10, arrow). The bone lost about 40% of the head's surface and micro-cysts formed,indicating an active process. Despite its robust appearance, the mandibular cortex was thin and medullary trabeculae were few and coarse. Faulty masticatory motions were instrumental in these changes.
Alterations accompanying jaw joint derangement usually begin on the posterior portion of the temporal bone's articular eminence and the articular surface of the mandibular condyle, followed by flattening of both surface contours. Today, temporo-mandibular joint remodeling is frequent in edentulous individuals who do not use dentures, or who's dentures fit poorly.
Temporo-mandibular joint attrition, mostly less severe, was in 6.1% of Crow Creek mandibles (Table 6.3, and Ch. 9), and was observed in many other skeletons during the Dry Bones study (Table 6.2).
The effect of diet, mastication, and other factors upon the temporo-mandibular joint in ancient skeletons has not been investigated to any extent (6-586). Exceptionally severe bilateral temporo-mandibular joint disease with extensive remodeling, more pronounced than any Upper Missouri Basin skeletons, was reported in an aboriginal skeleton from Tennessee (132).
In Figure 6.11, the femur's anterior (left) and lateral (middle) surfaces and the tibia's anterior surface (right) show erosion of the articular surfaces exposing underlying bone (left-arrow), cystic change in contiguous bone, and joint modification peripherally (middle, arrow). Minimal eburnation in surrounding bone suggests the distal femoral articular surface process was of recent origin (see osteochondritis dissecans, to follow).
Severe degenerative changes are etched into both knee joint surfaces (Fig. 6.12). The extent of modification indicates continued activity with a damaged knee for some time. The pathogenesis for these findings is not obvious, but it probably started with joint injury many years previously.
Joints of the hands.
Figure 6.13. 39SL4 Sully Site. Arikara adult female.
Cartilage and bone enlargement on surfaces of finger distal interphalangeal joints (Heberden's nodes) are part of primary degenerative joint disease (Figs. 6.3, 6.13- arrows). Similar nodes form at proximal interphalangeal joints (Bouchard nodes). Gross deformity in the hands and feet secondary to degenerative arthritis usually is not manifest until the disease is far advanced. Occasionally ossified nodes were in Dakota Territory skeletons; usually multiple and more common in women.
Short life span (Ch. 8) is a factor in the paucity and small size of these changes in regional skeletons.
DIARTHRODIAL JOINT Secondary Arthritis.
Joint alteration due to something other than ageing alone appears to have been responsible for findings in Figure 6.14. Two specimens, both probably from Arikara males, have seriously damaged knees. Degenerative change is characterized by extensive remodeling of joint surfaces and widespread alteration of surrounding structures. The appearance of both specimens suggests prolonged use of uncomfortable injured extremities, accompanied by considerable disability. Traumatic pathways leading to such alterations include fracture (Fig. 2.10), meniscus cartilage injury, dislocation, infected penetrating wound, and strenuous physical exertion, especially too soon after injury. Infectious (septic) arthritis, either secondary to penetrating wound or from blood stream spread could produce such changes. In addition, pain perception alteration by central nervous system disease might have predisposed to a Charcot joint. Because the femur in 6.14B was an isolated specimen without provenience, no analysis was possible.
Hip dislocation.
In Figure 2.13, as sequellae to long standing hip dislocation the femoral head, acetablum, and innominate bone lateral surface underwent extensive remodeling. The undisturbed epiphyses and bone development confirm injury during adulthood.
The degree of modification indicates an accident occurred long before and the injured hip was used for an extended interval thereafter. Absence of osteoporosis, implying adequate nutrition and minimum debility, indicates the individual and this limb were functional until death.
In contradistinction, changes in a sub-adult skeleton with long standing hip dislocation (Fig.7.26) include asymmetrical growth of the hemipelves and lower extremities, bone atrophy and osteoporosis, pseudo-joint formation, cystic alteration in adjacent bones, and aseptic necrosis of the femoral head, but very little osteoanagenesis. In addition, degenerative changes were on this skeleton's left scapula and navicular bones'articular surfaces (7.26E,F). Foot changes were caused by altered gait to accommodate the unreduced hip dislocation. Scapular articular cartilage erosion was induced by unusual pressure upon the joint while using a crude crutch (Lynn Deitrick, Anthropology Department, University of Tennessee, Personal communication, 1980).
