GYNAECOLOGY
A Review of the Epidemiology and
Pathophysiology of Pelvic Floor Dysfunction:
Do Racial Differences Matter?
Shunaha Kim, BSc, Marie-Andree Harvey, MD, Shawna Johnston, MD
Department of Obstetrics and Gynaecology, Queen's University, Kingston ON
Abstract
Objective: To describe the current state of knowledge regarding
etiology of pelvic floor dysfunction with special consideration to the
effect of racial background on the epidemiology and
pathophysiology of this disease.
Methods: We performed a nonsystematic review of the literature to
detail the current knowledge of the etiology of pelvic floor
dysfunction. Additionally, we performed a systematic search of
MEDLlNE, Cinahl, and the Cochrane database for English-
language articles registered from January 1, 1989, to June 31,
2003, that evaluated racial differences in the epidemiology and
pathophysiology of pelvic floor dysfunction. We also reviewed the
references of identified articles.
Results: We identified 11 articles that examined the effect of racial
background on stress urinary incontinence (SUI), urodynamic
stress incontinence, and (or) pelvic organ prolapse. We identified 2
studies that measured the prevalence of subjective stress urinary
incontinence. Six cross-sectional studies compared the prevalence
of urodynamically confirmed SUI and (or) pelvic organ prolapse
among different groups. White women had a higher risk of
developing urodynamic stress incontinence. Three studies noted
anatomical and physiological differences among the different
groups.
Conclusions: Both quantitative and qualitative defects in collagen
(endopelvic fascia) and compromised levator ani muscle function
have been identified as important etiologic factors in the
development of pelvic floor dysfunction. Parity, vaginal delivery,
menopause, and aging have been most clearly associated with
collagen defects and levator ani muscle dysfunction. The literature
suggests that white women are at increased risk for SUI. At
present, there is insufficient evidence to draw any conclusions
regarding the role of racial differences in pelvic organ prolapse. It
is possible that differences in prevalence rates for both SUI and
pelvic organ prolapse may be attributed to inherent anatomical and
physiological differences among racial groups.
~ ~;PeIVicfloQr dY6f!Jnction. ~jc o~ pfOlapse, urinary
In~. ost;e$s.uririary IDcontinence, racial ••thnicity
~ngh;rtttreirts; Nonedecisred. . inherentes aux differents groupes raciaux.
R~~~30.2004
~on~niber2,·2004
Resume
Objectif: Decrire I'etat actuel des connaissances en ce qui concerne
I'etiologie de la dysfonction du plancher pelvien, en portant une
attention particuliere aux effets de I'ethnicite sur I'epidemiologie et
la pathophysiologie de cette maladie.
Methodes: Nous avons mene une analyse non systematique de la
litterature en vue de rendre compte des connaissances actuelles
sur I'etiologie de la dysfonction du plancher pelvien. De plus, nous
avons mene des recherches systematiques dans les bases de
donnees MEDLlNE, Cinahl et Cochrane en vue d'en tirer les
articles de langue anglaise, publies entre Ie 1er janvier 1989 et Ie
31 juin 2003, qui evaluaient les differences raciales en matiere
d'epidemiologie et de pathophysiologie de la dysfonction du
plancher pelvien. Nous nous sommes egalement penches sur les
references contenues dans les articles retenus.
Resultats : Nous avons identifie 11 articles examinant I'effet de
a a
I'ethnicite sur I'incontinence I'effort (IE), I'incontinence I'effort
confirmee par test urodynamique etlou Ie prolapsus d'un organe
pelvien. Nous avons identifie deux etudes qui evaluaient la
a
prevalence de I'incontinence I'effort subjective. Six etudes
transversales ont compare la prevalence de !'IE confirmee par test
urodynamique etlou du prolapsus d'un organe pelvien parmi
differents groupes. Les femmes de race blanche couraient un
risque accru de presenter une incontinence a I'effort confirmee par
test urodynamique. Trois etudes ont constate des differences
anatomiques et physiologiques parmi les differents groupes.
