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Connective tissue responses in Negroes in relation to disease.

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Connective Tissue Responses in Negroes in
Relation to Disease
Birth Defects Institute, State Department of Hectlth, Alb a n y , N e w York
KEY WORDS Adaptation . Racial differences . Infectious diseases . Immunoglobulins . Fibroblasts . Pigmentation.
There is considerable evidence that Negroes have a tendency
toward overgrowth of those connective-tissue components concerned with
two functions - protection against infection (macrophages and plasma cells)
and repair after injury (fibroblasts and their products). Thus, adaptation to
the tropical environment in Africans may have involved a tendency toward
connective-tissue overgrowth, as well as hypertrophy of the pigmentary
apparatus. Both tendencies may have consequences in terms of: (1) susceptibility to certain chronic diseases; and (2) responses to disease processes or
drug therapies. Some of these possible consequences are discussed.
In 1937, Moehlig proposed that Negroes had a tendency, presumably genetic, toward "connective tissue overgrowth."
In support of this Moehlig cited the high
frequency among Negroes of keloids, or
raised scars formed in response to injury. This observation has been confirmed
among African Negroes (Alland and Keen,
'54; Verhagen, Koten, Chaddah and Patel,
'68) and U.S. blacks (Cosman, Crikelair,
Ju, Gaulin and Lattes, '61; Kenney, '65).
Moehlig's ('37) hypothesis is also supported by racial differences in other diseases involving connective tissue overgrowth, discussed below.
We are concerned mainly with connective tissue proper, one of four major types
of connective tissue - the others being
blood and lymph, cartilage, and bone. In
addition to providing mechanical support, the functions of connective tissue
include protection against infection and
repair after injury. These two functions
are discussed, along with their implications for explaining racial differences in
certain diseases.
Protection against infection
The reticuloendothelial system (RES)
or macrophage system is a connective
tissue component important in the pathology and natural history of infectious
diseases. Wassermann ('65) has reviewed
AM. J. PHYS. ANTHROP., 41: 49-58
evidence for hypertrophy of the RES in
Africans, and suggested adaptation to
tropical diseases as an explanation. Relatively high levels of immunoglobulins
were considered as evidence for this
In comparison with whites, healthy Negroes-both
in Africa (Weithaler and
Maruna, '67; McFarlane, '68; Ezeilo, '70)
and in the U.S. (Lichtman, Vaughan and
Hames, '67; Buckley and Dorsey, '71)have higher levels of serum immunoglobulin. High levels of gamma globulins
also characterize certain other tropical
populations, including New Guinea natives (Kariks and Hipsley, '61; Curtain,
Gajdusek, Kidson, Gorman, Champness
and Rodrigue, '65), Australian aborigines
(Curnow, '57), Malayan aborigines (Bisseru and Ahmad, '70; Brearley, '70), Indians (Rama Rao, Amrithalochani and
Narasimha Rao, '62; Chandra, Guha and
Ghai, '70; Sehgal and Aikat, '70), and
Mexicans (Golubjatnikov and Steadman,
It is uncertain to what extent these differences in gamma globulin level: (1)
represent a genetic adaptation to infectious disease; or (2) result from early
exposure to infectious disease. Supporting the genetic hypothesis is the finding
that Negro-white differences exist within
a similar tropical environment - that is,
Interestingly, high immunoglobulin (IgG)
levels are characteristic of this disease,
and the myeloma cell is of plasma cell
origin. The principal producer of antibodies - i.e., the immune globulins of
the blood involved in defense against infection - is the plasma cell, which is
a connective tissue component. Thus,
connective tissue overgrowth is apparently involved in multiple myeloma.