Pseudoarthrosis.
In Figure 2.25 joint alterations in the elbow were caused by a fracture at the base of the olecranon process that healed with a false joint, allowing abnormal elbow mobility. Corresponding joint changes were in the wrist. Degenerative change in elbow and wrist, alone or accompanying fractures, was in several regional skeletons.
Figure 6.11 (left- arrow). Articular cartilage erosion exposed underlying joint surface bone that is being eroded. At the periphery of the eroded area and slightly in the depths of the defect, bone was sclerotic, indicating osseous response to the disease. This finding accompanied primary joint degenera- tion, but osteochondritis dissecans was also possible. That condition is characterized by necrosis (death) of a segment of the bone's articular surface followed by degenerative change in the overlying cartilage, probably caused by impaired blood supply to to the affected bone segment. It most frequently involves the knee(203b).
Four distal Crow Creek femurs had changes for which osteochondritis dissecans was considered; in two it seemed likely.
Views of the spine and pelvis from three angles show changes typifying poker spine (Marie Strumpel disease (Fig. 6.15). Paraspinal ligaments between the neck and sacrum were firmly fused by dense bone. Vertebrae were fused antero-laterally on both sides but the anterior longitudional ligament was unaffected. Attachments of articular ligaments between cervical 6 and 7 and thoracic vertebrae had hyperostotic changes that increased in density progressively caudally. Costovertebral ligament insertions into ribs were accentuated, especially for the lower seven ribs. Bone mass and medullary trabeculae in all vertebral bodies were severely affected by secondary osteoporosis.
Figure 6.15. 39WW2 Mobridge vicinity, collector specimen. Arikara male 32-37 yr.
Figure 6.16. Schematic representation of foci involved in ankylosing spondylitis.
Thoraco-lumbar intervertebral spaces were narrow producing kyphosis (anterior bending of the spine). The sacro-iliac synchondosis was fused, but the pubic symphysis was not. The hips, shoulders, manubrial-sternal, and joints of extremities, were not obviously involved in the process. The individual represented by the skeleton was disabled, but survived for many years with the disease. Although nothing indicates the cause of death, pulmonary complications are most likely. With disability this severe, productive activity would have been limited, requiring much physical support during life.
Ankylosing spondylitis is a form of chronic progressive arthritis affecting primarily the spine. The common and less frequent joints affected are illustrated in Figure 6.16. In England today it appears in about 0.05% of the population (1:2000) (35;76-194).
In the upper Missouri Valley ankylosing spondylitis is not frequent in Native Americans, but reports from other parts of North America indicate the prevalence as high as 9.5% (294-228;145). Although Marie Strumpel disease has been identified as a rheumatoid variant, recent investigations have implicated an autoimmune reaction and a familial pattern for this disease (76-194).
In a study of over 2600 Indian skeletons from the Dakota Territory, 1415 of which were over 16 years of age, only one skeleton had ankylosing spondylitis (0.07%) (35). We know of no other examples of this disease in this region.
As part of ageing the skeleton is subject to marrow space replacement by fatty and fibrous tissue, and to demineralization and loss of resilience in compact bone. Quite often cartilages underwent mineralization or ossification (220-406). Gross physical evidence suggesting osteoporosis in old skeletons was light weight bones that crumbled or fragmented easily, thin cortices and decreased or absent medullary trabeculations, or remodeling with no evidence of hypertropic arthritis, previous fracture, or degenerative joint disease.
Because osteoporosis is difficult to quantify accurately in dry bones (260,261) several techniques, including measurement of longitudinal and cross sections of bones, standardized radiographs, photon beam absorbiometry, and neutron activation analysis, were potential diagnostic aids (21;104;215;285-205;313). Of necessity, analysis of Missouri Basin skeletons for osteoporosis was limited to evalation of gross specimens and radiographs.
Light weight, very thin cortex, and few, spindly medullary trabeculae, identify primary osteoporosis in the cross section of an almost completely edentulous elderly female's mandible (Fig. 6.17). For comparison, the insert shows the cross section of her contemporary normal adult female mandible. Two other mandibles illustrating temporo-mandibular joint derangement (Figs. 6.9, 6.10) show similar cortex and medullary changes.
