By definition a tumor is a mass, swelling, or enlargement. Cysts are abnormal membranous sacs containing gas, liquid, or semi-solid substances. Biologically, tumors are malignant (cancer: invades and spreads, destroying the host), or benign (remain localized, but may enlarge).
During the interval 1900-1968, in the United States cancer moved from 7th to 2nd place as cause of death, and increased in frequency from 64 to 159 per 100,000 population (Table I.1, Fig.3.1). Much of the change in causes of death accompanied greater longevity brought about by control of infectious diseases and better socioeconomic conditions.
Cancer is a disease of an aging population, promoted by exposure to carcinogens. Primary cancer arising from the cellular constituents inbone (sarcoma) is not common today, and has been diagnosed infrequently in ancient skeletons (62-330;82-16;225-23;226;246-365;302-318;309).
Especially in individuals past 50 years disseminated (metastatic) cancer is the commonest malignant affectation of bone. Many cancers spread to bone, but the most frequent primary sources are breast (female), lung (males but increasing in females), prostate (male), thyroid, and kidney; less frequently Hodgkins disease, endotheliomas, and lymphomas. In infants and children neuroblastoma and leukemia disseminate widely. Malignant metastases usually involve red marrow, most often in vertebrae, thoracic being commonest followed by lumbar, and the sacrum (302-385;190). Other metastatic recipients include the skull, ribs, pelvis, proximal humerus and femur, and sternum. Reports of metastatic cancer in bone are few in the literature of paleopathology (7;70;201-53;226;246-391;302-385;363).
Benign soft tissue and bone tumors are common today but because they are asymptomatic during life many are unrecognized unless discovered accidentally. In skeletons sans soft tissue tumors such as osteo mas, exostoses, enchondromas, and cyst-like processes are easily recognized, producing an apparent in creased frequency in skeletal populations.
The common locations for primary cancers are in Table 4.1 (68;298-45,65); the age adjusted death rates per 100,000 by race are in Table 4.2 (172- 17,64); and cancer deaths by site of origin in South Dakota Native Americans are in Table 4.3.
Table 4.1. U. S. Cancer Deaths, Whites*
Cancer_Location______________Male______Female
Lung 34% 16%
Breast -- 19%
Colon and rectum 14% 15%
Prostate 10% --
Leukemia and lymphoma 9% 9%
* U.S. and South Dakota Vital Statistics.
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Table 4.2. U. S. Age Adjusted Cancer Death Rate,
by Race, 1975 (per 100,000)
Native Americans 100.7
Japanese 158.3
White 174.0
Black 189.4
Chinese 189.7
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Table 4.3. Cancer Deaths, 1982, South Dakota Native Americans
Cancer_location______________Male_______Female
Respiratory & intra- 9 1
thoracic organs
Digestive organs and 3 6
peritoneum
Genital organs 3 1
Urinary organs 1 -
Breast - 2
Lip, oral cavity, pharynx - 1
Leukemia 1 -
All other and un- 6 6
specified_sites______________________________
23 17
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Despite increased frequencies of certain malignancies in American Indians during the past 30 years, in 1975 their age adjusted death rate for malignant neoplasms was 39% lower than for other races (Table 4.2). Some increase parallels greater longevity (See Fig. 8.7); some is attributable to carcinogen expo sure. In males the shift to first place for lung cancer deaths correlates with increased tobacco use. In both sexes, primarily in women, biliary passage, liver, and pancreatic cancer are common primary cancer sites (26-43,61,63,116,117). The great number in these organs may reflect dietary changes, and be at least partially due to increased consumption of alcohol. Cervical cancer is increasing in Indian women, the highest mortality being in the upper reaches of The Missouri River Basin in northern Montana (26- 101,123). Nationwide, cancers of the nasopharynx, testis, cervix, kidney, and female thyroid (172-17,64) have increased.
In 1982, 1,290 South Dakota deaths (184 per 100,000, 19.3%) placed cancer second in frequency as their cause. During the same time there were 40 Native Americans cancer deaths (9.4%; 89 per 100,000) (Table 4.3). The small number of cases and incomplete information as to tumors' anatomic site and histo logical characteristics makes statistical analysis tenuous. In addition, caution is imperative when death certificate data are the source of statistics concerning cancer deaths, because accuracy may be marginal (123). Little dependable information is available relating to cancer morbidity in regional Indian people.