Conclusions: Des anomalies quantitatives et qualitatives du
collagene (fascia endopelvien) et I'alteration de la fonction du
muscle releveur de I'anus ont ete identifiees comme etant des
facteurs etiologiques importants dans I'apparition d'une
dysfonction du plancher pelvien. La parite, I'accouchement vaginal,
la menopause et Ie vieillissement ont ete les facteurs les plus
clairement associes aux anomalies du collagene et la a
dysfonction du muscle releveUr de I'anus. La litterature semble
indiquer que les femmes de race blanche courent des risques
accrus d'IE. A I'heure actuelle, nous ne disposons pas de donnees
a
suffisantes pour tirer quelque conclusion que ce soit I'egard du
role des differences raciales en ce qui concerne Ie prolapsus d'un
organe pelvien. II est possible que les differences en matiere de
prevalence de I'IE et du prolapsus d'un organe pelvien puissent
etre attribuables aux differences anatomiques et physiologiques
J Obstet Gynaecol Can 2005;27(3):251-259
MARCH JOGe MARS 2005 • 251
GYNAECOLOGY
INTRODUCTION
P
elvic floor dysfunction (PFD) is a general term used to
describe conditions that compromise the female conti-
nence mechanism (urinary and fecal) and (or) pelvic
organ support. Both the epidemiology and pathogenesis of
PFn are still poorly understood, although recent work has
provided several new insights and suggested opportunities
for further research. While trauma to pelvic floor structures
during childbirth remains central in discussions regarding
the etiology of PFD, other possible factors, including genet-
ics and aging, may also be involved. The exact mechanisms
by which racial background influences the prevalence of
PFD are not known. We recognize it is possible that the
concept of race is outdated.
However, the use of racial designators is not intended to be
offensive or exclusionary to any individual or group of indi-
viduals. Unlike alternative terms such as "ethnicity," which
includes shared cultural traditions, I racial designators con-
note shared physical characteristics determined by a com-
mon genetic origin.2 Therefore, we use "race" or "racial
background" in an attempt to explain a possible genetic link
as an etiologic factor in PFD. The following review outlines
the current state of knowledge regarding the epidemiology
and the pathophysiology ofPFD, with a particular focus on
the relation between stress urinary incontinence (SUI), pel-
vic organ prolapse (prolapse), and racial background. For
this review, the databases searched included MEDLINE,
Cinahl, and the Cochrane Library. We also performed a
manual review of available references and of proceedings of
recent meetings of the International Continence Society
(1997 and 1999-2003), the International Urogynecologic
Association (2002-2003), and the American Urogyne-
cologie Society (1997-2003); we included only English-
language articles.
DEFINITIONS AND EPIDEMIOLOGY
Urinary Incontinence
Urinary incontinence (UI) is deflned as the involuntary loss
of urine. In women, it is most commonly associated with
activities causing increased intra-abdominal pressure, such
as coughing or lifting (stress urinary incontinence [SUI]), or
with urinary urgency (urge urinary incontinence [UUI]).
These terms, SUI and UUI, refer to subjective symptoms
reported by patients. Urodynamic studies are performed for
objective diagnosis. Urodynamic (formerly, "genuine")
stress incontinence (USI) is defmed as the objective loss of
urine associated with increased intra-abdominal pressure in
the absence of a detrusor contraction. Detrusor overactivity
(formerly, "detrusor instability") is diagnosed when unin-
hibited detrusor muscle activity (with or without urine loss)
252 • MARCH JOGe MARS 2005
is seen on urodynamic testing. It must be stressed that the
diagnosis of urine loss by symptoms alone can be inaccu-
rate. In a recent meta-analysis, SUI had a positive predictive
value for USI of only 79%.3
Urinary incontinence is one of the most common and
important chronic health problems occurring in modern
society. It is associated with a signiflcant negative effect on
quality of life, including daily social, sexual, and mental
functioning. 4,5 The direct and indirect health care costs of
UI can be substantial. In 2002 Langa et al 6 estimated the
average additional annual cost of informal care associated
with UI in American women older than age 70 years using
pads to be US $2000. In 1995 Wagner et aU reported an
annual expenditure exceeding US $27 billion for the man-
agement of urinary incontinence in the US. UI has been
recently estimated to account for approximately 2% of
health care costs in the US.8
Although UI is generally recognized as being a fairly com-
mon condition, actual reported prevalence rates of UI in
women have varied considerably.9 Estimates of prevalence
range from 17% to 45% in adult women. IO Such wide varia-
tion may be related to differences in the populations of
women studied, so the ability to generalize and compare the
results across different populations is limited. Further, the
deflnition of UI has differed, often dramatically, among
studies. Validated questionnaires have only recently been
developed and used to assess the epidemiology of urinary
incontinence.