A variant of osteoporosis accompanying atrophy of disuse occured when teeth were lost. Absence of pressure transmitted through tooth root sallowed alveolar margin bone resorption. Later, bone in the maxillae and mandible were lost, ending in decreased mass and flattening of alveolar margins (51-102).
Figure 6.17. 39BF11 Crow Creek. Proto-Arikara female adult.
Figure 6.18. 39BF11 Crow Creek. Proto-Arikara. adult, sex ?
The final result is seen in Figure 6.18, another edentulous pre-Columbian adult mandible of undetermined sex, and its radiograph. Grossly the bone was atrophic. In the radiograph the cortex was very thin; in some places medullary space trabeculae were almost totally absent. In extreme cases the mandible became wasted such that only a thin rim remained (132). Such change renders mandibles susceptible to fracture. In addition, absence of teeth made mastication difficult, compounding the problem of maintaining satisfactory nutritional status.
Collapsed vertebrae, especially in the thoracic and lumbar areas, an accompaniment of decreased bone density, were represented in several skeletal groups (Fig. 2.6). These were more frequent in females.
Decreased bone mass complicating congenital hip dislocation or Perthe's disease is exemplified in fragmentary remnants of a child's innominate bone and proximal femur (Fig. 7.25). The degree of degeneration indicates the process was active for a long time. This skeleton was in the mass burial, so it is evident the child was living with the disease until death, and life support measures were available.
Similar secondary osteoporotic changes were in an early 17th century, sub-adult, probably male skeleton (Fig. 7.26), also with congenital hip dislocation. Difference in development of the hemipelves and lower extremities, decreased cortical and medullary bone density on the affected side, and changes from adaptation to the malformation, indicate this was a lengthy process, and osteoporotic changes were the result of disuse atrophy.
In Figure 3.8, alterations throughout the skeleton, especially in thoracic and lumbar vertebral centrums of a 16-18 year old Arikara woman, exemplify metabolic change secondary to protracted debilitating infection, disseminated tuberculosis. Several thoracic and lumbar vertebrae were collapsing and bone mass in all other vertebrae was markedly decreased.
Changes of metabolic and nutritional origin in the remnants of Crow Creek massacre victims are discussed in Chapter 5.
During childhood, bone formation normally exceeds resorption. Physical maturity today is reached about the 18th birthday. The skeleton reaches its greatest mass and a state of equilibrium around age 25. To facilitate weight bearing this mass is maintained for about 20 years. With ageing, bone resorption gradually exceeds new bone formation, leading to varyable decrease in mass (110,341). Primary resorptive disease (osteoporosis) mostly involves trabecular bone, i.e., vertebral bodies and long bone ends. Through the effect of pregnancy and sex hormones, female bone mass alterations begin earlier, and are more pronounced after menopause.
Except for minor variations, it is unlikely that basic physiological processes changed appreciably in Upper Missouri River Basin inhabitants during the past millennium. Joint degeneration and osteoporosis, the major deteriorative processes, left residua in remnants of many past inhabitants. Both appeared in primary and secondary forms. The primary types were similar to what exists today in the regional general, and apparently to a lesser extent in Native American populations. Secondary joint disease and osteoporosis follow other patterns today, mirroring different socioeconomic conditions and life style of the population.
PRIMARY DEGENERATIVE JOINT DISEASE.
The hunter-gatherer and agrarian lifestyle of the people under study entailed activity
very different from today. Their physical efforts promoted cervical and lumbar spine
degenerative disease. Pathological alteration of knee joints was quite frequent and there
was some degenerative shoulder, jaw, elbow, hip, and ankle disease. Hand and foot joint
modification was uncommon.
Studies by Zimmerman and co-workers of pre-Columbian (361) and Bradtmiller (57) of post-Columbian skeletons, and other research in this region (128), indicated that lower back neural arch defects were frequent in people who lived here in the past, unrelated to culture or time period. Neural arch abnormalities were responsible for some serious lower back problems in past inhabitants. No good data are available to compare findings from the past with present day Native American inhabitants.