Nothing to suggest the effect of primary bone cancer (sarcoma) has been forthcoming in Upper Missouri Basin aborigines. Histological confirmation of tumors was not possible in skeletons, and museum specimens could not be damaged, so we had to rely on gross examination and radiographs to differentiate suspected tumors. The appearance of cancer in radiographs is osteolytic, osteoblastic, or mixed. Blastic response is the host bone's reaction to invading tumor. Marginal sclerosis accompanies slow growing cancers and benign lesions, but is usually absent with rapidly growing tumors. Metastatic cancer may also evoke periostial reaction. Some metastatic cancers, notably kidney and thyroid, produce solitary slow growing expansile lesions.
While evaluating extensive facial destruction (Fig. 3.12), an invasive malignancy was consider ed, but abandoned in favor of a granulomatous infection (Actinomycosis).
Figure 4.1. 39CO32 Nordvold Site. Arikara male 40+ yr.
Table 4.4. TUMORS and CYSTS.
Site Torus** Stafne
Skeletons______Culture__Osteoma*_____Cyst_______Spur____Palatinus__Defect__Hemangioma
Swan Creek
39WW7 Arik Frontal Clavicle -- -- -- --
N= 82
Mobridge Frontal Frontal Fibula -- -- --
39WW1 Arik Parietal Patella Fibula
N= 55 Innominate
Four Bears -- -- Tibia -- -- --
39DW2 Arik
N= 41
DeSpeigler -- -- Fibula -- -- --
39RO2 Woodland
N= 50(est)
Ufford -- -- -- -- -- --
39CL2 Woodland
N= 40
Double Ditch -- -- -- -- -- --
32BL18 Mandan?
N= 24(est)
ND Hist. Soc. -- -- -- 3 -- --
N = 151*** Several
Over Coll. Frontal Metatarsal Tibia & 7 1
N= 228 Several Maxilla & Radius Fibula
Parietal Radius Tibia
Occiput Innominate
Radius Fibula
Occiput Tibia
Femur
Misc. Coll. Frontal -- Tibia 29 -- Parietal
& Spec. Several Maxilla Tibia Frontal
N= 2427**** Parietal & Fibula Parietal
________________________Maxilla_________________Tibia
Total 3098 14 6 15 39 1 3
* Outer ear canal osteoma (exostosis), see Ch. 4, Epilogue.
** See Ch. 9.
*** Evaluation primarily emphasized the skull.
**** For about 50% of 2186 primary emphasis was upon the skull.
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Osteolytic defects for which metastatic cancer was possible were in three Arikara skulls from different geographic locations and periods in time, two adults and one child. For one adult skull (Fig. 4.1) we feel the likelihood of neoplastic origin is good.
Skull One. Figure 4.1 a round 2.0 cm defect involved the frontal bone's entire thickness. At its periph ery cortical bone was thickened and the edges were elevated as flanges circumferentially, indicating response to an expanding intramedullary mass. No other abnormality was in the skull or skeleton. In radiographs circumferential marginal sclerosis 1-3 mm wide indicated a slowly expanding intra-diploic mass. Although this could represent a walled off infectious process, infections usually cause more in flammatory reaction within and at the periphery of the lesion. The residual of physical trauma and an intradiploic cyst were additional possibilities. All factors considered, the consulting radiologist and we believe this is a metastatic cancer implant (141).
To facilitate identification of the neoplastic primary source, it is assumed that in regional prehistoric Indians cancer behaved the same as it does in the general population today. For a male of stated age, not exposed to modern carcinogens, solitary metastasis from a cancer in the thyroid or kidney offers the best explanation for these findings.
Skull Two. An adult male's calvarium (Fig. 3.14) had multiple discrete osteolytic defects for which metastatic tumor implants were suspected, but a granulomatous infection was postulated as more likely (141).
Skull Three. Round irregular defects involved all tables of a child's skull (Fig. 5.1). Available long bones were not involved. In radiographs the defects were mildly sclerotic peripherally. Metastatic cancer (kidney, leukemia, lymphoma) were considered, but the radiologist felt Histiocytosis X was more likely (141;364-131=135). In an adult over 45 years multiple myeloma (cancer arising in marrow cells) could cause similar skull defects.