Scleroderma is a rare connective tissue disease involving excessive collagenization, producing a thickening of skin
and mucous membranes. Systemic lupus
erythematosus (SLE) involves widespread
lesions of connective tissue, often with
joint pain and swelling. Both diseases
are much more frequent in females. In
the U.S. both SLE (Siegel, Lee, Widelock,
Reilly, Wise, Zingale and Fuerst, ’62;
Siegel, Holley and Lee, ’70) and fatal diffuse scleroderma (Masi and D’Angelo, ’67)
are more frequent in Negro females than
in white females. These diseases “reflect
a local response of a particular tissue to
irritants or injurious agents” (Gardner,
’72:97). We have mentioned keloids as one
example of a local (dermal) response of
connective tissue to injury.
It has been suggested (Siegel et al.,
’62) that the higher rates of SLE in
U.S. Negro females might be related to
their higher gamma globulin levels relaDiseases of connective tissue
tive to whites. In a recent study, mean
Certain tumors of connective tissue IgG and IgM levels were both significantly higher in SLE patients than in concommon in some parts of Africa-notably, Burkitt’s lymphoma (Burkitt and trols (Alarcon-Segovia and Fishbein, ’72),
Wright, ’70) and Kaposi’s sarcoma (Tay- but abnormal elevation of IgM was the
most common pattern. In the Southern
lor, Smith, Bull and Pike, ’72)-involve
the RES. Evidence is accumulating for U.S., black females have significantly
an association between Burkitt’s lym- more IgM than white females (Buckley
phoma and malaria (Anon., ’70). Chronic and Dorsey, ’71), but males do not differ.
infection with malarial parasites stimu- This finding is interesting because: (1)
lates the RES. In tropical populationsSLE is much more common in females;
perhaps genetically prone to overgrowth and (2) Negro-white differences in SLE
of the RES as an adaptation to infectious frequency are confined to females.
diseases - such stimulation may be cruThus, connective tissue hypertrophy
cial in tumor formation (Edington, von in Negroes (high immunoglobulin levels)
Lichtenberg, Nwabuebo, Taylor and Smith, may be involved in their increased sus’70).
ceptibility to SLE, but this is uncertain.
Multiple myeloma is one of the most Although most of the cellular, tissue, and
common primary malignant tumors of organ damage in SLE can be attributed
bone. According to some studies multiple to immunological disturbances (Alexanmyeloma is more frequent in U.S. Negroes der and Good, ’70:106), the role of hyperthan in whites (MacMahon and Clark, gammaglobulinemia in causation is un’56; McPhedran, Heath and Garcia, ’72). clear. The occurrence of “autoimmune”
in South Africa (Milner and Calitz, ’71)
and Egypt (El-Hehawi, ’69). Also, American Negro-white differences are independent of socioeconomic status (Lichtman,
Vaughan and Hames, ’67; Buckley and
Dorsey, ’71). Longitudinal (Trevorrow,
’70) and family (Lichtman, McDonough
and Hames, ’67) studies suggest that genetic factors may be involved in determining IgG level.
Both malaria (Edozien, Boy0 and Morley, ’60) and schistosomiasis (Cook, Woodstock and Jordan, ’72) infection are accompanied by elevation of serum globulin
(particularly IgG) as well as by increased
phagocytic activity. Thus, these diseases,
common in tropical Africa, are associated
with overgrowth of the RES. The relative
contributions of genetic and environmental factors in causing an RES response,
however, remain to be clarified. In any
case, an ability to respond to these infections by an RES mechanism presumably
would be adaptive.
Thus, a tendency toward hypertrophy
of certain connective tissue elements may
be an adaptation to the tropical African
environment, in particular to infectious
disease (Wasserman, ’65). On the other
hand, this tendency might also predispose to other diseases, to which we now
diseases, such as SLE, in agammaglobulinemic patients argues against a causal
role according to some authors (Rowell,
’67) but not others (Alexander and Good,
It was once generally believed that
SLE was rare in U.S. Negroes. Similarly,
SLE was believed to be rare in tropical
Africa, but recent surveys suggest that
i t is at least as common as elsewhere and
“might be found more often when modern diagnostic methods become available”
(Verhagen et al., ’68).