Pelvic Organ Prolapse
The term "prolapse" includes a group of disorders that
compromise normal pelvic organ support. In women, con-
nective tissue (fascia and ligaments), muscles, and bony
structures together provide normal support to the pelvic
organs, including the uterus, the bladder and urethra, and
the rectum and anus. Prolapse presents with mechanical
symptoms (pelvic heaviness, introital lump, vaginal pain,
and possibly low back pain), and (or) bladder, bowel, or sex-
ual dysfunction. Findings on examination include laxity or
descent of the anterior vaginal compartment (commonly
referred to as cystocele), posterior compartment
(rectocele/ enterocele), or apical compartment (uterine or
vault prolapse). However, these symptoms have not been
shown to be associated speciflcally with severity of prolapse
or with speciflc compartmental defects. 1I Until such associ-
ations have been deflned, prolapse will continue to be
diagnosed only when descent of the vaginal walls is demon-
strated on pelvic examination, ideally with a standardized
and validated method such as the Pelvic Organ Prolapse
Quantiflcation system (pOP-Q).tZ While prolapse is rarely
associated with mortality or severe morbidity, the condition
 A Review of the Epidemiology and Pathophysiology of Pelvic Floor Dysfunction: Do Racial Differences Matter?
does exert a significant negative effect on a woman's sexual
functioning13 and quality oflife. 14
Surprisingly, although more than 400 000 surgical proce-
dures for prolapse are performed annually in the VS,15 the
prevalence of prolapse has not been well studied.
Samuels son et al. 16 documented prolapse on pelvic exami-
nation in 30.8% of 487 premenopausal Swedish women
(aged 20 to 59 years). Similarly, Versi et al. 17 found a
cystocele in 51 % of 285 women presenting for evaluation of
menopausal complaints, a rectocoele in 27%, and uterine
descent in 20%. It is estimated that 11 % of women will
undergo surgery for prolapse or VI by age 80 years; 30% of
this group will require repeat surgery.18
FUNCTIONAL ANATOMY OF THE PELVIC FLOOR
Pelvic floor integrity in women is maintained by the coordi-
nated actions of muscles Oevator ani, urethral, and anal
sphincters), nerves (sacral plexus and pudendal nerve), and
connective tissue (endopelvic "fascia," perineal body, and
utero-sacral and cardinal ligaments) anchored to the bony
pelvis. Levator ani muscle integrity is of paramount impor-
tance-it is the primary support mechanism. Its function is
twofold. First, the levator ani muscles close the urogenital
hiatus, preventing protrusion of organs through that aper-
ture: Second, the fused posterior component of the muscles
(the levator plate) provides hammock-like support for the
pelvic organs, preventing stretch and tension on the sup-
portive connective tissue. 19 Should the levator ani muscles
fail in providing support, the endopelvic connective tissue
would be placed under tension and, with time, may attenu-
ate or tear. Thus the interaction between the levator mus-
cles and the connective tissue network provides functional
support to the pelvic viscera. The pathophysiology of PFD
is directly related to the functional anatomy of the pelvic
floor. In this context, any force or process that interrupts
the integrity of the neuromuscular or connective tissue
supports may result in PFD.
ETIOLOGIC FACTORS
Parity
It is possible that pregnancy may be an independent risk
factor for the development of PFD, but this is difficult to
establish because most studies have examined only parity as
a risk factor, instead of considering gravidity as well. Vagi-
nal birth is presumed to be one of the most important deter-
minants of PFD. Parity has been clearly identified as a risk
factor for urinary incontinence20-24 and pelvic organ pro-
lapse. 25-28 Specifically, forceps delivery has been associated
with a significant increase in the risk of SVI29 (odds ratio
[OR] 10.4; P = 0.04; 95% confidence interval [CI],
1.2-93.4).30 The duration of the second stage oflabour may
also be important, though it has not been clearly established
as an independent risk factor for the development of
PFD.31 In most women, it is likely that the consequences of
childbirth trauma are not immediately apparent but are
present later in life, when they are compounded by age-
related deterioration and possibly hormonal deprivation
following menopause.