Table 4.5. Crow Creek Skeletons. Tumors and Cyst Like Lesions
Bones Lesions
Abnormality_______________Location________Counted__Counted____%____Total
Neoplasms
Fibrous dysplasia---------Tibia 531 1 .1 1
Osteochondroma------------Humerus 413 1 .2 1
Osteoid osteoma-----------Tibia 531 1 .1 2
Humerus 413 1 .2
Osteoma-------------------Femur 734 3 .4 55
Tibia 531 1 .1
Parietal --- 2 --
Temporal 963 1 .01
External ear
canal 963 45 4.6
Torus
palatinus 129 3 2.3
Bone spur-------------------Clavicle 233 1 .4 7
Tibia 531 4 .7
Fibula 299 1 .3
Femur 734 1 .1
Heterotopic bone------------Humerus 413 2 .4 14
Tibia 531 2 .3
Fibula 299 7 2.3
Pubis --- 1 --
Innominate 1133 2 .1
Cyst like lesions-----------Frontal --- 1 -- 12
Parietal --- 1 --
Orbital roof --- 1 --
Clavicle 233 2 .8
Scapula 521 2 .4
Radius 206 1 .4
Ulna 244 1 .4
Fibula 299 1 .3
Pubis --- 1 --
____________________________Femur___________734________1______.1________
Total 92
From: Zimmerman et al, 1980, p. 214.
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Non-malignant tumors and cysts from different skeletal populations are in Table 4.4. In some, listed Miscellaneous Collections and Specimens, skeletons were partial and/or examination was limited to the skull, so post-cranial benign tumor representation is under-reported.
Benign tumors and cyst-like defects at Crow Creek are in Table 4.5. Osteomas (including exostoses) were commonest, followed by heterotopic (formed in unusual places) bone, cysts, and bone spurs.
Many of the latter three were residua of trauma. Some cyst-like defects may have been fluid fill ed, but during life most probably contained soft tissue. Except for discomfort accompanying their causative injury, it is unlikely lesions of traumatic origin were symptomatic.
OSTEOMA
Varyably sized, usually small, round or oval shaped localized ivory-hard lamellar (in plates) islands, protruding from bones' surfaces, variously called compact osteomas or exostoses, have long titilated the fancy of paleopathologists. They are common in skulls, with predilection for the mandible, palate, and external ear canals. Figure 4.2A, shows a "button osteoma." Other osteomas appear in 4.2 B-F.
It is doubtful these are true neoplasms; more likely they represent osteoblastic stimulation by local irritation or periostial injury (27-134;82;199-9,41,116). Numerous references to these tumors are in the paleopathology literature (62-15,43,322,552;168;225;302-325).
EXTERNAL AUDITORY CANAL EXOSTOSES.
Discussion of these tumors is germaine to Chapter 4, but the Dry Bone findings are more effective as a suppliment (See Ch. 4, Epilogue).
OSTEOID OSTEOMA
Figure 4.3. 39BF11 Crow Creek. Proto-Arikara adult male.
In the middle third of a tibia's anterior cortex there is a 13 x 12 mm oval defect with slightly raised edges and saucer-like center. An island in the concavity's midportion and the defect's edges are dense cortical bone. No other abnormality was in the tibia, and other skeletal components were unavailable.
Osteoid osteomas are benign tumors more common in males, children and young adults. In radiographs they are small rounded radiolucent areas surrounded by reactive sclerosis. The amount of sclerosis increases with the lesion's proximity to the bone's surface. It has been questioned whether these are actually neoplasms, or perhaps they represent obscure bone infections, possibly previous osteomyelitis. This and another osteoid osteoma, in an adult humerus, were in pre-Columbian Crow Creek skeletons. Similar tumors were seen in other skeletons from the Dakota Territory. These lesions are usually painful during life. Reference to these tumors have appeared in the paleopathology literature (62-325;225-21;302- 235;347).
OSTEOCHONDROMA
Figure 4.4. 39BF11 Crow Creek. Proto-Arikara adult, probably male.
A tumor mass protrudes laterally from the proximal portion, lateral surface, of an adult male humerus (Fig. 4.4). Grossly it appears quiescent. Skeletal disruption in the common grave precluded investigation for similar lesions in the individual, but similar abnormalities were not found. Radiographs show increased bone volume with a laminated trabecular pattern, appearing to flow toward the lesion, suggesting progressive growth. This appearance identifies it as an osteochrodroma, and distinguishes it from other calcified masses inherent to bone surfaces (Lent Johnson, Orthopedic Surgery Division, Armed Forces Institute of Pathology, Personal communication, 1979). This is the only such bone tumor identified in regional skeletons.
Osteocartilagenous exostosis or osteochondroma is probably the commonest benign bone tumor. They arise most often at the ends of long bones and are fundamentally osteomas arising from cancellous bone. Characteristically they point away from the end of their bone of origin. They may be regarded as miniature bones in that they have epiphyseal cartilage caps by means of which they increase in size, as long as skeletal growth continues. When single their malignant potential is less than 1%, but if multiple it is 20%. Osteochondromata have been reported in the paleopathology literature (62-323,330;302-319).