Since most of the diseases discussed
above (multiple myeloma, scleroderma,
and SLE) are chronic disorders affecting
primarily older persons, natural selection
would not be expected to operate. Burkitt’s lymphoma, however, has a peak
incidence at age 5-9 years and apparently
involves an infectious (viral) agent. lndividuals with sickle cell trait may be more
resistant to Burkitt’s lymphoma (Pike,
Morrow, Kisuule and Mafigiri, ’70). This
finding, if confirmed, strengthens the
argument for an association between malaria and Burkitt’s lymphoma. Thus,
individuals with sickle cell trait may be
protected both from malaria and Burkitt’s
lymphoma. This might be explained by
the fact that the incidence of heavy
p. falczparum infections is lower in children with the sickling trait than in those
without the trait (Allison, ’64). Without
chronic malarial infection providing stimulation of the RES, susceptibility to RES
tumors might be lower.
Repair after injury, and granulomatous diseases
Repair of tissues after injury, a function
of connective tissue, may occur by substitution. Fibroblasts are the principal
agents of this repair. Substitution by
fibroblasts may lead to fibrous scars in
the tissues involved. Keloids, for example,
are dermal scars developed after skin injury. Histologically, keloids consist of
elastic fibers and collagen, with a granulomatous infiltrate containing fibroblasts,
plasma cells and lymphocytes (Kelley, ’63).
In the dermis, Japanese have significantly more fibroblasts than Caucasians
(Andrew, Behnke and Sato, ’65), but
Negroes apparently have not been studied. In a biopsy study of connective tissue,
however, Negroes developed a scleroprotein with a higher percentage of collagen
relative to whites (Boucek, Noble, Kao
and Elden, ’58). Collagen is produced by
fibroblasts, as in the repair of connective
In syphilis, a granulomatous infiammation, the response to tertiary lesions
involves “gummas.” Gummas consist of
fibroblasts, and “epithelioid cells” (macrophages transformed by ingestion of
certain substances). In the earlier literature osseous gummas were reportedly
more common in Negroes than in whites
with tertiary syphilis (Lewis, ’42). This
conclusion was supported by Frazier and
Hung-Chiung’s (‘48) study of 11,353
cases of syphilis at Johns Hopkins Hospital in 1920-1931.
Chronic granulomatous inflammatory
processes are produced by agents other
than the spirochete responsible for syphilitic lesions. Sarcoidosis is an infectious
granuloma of obscure etiology. The sarcoid granuloma consists of “epithelioid
cells” surrounded by fibrous connective
tissue, and lesions may occur in various
organs. Recent data from the U.S. (Terris
and Chaves, ’66; Dauer, Korns and Schuman, ’68; Keller, ’71) indicate that this
disease is much more frequent in Negroes
than in whites. Hypergammaglobulinemia is found in one-third to one-half of
patients with sarcoidosis, and “particularly among Negro patients” (Siltzbach,
’70:831). The disease may involve a tissue
response to various agents (viral, fungal,
or pollen), or to tuberculosis. Tuberculosis is another granulomatous inflammation which is much more frequent and
severe in Negroes than in whites, independently of childhood infection (Lurie,
Further evidence of a tendency of Negroes to form granulomatous connective
tissue, in response to injury, may involve
endomyocardial fibrosis.
Fibroblasts are involved in the healing
of defects not only in connective tissue
proper, but in other tissues such as heart
muscle. Heart muscle that degenerates,
following myocardial infarction or other
injury, is replaced by a connective tissue
scar. In endomyocardial fibrosis (EMF),
dense fibrous tissue scars replace the
endocardium and adjacent myocardium.
Although not confined to the African continent (Davies, ’69), EMF is relatively
common in parts of Africa (Shaper and
Coles, ’65; Shaper, ’66; Connor, Somers,
Hutt, Manion and DArbela, ’68). Few
cases have been reported in the United
States, but a probable familial occurrence
in North American Negroes has been reported (Bishop, Bousvaros, Cunningham,
Jain and Davies, ’68). Two diseases apparently related to EMF - i.e., “idiopat hic myocardial hyper trophy” (Phillips
and Burch, ’60) and endocardia1 fibroelastosis (McLoughlin, Schiebler and
Krovetz, ’66) - are reportedly more common in U.S. blacks than in whites.