Anatomic and functional changes have been observed in
women following vaginal delivery. Peschers et al. 32 noted
greater mobility of the bladder neck on ultrasound in
postpartum women who delivered vaginally, compared
with women who had elective Caesarean sections or with
nulligravid women. Additional observations include wors-
ened levator function in parous women, compared with
nulliparous women,33 and excessive pelvic floor descent in
women who have had 3 or more deliveries, compared with
those who have had fewer than 3 deliveries. 34 With respect
to specific obstetric history risk factors, Kearney et al. 35
showed that women with a defect of the pubovisceral mus-
cle on magnetic resonance imaging (MRI) had a second
stage of labour that was 1 hour longer, that they were 3.5
times more likely to have had an operative delivery, that
they were twice as likely to have had an episiotomy, and that
they were 3 times more likely to have sustained an anal
sphincter rupture, compared with women without defects
of the pubovisceral muscle. All these observations point to
muscle or connective tissue damage as possible sequelae of
vaginal delivery in women with PFD.
Vaginal delivery may alter pelvic floor function by causing
neuropathy in the pudendal or sacral nerves. Nerve injury
(from pressure necrosis) can occur following pressures as
low as 80 mm Hg applied for as little as 2 hours.36 During
labour, pressures as high as 240 mm Hg can be applied to
the pelvic floor,37 sometimes for several hours duration.
Wall et al. 38 have shown that excessive stretching on periph-
eral nerve tissue is also deleterious and often permanent.
The pudendal nerve may therefore also be injured by exces-
sive stretching during descent of the fetal head, particularly
in its most caudad portion, from Alcock's canal (at which
site the nerve is fixed to the surrounding structures) to the
muscle attachments. Observations supporting this hypo-
thesis include prolonged pudendal nerve terminal motor
latencies, present in 16% of primiparous women following
vaginal delivery,39,40 and evidence of partial denervation
documented on electromyography (EMG),31 following
vaginal delivery (with later re-innervation).
Age and Menopause
Increasing age is another factor often cited as a risk factor
for PFD, though scant epidemiologic evidence exists to
support this conclusion unequivocally. Most of the studies
reported are cross-sectional in design rather than
MARCH}OGC MARS 2005 • 253
GYNAECOLOGY
prospective cohort series, and most include only older
women. Nonetheless, from the available data, it appears
that all types of urinary incontinence in women increase in
prevalence with advancing age,15,18,22 though some data are
conflicting. 10,42 Specifically, Olsen 18 found that among sur-
gi<:ally managed cases of pelvic organ prolapse and UI, the
age-specific incidence of pelvic organ prolapse and UI
increased with advancing age. Additionally, GureI27 found
on univariate analyses that age was significantly correlated
with prolapse,compared with control subjects without pro-
lapse. Perucchini et a/.43 noted that striated muscle layers of
the urethra were thinner at the vesical neck in older women.
Because age and menopause are integrally linked, it is diffi-
cult to define a clear role for age in the development ofPFD
without considering that the underlying etiology may, in
fact, be estrogen deprivation alone. 23 Menopause is
assumed to be a risk factor for SUI, especially if one consid-
ers the close anatomic and embryologic associations of the
reproductive and urinary tracts. Both the urethra and the
bladder contain estrogen receptors in high number,44 and
therefore, both tissues are similarly responsive to the pres-
ence or loss of estrogen. Estrogen receptors have also been
found in endopelvic fascia, levator ani, and uterosacralliga-
ments. 45,46 However, research thus far has not delineated a
clear causal role for menopause in the development of
PFD. Investigators have not found any consistent increase
in the risk of UI around the time of menopause. 10,47,48
Versi49 reported a fall in proximal urethral pressure after
menopause, but found that the prevalence of prolapse did
not correlate with menopausal statusP Randomized con-
trolled trials have failed to show a beneficial effect (over pla-
cebo) with estrogen replacement on SUI in menopausal
women. 50 Clearly, further study is needed in this area.