BONE SPUR. MYOSITIS OSSIFICANS.
Seven bone spurs were in 486 Crow Creek skeletons (Table 4.5), the tibia being affected most often (4/531, 0.75%). In 14 instances heterotopic bone was found. Fibulae were involved most often 7/299 (2.3%), followed by two lesions each in humeri, tibii, and innominates.
Deitrick reported heterotopic bone formation in 36/628 (6.1%) cemetery skeletons and 9/71 (13.1%) earthlodge skeletons from the mid-18th century Larson Site. Fibulae were involved most often in both cemetery (17/777, 2.2%) and earthlodge (3/125, 2.4%) skeletons. In addition, she found similar changes in 5/261 (2.1%) early 19th century Leavenworth cemetery skeletons (Table 2.4), but specific bone involvement was not indicated (89).
The configuration of bone spurs in adult
skeletons (Fig. 4.5) suggests traumatic origin.
4.5A. Innominate tumor representing bruising or penetrating trauma to the pelvis' lateral
surface.
4.5B. Residua of tearing injury to tibia ligamentous attachments.
4.5C. Right tibia and fibula. A sprain or sprain/dislocation explains distal tibia/fibula
findings. Additional pathology in this skeleton: degenerative changes proximal ulna; flint
chip distal left fibula.
4.5D. Proximal femur changes, aftermath of blunt soft tissue injury. All lesions are
healed; probably occurred long before death.
Figure 4.5. Representative bone spurs from different geographic locations and time
periods.
A. 39BF11 Crow Creek. Proto-Arikara male adult
B. 39WW2 Larson Site. Arikara female 40 yr.
C. 39LM33 Dineharts Village Over Collection #3560.(date and culture unknown). Male 36-40
yr.
D. 39ST1 Cheyenne River Site. Over Collection #13506. Arikara male 35-40 yr.
Once healed it is unlikely these injuries caused significant functional impairment. Although resembling tumors and considered separate entities, these processes are usually of traumatic origin, representing ossification in tissues subjected to physical stress.
Heterotopic ossification occurs with trauma, aging, or other stimulus to structures of embryonic mesodermal origin, producing bone where normally it does not exist, i.e., muscle, tendon, ligament, or cartilage. Ectopic ossification usually conforms to the shape of affected structures, but can appear as sheets, strands, or formless masses. Bone spurs are a form of ectopic bone.
Myositis ossificans is localized heterotopic bone and cartilage, usually near bone or in muscle (114). Two forms are recognized: 1) a rare progressive disease; and 2) post traumatic ossification complicating fractures and fracture dislocations most often when large muscle masses and connective tissue are crushed against bone (see Fig. 4.5A,B), or following disruption of tendon and fascial attachments (82-633,708;199-2,389). Myositis ossificans has been discussed from the standpoint of paleopathology (62-325;225-21;302-322).
Two knobby tumors with a shallow depression between them protrude from an adult innominate bone's medial surface (Fig. 4.6). Inset shows the mass enlarged. The tumors are lobulated cortical bone that appears old. There was no other abnormality. A radiograph showed a homogeneous mass with a small radiolucent defect in its midportion, probably a retained projectile point. This was a museum specimen, precluding definitive analysis by invasive methods.
It is surprising that despite the location of this mass, its probable pathogenesis, and the trajec tory through which a projectile had to enter the bone, the affected individual did not die of peritonitis. The amount of tumefaction indicates it began quite some time before death.
Figure 4.6. 39WW1 Mobridge Site. Arikara male 30-35 yr.
Expanding trabeculated bone in the medullary cavity is pressing upon and thinning the distal cortex in an adult male tibia (Fig. 4.7). The medullary architecture is replaced by evenly spaced fiber bone trabeculae that anastomose producing a regular retiform (network) pattern. Small, flat, slightly raised excrescences are on the tibia's surface (arrow). Structurally the tumor is similar throughout, but there are a few small pseudo-cysts. To the examining finger the tumor's cut surface feels like coarse sandpaper. The gross and operating microscopic patterns suggest late stage inactive fibrous dysplasia (Lent Johnson, Armed Forces Institute of Pathology, Personal Communication, 1979). The cause of fibrous dysplasia is unknown.
Figure 4.7. 39BF11 Crow Creek. Proto-Arikara male adult.