The initial injury to the heart in these
fibrotic diseases may be caused by an
infective agent (virus or bacteria). The
correspondence in distribution of EMF
and Burkitt’s lymphoma suggests that an
immunological response to malaria may
be involved in EMF (Miall and Bras, ’72).
The theory that EMF is an “autoimmune”
disease is particularly interesting in view
of the above discussion of immunoglobulin levels in Negroes.
Thus, Negroes appear to be more susceptible to various diseases or disease
manifestations involving granulomatous
inflammatory responses. This may be due
to a tendency to form granulomatous
connective tissue (including fibroblasts
and their products) in response to injury.
Both African and U.S. Negroes, however,
may be more subject to the environmental agents responsible for these injuries
- specifically, to various infectious agents.
Scleroderma and SLE, as noted above,
reflect local tissue responses to irritants
or injurious agents. The response is excessive collagen production by fibroblasts,
and the injury may be caused by imminological disturbances.
ly common in East Africa (Verhagen et al.,
’68) and in U.S. blacks (White, Strudwick,
Ricketts and Sampson, ’61). The high
prevalence of soft-tissue fibrosarcomas in
Africans, and in other populations such
as Afghanistan (Sobin, ’68), may be related to viral and other agents introduced
through the skin by arthropod vectors.
There is some evidence, although inconclusive, that fibrosarcomas of bone in
children may be more common in Uganda
than in the U.S. (Dodge, ’64).
Fibromas are common benign neoplasms consisting of fibroblasts and collagenous tissue. Uterine fibromas (fibroids, fibromyomas, or leiomyomas) are
more frequent in U.S. black women than
in whites (Damon, ’60). A small proportion
of uterine fibroids become malignant tumors (leiomyosarcomas). There is some
evidence that these sarcomas are also
more frequent in U.S. blacks than in
whites (Christopherson, Williamson and
Gray, ’72).
Neurofibromas consist of masses of
nerve bundles (Schwann cells) and a
variable amount of collagen, and occur
in the subcutaneous tissue along the
course of peripheral nerves. The tumors
are classified as fibroblastomas. Multiple
neurofibromas (neurofibromatosis or Von
Recklinghausen’s disease) is reportedly
frequent in some parts of West Africa
(Basset, Collomb, Quere, Sicard and
Faye, ’66) and East Africa (Verhagen
et al., ’68). The frequency of the disease
in U.S. blacks is difficult to determine
from the literature.
Albright’s syndrome, involving fibrous
dysplasia of bone, is clinically similar to
neurofibromatosis. Normal bone is replaced by fibrous tissue. Apparently, the
racial distribution of this disease has
not been studied.
Fibroblasts and tumors
We have mentioned racial differences
certain connective-tissue tumors,
namely, Kaposi’s sarcoma and Burkitt’s
lymphoma. Both are lymphomas or lymphosarcomas, and involve uncontrolled
proliferation of lymphocytes. Malignant
neoplasms arising from fibroblasts are
known as fibrosarcomas.
In addition to dermal scars (keloids),
fibrosarcomas of the dermis are reported-
Fibroblasts and bony overgrowth
There is some evidence that in certain
pathologic states, fibroblasts may develop
into bone cells (Bloom and Fawcett,
’68:143). This might explain the frequent
occurrence of bony hypertrophy in certain diseases among Negroes, but this is
speculative at present.
Osseous lesions in tertiary syphilis may
involve new bone formation, as well as
bone destruction and fibrosis (gummas).
As noted above, osseous lesions are more
frequent in U.S. Negroes than in whites
(Frazier and Hung-Chiung, '48).