Raised Intra-Abdominal Pressure
Raised intra-abdominal pressure, especially if chronic, may
also contribute to the development ofPFD.51 Several stud-
ies have confirmed that obesity or increased body mass
index (BM!) is a risk factor for PFD,52-54 as well as chronic
cough and chronic constipation. 55,56 In fact, a decrease in
BMI appears to improve SUI. 57 There is no clear consensus
on the role of smoking as a risk factor for SUI,I8--21,58--60
although there is at least an indirect link because smoking
predisposes individuals to chronic cough.
Collagen
Connective tissue is composed primarily of collagen and
elastin proteins in the form of fibres embedded in a ground
substance of polysaccharides. 61 The collagen provides ten-
sile strength, while the elastin provides flexibility.62 More
than 12 types of collagen have been identified. 63 Type I col-
lagen is very strong, usually organized into large fibres, and
254 • MARCH lOGe MARS 2005
more often found in tendons. Type III collagen forms ran-
domly organized, branched fibres and is found in more flex-
ible tissues such as the skin, aorta, and uterus. A mixture of
Type I and III collagen is the main structural component of
pelvic connective tissue. 64 Further strength is conferred
upon this collagen through cross-linking between the indi-
vidual tropocollagens. 61
If collagen is responsible for the strength of the pelvic con-
nective tissue, then one can hypothesize that abnormal con-
nective tissue is a key factor leading to PFD, even in the
absence of extrinsic insults on the pelvic floor. This would
explain the development of PFD innulligravid women.
Further, milder degrees of abnormality in the fascia and lig-
aments may still allow adequate function when exposed to
normal stressors but inadequate function when exposed to
excessive outside stressors such as vaginal delivery. This
would potentially explain the development of PFD in some
women, whereas other women with similar circumstances
at delivery would not develop PFD.
Several preliminary observations that support this hypo-
thesis have been made. A higher incidence of prolapse has
been reported in women with Ehlers-DanIos syndrome, a
collagen disorder. 65 Joint hypermobility is thought to be a
surrogate marker of defective collagen, because it is associ-
ated with disorders like Ehlers-DanIos syndrome. 64 Norton
et al. 66 found that joint hypermobility did not appear to be
associated with SUI but that subjects with joint
hypermobility had a significantly higher prevalence of pro-
lapse when compared with women with normal joint mobil-
ity. Bai et al. 67 found that among Korean women aged
between 40 and 59 years, the average finger extension angle
was significantly higher for women with prolapse than for
women without prolapse. At the tissue level, Bakas et al. 68
found that the amount of Type III collagen was significantly
reduced in women with USI. Chen et al. 61 showed that
women with SUI and prolapse had higher rates of collagen
turnover than did control subjects. Norton et al. 69 found
that women with prolapse had an increased proportion of
Type III collagen in biopsies taken from vaginal skin. In
contrast, Norton et al. 69 found no difference in the ratio of
Type I to Type III collagen at the vaginal apex between
women with SUI only and control subjects. Overall, these
early results suggest that a qualitative or quantitative disor-
der of collagen may exist in some patients with PFD,
though it is difficult to draw conclusions because all the
studies reported thus far have had small sample sizes.
Family History
There has been speculation as to whether family history is a
risk factor for PFD. Van Dongen70 observed that prolapse
occurred equally in identical twins who were given the same
conditions of physical stress. Mushkat et a/. 71 noted a
 A Review of the Epidemiology and Pathophysiology of Pelvic Floor Dysfunction: Do Racial Differences Matter?
threefold increase in prevalence of USI among first-degree
relatives of female subjects with USI. More recently, Elia et
al.72 reported that the odds ratio for having at least one
relative with urinary incontinence was greater for an incon-
tinent woman (OR 2.6; 95% CI, 1.50-4.48) than for a conti-
nent woman presenting to a urogynaecology clinic. This
was also true when studying incontinent and continent
women from a general gynaecology clinic (OR 9.6; 95% CI,
4.17-22.25). Data from the Norwegian EPICONTl3 popu-
lation study showed that daughters of incontinent women
had an OR of 1.4 (95% CI, 1.3-1.6) for being incontinent
when compared with daughters of continent women.