It is more frequent in males, usually appears during infancy or childhood, but occurs in adults (82). Mostly it involves long bone ends, the proximal femur being most frequent (114). Radiographs show ill- defined zones of decreased density with overlying thinned or expanded cortex. There is usually no periostial reaction (199-11, 13,391).
Although often discussed in conjunction with bone tumors, it is more likely this disease represents faulty repair following trauma. In the living, nests of fibrous tissue fill interspaces between bony trabeculae. Because this process was at the tibia's distal end involving the ankle, walking may have caused some discomfort. Monostotic fibrous dysplasia does not have a significant malignant propensity but the structurally weak bone is susceptible to pathological fracture.
Findings similar to Figure 4.7 were in the distal tibia of an American Indian male skeleton 18-22 yr. (probably Woodland) found in 1985 near Worthington, MN. Gross findings and radiographs were interpreted as fibrous dysplasia. No other representation of this disease has been forthcoming from this region.
Other reports of fibrous dysplasia have been in the literature of paleopathology (91;137;225- 22;302-336;345), but one skeleton from Alaska, postulated as isolated metastatic cancer in the mandible (from esophagus) (70), appears to us more likely an example of fibrous dysplasia.
An irregular cavity in the head of an adult metacarpal bone with smooth lining and edges was an isolated abnormality in the skeleton (Fig. 4.8).
Figure 4.8. 39CA4 Rygh Site. Arikara male 30-40 yr.
Nothing suggested reactive response to the defect. During life the defect contained solid tissue, probably cartilage, identifying it as an enchondroma. Enchondromas appear near cartilagenous epiphysis in metaphyses of bones that develop by enchondral ossification (bone formation in cartilage). Usually they are single; most are in short cylindrical bones of hands and feet. Enchondromas are rare in children, usually appear in adolescence. The average age of discovery is 35 years. They usually are asymptomatic, and do not have a malignant potential (199-29,57,180,372). We have not observed similar lesions. References to these neoplasms are in the paleopathology literature (62-327;225-21;302-235;309).
Figure. 4.9. 39WW1 Mobridge Site. Arikara male 30-35 yr.
A sharply demarcated 7 mm cyst-like lesion in the frontal bone's anterior cortex involves the outer table and diploe, and has osseous reaction within (Fig. 4.9). Otherwise the skull and available skeleton were normal. A developmental cyst was possible, but an encapsulated foreign particle is more realistic. No comparable abnormalities were in skeletons from this area, but a slightly larger similar lesion in the same location, is in the San Diego Hrdlicka Paleopathology Collection (1915-2-97) (329). We have not seen discussions of similar lesions elsewhere.
Non-artifactual localized vacancies in bone can represent true cysts, or pseudocysts. True cysts are inborn, caused by trauma, secondary to metabolic changes or infections, or of neoplastic origin. In old bones cyst-like defects representing islands of soft tissue during life very often make interpretation difficult.
In an adult parietal bone there is a 2.5 x 2.5 x 1.5 cm cyst-like cavity (Fig. 4.10). Its floor is thin and smooth, the interior is remodeled, and the edges are raised and irregular. On the medial surface the middle meningeal artery groove is intact. The superior temporal line on the lateral surface (arrows) is accentuated from ligamentous stretching. The skull had no other abnormality. This is the aftermath of cranial fracture, aseptic necrosis of a bone fragment, and cystic degeneration of devitalized bone. The process occurred several months ante-mortem, and appears inactive at death. This was an isolated circum stance in this population and in our experience. We have found no reference to similar defects.
A 13 x 7.5 mm oval defect is in the medial cortex anterior to the angle of the mandible (Fig.4.11). It extends into the medullary space but does not involve the lateral cortex. The edges are smooth and there is no evidence of osteoanagenesis or periostial reaction. Other abnormalities in this skeleton included small bilateral paracondyloid processes, small anterior linear ear canal exostoses, occipital botton osteoma, separate neural arch L-5 & S-1, and marked skull osteoporosis. This is the only Stafne defect we identified in regional skeletons.
Finnegan and Wittey reported an adult skeleton with a Stafne defect, and stated they had "seen 4 or 5 of these defects" (107). In a personal communication Allison and Gerszten (Medical College of Virginia) reported a similar defect in the mandible of a late Woodland Indian (c. 1,550 A.D.).
Batsakis considers Stafne "bone cysts" as rare, static, benign, developmental defects near the groove of the facial artery as it crosses the mandible. Most are due to ectopic submaxillary gland tissue that develops in the bone's medial cortex (38). They occur predominately in females, may be bilateral, and usually are found between 33 and 72 years of age. Stafne defects are asymptomatic and are often found incidentally in radiographs.