Among West African Negroes in Dakar,
Senegal, bony hypertrophy is reportedly
common in Von Recklinghausen's disease (Basset et al., '66). The origin of
these bony overgrowths is unclear, although a mesenchymal source has been
postulated (Basset et al., '66). Bony overgrowth -cysts (lined by fibrous tissue)
and elephantiasis - is rare in whites with
neurofibromatosis (Benedict, Szabo, Fitzpatrick and Sinesi, '68; Sane, Yunis and
Greer, '71). Griffith, McKinney, Monroe
and Howell ('72) reported three cases of
bone cysts in 50 patients with neurofibromatosis in Chicago children. Interestingly,
eight of the 50 cases (16%) were Negroes,
but the racial distribution of bone symptoms was not reported.
by melanocytes is increased. Hyperplasia,
or an increase in the number of cells
(melanocytes), is not involved in racial
differences in pigmentation (Szabo, Gerald, Pathak and Fitzpatrick, '69). This is
in contrast to the connective tissue overgrowth described above, which may involve both hypertrophy (increased immunoglobulin production by plasma cells, or
collagen production by fibroblasts) and
hyperplasia (increased numbers of plasma
cells, macrophages, and fibroblasts). This
distinction is partly hypothetical, since
the actual numbers of these cells have
not been studied in Negroes and whites.
There is evidence of decreased adrenocortical activity in Africans. Barnicot and
Wolffson ('52) found that 17-ketosteroid
excretion was significantly lower in West
Africans than in whites. Politzer and
Tucker ('58) found no difference in
17-ketosteroid excretion in healthy South
Possible analogy with hypertrophy
African Bantu and whites, but 17-ketoof pigmentary apparatus
genic steroid excretion was significantly
An analogy to the above relationships lower in men. While part of the total urimay involve pigmentation of skin and nary 17-ketosteroids are derived from
other organs. Increased amount and dis- testicular
persal of melanin in dark-skinned popu- steroids are produced in the suprarenal
lations (including Negroes) is believed to cortex only. This suggests decreased proaccount for their low rates of skin cancer. duction and excretion of adrenocortical
In contrast to infectious diseases, how- steroids in African Negroes (Politzer and
ever, skin cancer may occur too late in Tucker, '58). Noteworthy in this regard
life to be a major factor in natural selec- is the smaller size of the adrenal cortex
tion. Wassermann ('65) has proposed in relation to the medulla in American
that dark pigmentation in tropical popu- Negroes (Swinyard, '40) and East Afrilations may represent a secondary adap- cans (Allbrook, '56) relative to whites.
tation to infectious disease.
Since hydrocortisone (cortisol) supA tendency toward hyperpigmentation presses the secretion of melanocyte-stimmay predispose Negroes to certain dis- ulating hormone (MSH), Wassermann
eases, and to certain responses to disease ('65) has suggested that reduced adrenoor drugs. Thus, the skin of Negroes is cortical activity could be a mechanism for
especially liable to postinflammatory hy- increased pigmentation in Africans.
perpigmentation (Kenney, '65). Excessive
(glucocortipigmentation is characteristic of Kaposi's coids) also alter the response of connecsarcoma (Master, Taylor, Kyalwazi and tive tissue to injury. Cortisone, which is
Ziegler, '70) and SLE (Verhagen et al., closely related to hydrocortisone, depress'68) in African Negroes, and is of diag- es serum gamma globulin levels (Snell
nostic importance. A tendency toward and Nicol, '56; Batchelor, '71). Adrenohyperpigmentation in Negroes is also an cortical steroids inhibit the formation of
important consideration in the drug treat- new fibroblasts and macrophages (Fauve,
ment of acne (Anon., '68), and in busul- '70; Thompson and Van Furth, '70) and,
fan (Myerland) treatment of leukemia hence, reduce the inflammatory reaction
and related disorders (Desai, '65).
to toxic and mechanical injury. CorticoIt should be noted that increased pig- steroids, namely hydrocortisone and its
mentation in Negroes involves hypertro- derivatives (e.g., "kenalog" or triamcinophy, in the sense that pigment production lone acetonide) have been used with some
the production of macrophages, and plasma cells (the principal producers of antibodies). There is evidence of increased
production of certain antibodies (immunoglobulins) in Negroes, which may account for their susceptibility to certain
diseases involving hypergammaglobulinemia.