Younger sisters of incontinent women had an OR of 1.9
(95% CI, 1.5-2.5) for being incontinent when compared
with younger sisters of continent women. Having 2 inconti-
nent foremothers further increased the odds of developing
incontinence (OR 2.9; 95% CI, 1.1-7.6). Chiaffarino et al. 74
also reported that the risk of prolapse was higher in women
with mothers or sisters reporting the condition. Even more
convincing evidence arises from Buchsbaum et al. ,75 who
found that 25 of 27 parous and nulliparous sister pairs had
identical staging of prolapse in the anterior and apical com-
partments. Certainly, it is possible that some families may
have an inherited disorder of collagen integrity.
RACIAL DIFFERENCES AND
PELlVC FLOOR DYSFUNCTION
It is also possible that the relation between family history
and PFD may run beyond familial relationships and be
explained by broader genetic factors among racial groups.
Accordingly, the possible etiologic role of racial differences
is a major epidemiologic question in the area of PFD. As
previously noted, racial signifiers connote shared physical
characteristics determined by a common genetic origin2 and
are used in the context of this review to define a broad
group of people with similar physical characteristics. We
acknowledge that the currently available literature is largely
based on the simple assumption that racial groups are
homogeneous. Clearly, this assumption is flawed . In our
society, there is significant ethnic and racial diversity even
among groups of people who are self-defined as white,
black, or Asian. Therefore, the following represents what is
known, with acknowledged limitations, about the role of
racial differences in the development of pelvic floor dys-
function. Conclusions drawn from this literature are thus
not perfect, but they do suggest a possible etiologic role for
racial differences in the complex problem of pelvic floor
dysfunction.
There are limited data comparing PFD among racial
groups. Most data are restricted to survey formats and are
based on subjective symptoms alone, possibly limiting their
validity, because several studies have shown that subjective
complaints are not helpful in differentiating the etiology of
incontinence. 54,76 Surveys are also limited by self-selection
bias77 and possibly language fluency and socioeconomic sta-
tus. Notably, all studies determine an individual's ethnicity
or racial background either by self-report or by assessment
of physical characteristics. While both of these methods are
open to subjective interpretation of physical characteristics
by either the woman herself or the observer, it can be
assumed that there is a reasonable degree of correlation
between the subjectively assigned and "true" racial
background.
RACIAL DIFFERENCES AND URODYNAMIC
STRESS INCONTINENCE
In a large population-based study of postmenopausal
women using a self-report questionnaire, Brown et al. 78
described the prevalence of urinary incontinence (all types)
and its associated risk factors. The prevalence of weekly
SUI was higher in white women than in black women (OR
2.8; 95% CI, 1.6-5.1), but only 8% of survey participants
were black. Thom et al. 54 conducted a mail survey of mem-
bers of a large health maintenance organization, 76.8% of
whom were self-described as white, 7.5% as black, 5.7% as
Asian, and 5.4% as Hispanic. These authors found that the
distribution by type of incontinence (urge, mixed, or stress)
did not differ significantly by self-identified background.
We found only 6 studies that compared objectively diag-
nosed USI and genital prolapse in different racial groups
(fable 1).79-84 Five of these relied on data collected only
from women who had been referred to urogynaecology
clinics.79- 83 From these limited data, it may be concluded
that there is a greater incidence of USI in white women,
compared with black women. Reports are inconclusive with
respect to differences between white women and women of
other backgrounds.
RACIAL DIFFERENCES AND
PELVIC ORGAN PROLAPSE
Scherf et al. 85 studied the prevalence of pelvic organ pro-
lapse in women from a homogenous black population
(mean age 32.6 years) in The Gambia, West Africa.
Speculum examination was performed on 1067 women.
Prolapse was objectively documented in 46% of these
women. This compares to a prevalence of 30.8% in a popu-
lation of women with a mean age of 39 years in the
Samuels son study16 and a prevalence of 51 % in a peri-
menopausal population in the Versi study.17
Reports from Heyns in South Africa cited genital prolapse
as being more common in white women than in black
women 86 ; subsequent studies have disagreed. Four studies
in the last 10 years found no significant difference in the
MARCH lOGe MARS 2005 • 255
GYNAECOLOGY

Table 1. Comparative studies assessing the prevalence of urinary stress incontInence (USI) and pelvic organ
prolapse (POP) and racial background
Study Population Proportion OR of having USI Proportion with Other findings Quality of
studied with USI POP evidence 93.94
Bump79 54 Black 27% Black NR 24% Black Black women with USI: Level 11-2
heavier, higher parity, greater
146 White 61% White 23% White diuretic use, more often dia-
=
(P 0.0008) betic, better passive urethral
closure pressure, and greater
urethral axis mobility than
white women.