Figure 4.10. 39BF11 Crow Creek. Proto-Arikara male adult. A. Medial surface. B. lateral surface.
All frontal bone tables were involved by a lobulated, irregularly round, eroded defect with smooth edges, suggesting diploic space origin (Fig. 4.12A). Otherwise the skull was normal. In gross appearance and in radiographs this was an hemangioma, a benign vascular tumor. A round eroded area in the inner cortex of an adult parietal bone just lateral to the midline (4.12B, arrow), is interpreted as a hemangioma.
A few lesions similar to 4.12B have been in other skeletons, but none like 4.12A has been identified. Usually asymptomatic during life these tumors are often incidental discoveries. Hemangiomas occur mostly in calvaria and vertebrae, less often in the pelvis and small hand bones. Gilmer et al reported vertebral hemangiomas (occasionally multiple) in 10% of the population (114). Very few possible hemangiomas have been reported in archaeological material(302-352).
By definition, cholesteatoma is a cystlike mass lined by stratified squamous epithelium (skin), filled with dead skin, that might be looked upon as a form of benign tumor. They appear in several locations but are most common in the middle ear and mastoid.
Figure 4.11. 39ST235 Stony Point. Over Collection #17416. Arikara male 35-40 yr.
They resemble invasive tumors in that they expand locally causing bone erosion and can destroy contiguous structures by pressure effect.
The evidence for middle ear and mastoid cholesteatoma in antiquity was presented and discussed in Chapter 3, Epilogue). External ear canal cholesteatoma, alluded to by Stewart (307), was discussed brief ly (Ch. 3). In clinical practice middle ear and mastoid cholesteatoma was quite frequent in the general and Native Americans populations, but outer ear canal lesions were seen only occasionally. Dehiscent tympanic plates suggesting canal cholesteatoms were in several adult dry skulls but were not distinguishable from developmentally patent foramina of Hushke.
A cholesteatoma (epidermoid cyst) is a differential possibility for the lesion illustrated in Figure 4.1 (259-228).
During the Dry Bones project the remnants of many people were examined. Nothing suggesting the effect of primary bone cancer was observed. To explain destructive facial disease in one skull the possibility of invasive cancer was entertained, but abandoned. Bony changes for which metastatic cancer was a differential consideration were encountered several times but three were especially difficult to interpret. For two of these it was finally decided the disease processes represented was not cancer. After thorough analysis, we concluded that the third probably represented a metastatic neoplastic implant, and speculated its origin in the thyroid gland.
The absence of cancer in regional skeletons is explained best by two observations: 1. the life span of people who lived here in the past was short; only a few survived to the cancer age group; and 2. many cancers relate to carcinogen exposure. Of 88 chemicals recognized as carcinogens today, only two, aflatoxin and cycasin, occur naturally (291). It is unlikely that previous inhabitants of this region had contact with either of these.
In addition, regional and national patterns of cancer in Native Americans today, are different than in the general population. Nationally, biliary tract, liver, and pancreatic malignancies are the most frequent cancer primary sites today. Bone metastasis from these cancers is not common. But with greater longevity of Native Americans and exposure to carcinogens, other cancers are occurring more often. In Sievers and Fisher's opinion the prevalence and anatomic distribution of cancer in North American Indians today is influenced more by cultural conditions and environmental factors than by inherited resistance or inborn susceptibility to specific malignant neoplasms (294-223).
If cancer existed in the original people of this region and behaved as it does today, the likelihood of finding bone metastases would be small. Despite the apparent absence of cancer in this region in the past, historical references to ancient Egypt, Greece, Rome, and elsewhere, belie the wishful thought that cancer did not exist in antiquity (105).
In skeletons examined during the Dry Bones survey, benign tumors were a frequent finding. Many were tumor by definition, but attributable to trauma or other cause. With a few exceptions there was no not able difference in the type and location of tumors in pre and post-Columbian skeletons. In general, the types of tumors, their locations, and their effect upon skeletons, were comparable to what has been found in other skeletal populations.
Benign bone tumors attributable to the effect of physical trauma during life were more frequent in mid-18th century skeletons than in pre-Columbian or early 19th century skeletons. Because the horse was becomming available in the region in the early 1700s, it is conceivable this event was a factor promoting skeletal trauma.