The role of natural selection and genetic factors in determining these connective tissue responses, however, remains uncertain. Relative to whites, U.S.
Negroes tend to be more subject to the
environmental factors producing these
responses - in particular, to infectious
diseases. Differences in disease patterns
It appears that the process of tissue re- between African and U.S. Negroes also
pair after injury, involving substitution may be due to environmental differences.
of fibrous connective tissue, is more prom- In the absence of malaria infection, for
inent in Negroes than in whites. This may example, we would expect that certain
help to explain the higher frequency in RES tumors (Burkitt's lymphoma and
Negroes of certain granulomatous inflam- Kaposi's sarcome) would not be frequent
matory diseases, and various tumors in- in U.S. Negroes, and this is indeed the
volving fibroblasts. This capacity to re- case (Phillips and Burch, '60; Dorfman,
spond to injury may have developed by '6 5).
Whatever mechanisms are involved,
natural selection in response to infectious
diseases in the tropical African environ- the connective tissue responses described
above may help to explain some racial
Collagen is produced by fibroblasts in differences in disease frequency. Table 1
the repair of connective tissue, and ex- summarizes the possible relationships.
cessive collagenization is involved in
Further studies of the racial distribuseveral diseases more frequent among tion of disease may clarify, or, conceivably,
Negroes (Africans, U.S. blacks, or both) contradict the relationships postulated.
than among whites. These diseases in- Racial distributions of cases of fibrosarclude scleroderma, systemic lupus erythe- coma, for example, are seldom reported
in the literature. Even if available, such
matosus (SLE), and neurofibromatosis.
In defense against infection, the local data from hospital admissions would be
reactive process of inflammation involves of limited value as an indication of the
success in the treatment of keloids in
blacks and whites (Cosman et al., '61;
Kelley, '63; Murray, '63) and in other
racial groups (Alhady and Sivanantharajah, '69). Corticosteroid therapy is also
useful in granulomatous diseases such as
sarcoidosis (Siltzbach, '71).
Thus, decreased adrenocortical activity could be a more direct mechanism
underlying both increased pigmentation
and increased connective tissue response
(gamma globulin synthesis, fibroplasia,
and granulomatous inflammation) in
Negroes relative to whites.
S u m m a r y of possible relationships b e t w e e n Connective t i s s u e overgrowth and disease in Negroes
Environmental agent
Disease manifestation
Viruses, parasites (?)
Overgrowth of reticuloendothelial system
(RES); i.e., increased macrophage production and immunoglobulin synthesis by
plasma cells
Production against infection
Burkitt's lymphoma, Kaposi's
sarcoma (Africa)
Systemic lupus erythematosus,
scleroderma, multiple myeloma ( U S . )
Irritants, injurious
agents (?)
Growth of fibrous connective
tissue (fibroplasia)
Keloids, dermal neoplasms
(Africa, U.S.); fibromas and
fibrosarcomas, granulomatous
Overgrowth of bone, possibly derived
from fibroblasts
Bony growths in tertiary
syphilis (U.S.), and in
neurofibromatosis (Africa)
true disease frequency. The best data
available are from surveys of hospital records (or tumor registries) and death certificate data - as in SLE (Siegel, Holley
and Lee, '70) and multiple myeloma
(McPhedran, Heath and Garcia, '72).
Again, these data have fundamental limitations in epidemiology.
At the histological level the mechanisms underlying the apparently enhanced
fibroplasia in Negroes could be investigated. First, the relative numbers of
fibroblasts and other connective tissue
components could be determined in Negroes and whites. Second, racial differences in cultured fibroblast activity could
be investigated, in health and disease.
Part of this work was supported by the
Fund for Research and Teaching of the
Department of Nutrition, Harvard University School of Public Health, Boston.
Part of this work was done while the author was Research Associate in Biological
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