The exact mechanism of primary arthritis accompanying ageing is unclear. In the United States today, most individuals of 70 years have joint problems; about 19% have some (mostly a symptomatic) weight bearing joint change by age 40 (231). Under age 45 joint problems are more in men, over 55 in women. In location and severity degenerative changes are related to work and life style.
Degenerative change in lumbo-sacral amphiarthrodial joints is life-style related, but inheritance is also implicated. Spondylolysis most commonly involves the fifth lumbar vertebra, and predisposes to spondylolisthesis. The cause of neural arch defects is conjectural, but they are not inborn because the defect is absent in new borns (98-1684;189;307-259). Spondylolisthesis can be genetically inherited, is commoner in males, and has racial overtones. In 4,000 skeletons, 6.6% of Caucasian males and 2.3% of females, and 2.8% of Black males and 2.3% of Black females had spondylolisthesis (282). Stewart found this defect in 50% of Alaskan Eskimos, and questioned whether it is due to inbreeding (303,307).
INFLAMMATORY ARTHRITIS (Rheumatoid).
The absence of articulation changes attributable to the rheumatoid catagory, other than
one instance of ankylosing spondylitis, showed that rheumatoid disease was not common in
Upper Missouri River Basin abo- rigines, and gives an indication of the antiquity of this
disease in this portion of the world.
BONE MASS LOSS.
Investigation of skeletal mass as an indicator of the health of past regional inhabitants,
has produced important evidence concerning them and their milieu. In addition, much is
being learned about their physical and nutritional status, and their patterns of growth
and development.
Ericksen showed that in Arikara skeletons of both sexes there was greater femoral medial-lateral cortex bone loss in the aged group than in Eskimo or Pueblo skeletons. Arikara males gained cortical bone during growth and young adulthood, but lost more mass than the other males thereafter. Cortical bone loss was consistently greater for females in all three skeletal groups. The small female sample size for Eskimo and Arikara skeletons, discouraged statistical analysis. Ericksen concluded that environmental factors, principally nutrition and the level of physical activity, are important in the pattern and amountof age-related femoral medial-lateral cortex bone loss (104).
In a similar study, Pfeiffer and King evaluated cortical bone formation and diet in two protohistoric Iroquoian samples (Kleinberg, 1600A.D., N= 561; Uxbridge, 1490 +/- 80 A.D., N=457). Mean values for the cortical index and percent cortical area were consistently below expected levels, suggesting that some low values represented the effect of disease, but also could be related to prolonged dietary insufficiencies. There was no evidence for a genetic factor, and no reason to ascribe findings to inactivity of Iroquoian horticulturists. Absolute calcium intake and the ratio of dietary calcium to phosphorus were considered as influential upon the findings. If bone forming characteristics associated with corn-based low meat diet are to be differentiated from those associated with protein-calorie insufficiency, it was suggested that future investigation compare corn based horticulturists with others who depend on different foodstuff (262).
Today, beginning about age fifty most women in this country lose 0.5% of skeletal mass per year (341); by age 90 the average woman's skeletal mass loss is 20%. With active primary osteoporosis, bone atrophy is at least twice the normal rate (1% per year). With 1% bone mass loss per year starting at age 50, osteoporosis appears at age 80; with 2% loss, at age 65; sooner with larger yearly loss (uncommon) (341). At 30% loss of maximum mass vertebral bodies are susceptible to compression fracture, and fractures occur often in other bones (femoral neck commonly).
In robust skeletons resorptive changes are less apparent. Male bone atrophy is usually less and doesn't begin until age 65-70. Skeletal alteration in males with active osteoporosis begins earlier and progress more rapidly. Past age 80 osteoporosis usually affects both sexes similarly.
Secondary (metabolic) osteoporosis is part of atrophy of disuse, but is also an accompaniment of several diseases, e.g., hyperparathyroidism, chronic nephritis, or circulatory and nutritional disturbances (Ch. 5) (215;246-288).
In the final analysis degenerative joint disease and bone mass alterations were frequent in Missouri Basin skeletons, but they appeared in individuals younger than is usual today. The two factors most likely as cause are the life style of the individuals represented, and their nutrition.
Markup by Larry Zimmerman, 4/21/98