The one area where findings during this research have differed with the findings of others relates to the locations and frequencies of exostoses in the external auditory canals. Although it has been reported elsewhere that these tumors can arise from any portion of the canal, in our experience they are found at the points where the tympanic ring and temporal bones fuse, and where the annular ligament and tympanic membrane attach to the bony ear canal. The high frequency of auditory canal exostoses reported from Mobridge, S.D., by Hrdlicka, has not been corroborated by the findings in large groups of skeletons exhumed from that region through salvage archaeology techniques during the 1960s and 1970s. Our findings in skulls at North Dakota and the U.S. National Museum, known to have been examined by Hrdlicka, corroborate his statistics regarding the frequency of exostoses in those specimens. The statistical discrepancies between Hrdlicks's data and ours are best explained on the basis that his results were compiled from random sample specimens, rather than from true population samples, as was possible with salvage archaeology specimens.
EXTERNAL AUDITORY CANAL EXOSTOSIS (Osteoma).
The outer ear ear canal is a frequent location for exostoses. These benign tumors have long been of interest to physicians, anthropologists, and paleopathologists. Many reports from these disciplines have appeared in the world literature (4,93,121,279,302,307).
In 1934 Hrdlicka reported his findings in 7,814 skulls, a small number of which came from North Dakota and South Dakota (Table 4.6) (168), summarized world-wide demographic information, and discussed hypotheses relating to the origin of external auditory canal exostoses. He noted that the diverse theories as to pathogenesis have in many ways confused the issue.
In the 'general discussion' accompanying his article, Hrdlicka listed personal observations (168-80=86) that assisted our investigations: 1. Exostoses are purely human. 2. They develop chiefly in later adolescence and the early half of adult life. 3. Males are affected much more frequently. 4. Bilaterality is the usual; unilateral lesions are more often on the left. 5. In Whites exostoses occur predominately in well-to-do classes. 6. They arise from the remnants of the free upper ends of the tympanic ring. He concluded:
The exciting cause of ear exostoses, where the predisposition to these exists, may be anything mechanical or chemical that produces prolonged irritation, with consequent hyperaemia to inflammation of any part of the bony meatus (168-86).
Originally the Dry Bones project was focused upon otological abnormalities, so it was natural that ear canal exostoses were included in the research effort. Data from the Upper Missouri River Basin relating to these tumors is considerable.
WET BONES Studies.
In clinical practice in South Dakota that entailed 6,000-7,000 patient contacts per year, exostoses were in about 4-5% of adult patients' external auditory canals, but not in children. Males were affected more often. They occurred with the same frequency in the general and Native American populations.
Table 4.6. External Auditory Canal Exostoses, North and South Dakota
Skulls Ears % ears
Location______________________Skulls__exostoses___%_____exostoses___exostoses
South Dakota (All, Mobridge, 109 30 27.5 48 22.0
Arikara, Misc.)
South Dakota (Mobridge alone) 76 23 30.3 37 24.3
North Dakota 29 2 6.9 2 3.45
From: Hrdlicka, 1934.
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DRY BONES Studies.
Early Dry Bones studies at the Over Museum showed exostoses in the outer ear canals of 3:221 individuals (1.3%) (165,166,301). In the first group of salvage archaeology skulls there were 9:358 (2.5%). At The Museum of The Historical Society of North Dakota exostoses were in 9/149 skulls (6%) (125) for an overall total of 21/728 (3%).
Our North Dakota results agree with Hrdlicka's report of his findings in skulls from that state (Table 4.6), suggesting to us the North Dakota skulls he had seen were the same as those we saw during the Dry Bones evaluation. It is notable the North Dakota skulls were largely museum specimens and basically randon samples in culture, time, and geography. Subsequently we examined many temporal bones from other museums, private collections, and salvage archeology skeletons, but our results did not corroborate data Hrdlicka reported for the Mobridge vicinity. To locate discrepancies between his and our results, we examined skulls he had evaluated, now at the U.S. National Museum. Our findings in the National Museum skulls were similar to his, indicating to us the disparity between his results and our findings was not differential interpretation (130,135). More likely, different archaeological techniques were used to procure his specimens (306). Stewart reminded us that Hrdlicka's specimens were often random samples from aboriginal cemeteries, or from other sources, and as such did not present true cross sections of the pathology in the population (T.D. Stewart, Personal communication, 1967).
Table 4.7. North and South Dakota Skeletons. Exostoses, External Auditory Canals
Temporal Total Right Ear Left Ear Bilateral % %
Culture_________bones______Skulls___M___F__?____M___F__?____M___F__?___Temp._Bones___Skulls_
Crow Creek 963 482+ 7 12 26 7.4 9.3
Proto-Arik.
Arikara 993 613 2 2 2 1 7 2.1 2.2
Arikara- 50 34 2 1 12.0 8.8
Mandan
Mandan 79 45 2 5.1 4.4
Woodland 87 50 1 1.1 2.0
Historic 301 178 2 1 1.3 1.7
Sioux
Undetermined______380_______230____________1____3___1__2____7_____________5.0_________6.1_
Totals 2853 1632+ 3 8 5 3 17 18 2 26 4.8 4.9
Pierre Indian 770 385 None None None
School Children,
Grades K through
12, primarily
Sioux
|
The great majority of skeletons we examined came from salvage archeology, providing more complete cross sections of populations for study, and a better means to assess epidemiology.
In Table 4.7 our findings relating to exostoses in Dakota Territory dry temporal bones are tabulated and compared with a group of contemporaneous South Dakota Indian School children. The greatest number of exostoses were in Arikara-Mandan skulls, but the number available was small (and specimens at the The Historical Society of North Dakota were not true population samples) making statistical analysis tenuous. No significant geographic or temporal patterns were apparent for exostoses, but they were only in adult temporal bones. The male to female ratio was 6:1; tumors were more often bilateral, but when unilateral 75% were in left ears. The overall frequency in old skulls is similar to clinical observations in the regional general and Native American populations today.
Four structurally different exostoses were in our specimens' ear canals and an isolated fifth tumor type presented posterior and superior to the ear canal (Fig. 4.13F) (130). For lack of accepted terminology to designate them, descriptive terms used were: 1) spongy (4.13A); 2) knob-like (4.13B,C,D); 3) linear (4.13C arrow); and spicular (4.13E). Linear exostoses were most common, followed by knobby tumors. Spicular defects occurred occasionally, but were usually smaller than 4.13E (130,301).
Typically, exostoses developed from dense (cortical) bone, except 4.13A, which came from osteocarti lagenous (cancellous) bone. This lesion had enlarged sufficiently to replace the tympanic ring and fill the ear canal. Radiographs showed the canal lesion but no other abnormality. Hearing in this ear should have been affected moderately. This was an isolated mass burial specimen, precluding investigation for bilaterality, but no similar temporal bone was in the grave (361-241=246). Another 50% occlusive unilateral spongy tympanic ring exostosis was in Over Collection Arikara skull #13483 (39ST1 Cheyenne River Site, Male 25-30 yr.), and other tympanic rings had mild spongy type changes (130,301).
LOCATION of Ear Canal Exostoses
Despite reports by Hrdlicka and others that exostoses occur almost anywhere in the outer ear canal, most often on posterior and anterior walls (93;121;168-86;279), in our specimens exostoses presented in two specific locations: 1) the anterior and posterior points of fusion between the primordial tympanic ring and the inferior-lateral temporal bone surface (Fig. 4.13B,C,D,E); and 2) at the annulus (where the the ear drum meets the bony ear canal), particularly along the floor and anterior wall (Fig. 4.13C).
Anatomic and physiological factors affecting ear canal development are diagrammed (4.14 middle). They include skull base growth (SB), force on temporo-mandibular joint (TMJ), mastoid process growth (M) affected by sterno-mastoid muscle pull, and outer ear canal growth (EAC). A--A' and B--B' are the direction and repositioning of the tympanic ring as the temporal bones develop.
Figure 4.13. Typical outer ear canal
exostoses.
A. 39BF11 Crow Creek. Proto-Arikara adult.
B. 39WW1 Larson cemetery. Arikara adult male.
C. North Dakota, no provenience. Male 40+ yr.
D. 39SL4 Sully Site. Arikara male 29+ yr.
E. 39WW2 Larson Cemetery. Arikara male 40 yr.
F. Over Collection, no provenience. Adult male.
TYMPANIC RING DEVELOPMENT.
When bone is stressed, there is the proclivity to remodel or form new bone. Growth subjects the tympanic ring to stress in three directions, accompanied by masticatory forces in a fourth direction. These forces are capable of stimulating osteoanagenesis at the points of fusion to the temporal bone. Stretching of the annular ligament by otitis media could stimulate fibrous tissue proliferation at ear drum edges, followed by metaplastic bone formation. However, another undetermined factor is the proximate stimulus to exostosis formation.
Notably, similar to Hrdlicka's findings, almost without exception Upper Missouri River Basin auditory canal exostoses, past and present, have been in adult temporal bones. This strengthens our conviction that these are developmental abnormalities, the result of stimulae to immature bone during its formative stages.
Markup by Larry Zimmerman, 1/4/98