Graham and 183 Black 22% Black NR No significant Being white most significant Level 11-2
Mallett 80 differences predictor of USI (OR 2.21 ;
132 White 46% White 95% CI, 1.31-3.73).
Mattox and 121 Hispanic 30% Hispanic NR 18% Hispanic Hispanic women had higher Level 11-2
81
Bhatia gravidity and higher parity,
50 White 6% White 18% White compared with white women
of comparable age.
Duon~ and 195 Hispanic 67% Hispanic NR NR Black women had signifi- Level 11-2
8
Korn cantly higher urethral closure
95 White 59% White pressures than did Hispanic,
white, or Asian women .
66 Asian 56% Asian

42% Black
83
Boreham et a/. 119 White NR White> Hispanic NR Parity and USI independently Level 11-2
(OR 0.31 ; 95% =
related (P 0.03)
125 Black CI, 0.14-0.71) >
Black (OR 0.18;
193 Hispanic
95% CI,
0.08-0.43)
Chang and 73 Wh ite NR NR Stage 2 or Black women had higher Level III
Sultana 84 higher body weight and were more
34 Black prolapse: likely to smoke than Asian
67% Asian women and white women.
60 Asian
28% White White women had lower
26% Black parity and used more hor-
mone replacement therapy.
OR: odds ratio; NR: not reported.

ANATOMICAL AND PHYSIOLOGICAL

incidence of prolapse between white women and black
women79- 81 ,84 (Table 1). However, differences in parity may
be an explanation, as Bump and colleagues found that black
women with more severe pelvic organ prolapse also had sig-
nificantly more vaginal deliveries than did white women
(4.2 vs. 2.7; P =0.004) with no other significant differences
found between groups.79 Chang and Sultana found that
Asian women had higher rates of pelvic organ prolapse than
did women in other racial groupS.84 In total, the available lit-
erature suggests that being white, or possibly Asian, may
predispose women to the development of prolapse. It is,
however, impossible to draw any firm conclusions.
DIFFERENCES AMONG RACIAL GROUPS
While inherent anatomical and physiological differences
among racial groups have not been proven, several interest-
ing preliminary observations have been made. Howard et aL
compared the structure and function of the urethral
sphincter in both black and white nulliparous continent
women. 87 The study was cross-sectional in design and
included 18 black women and 17 white women. Black
women demonstrated a 29% higher urethral closure pres-
sure than did white women during a maximum pelvic mus-
=
cle contraction (P 0.008). A nonsignificant trend toward
higher maximum urethral closure pressure at rest and larger
.urethral volume was also observed in black women.
Though both these findings would suggest better urethral

256 • MARCH JOGe MARS 2005

 A Review of the Epidemiology and Pathophysiology of Pelvic Floor Dysfunction: Do Racial Differences Matter?
function in black women, there was also greater bladder
neck mobility during maximum performance of a Valsalva
manoeuvre when measured with the cotton swab test (36%
greater, P = 0.02), compared with white women. Because
the women in this study were all continent, the importance
of these observations in the clinical context of PFD is
unclear.
Another recent study examined differences in pelvic floor
area between black women and white women. Baragi et aL88
measured the bony pelvises of 40 black and 40 white female
cadavers, concluding that the overall pelvic floor cross-
sectional area in black women was 5.1 % smaller than in
white women (P = 0.037). Weidner et aL89 also studied dif-
ferences between black women and white women, using
electromyography and MRI. All the women were
nulliparous and had neither symptoms nor signs of PFD.
Differences between white women and black women were
noted in the motor unit action potentials in the external anal
sphincter. Black women demonstrated much greater ability
to recruit motor units in the external anal sphincter than did
their white counterparts. 90 In another study, Weidner et al. 91
noted that black women had thicker levator ani muscles on
MRI than white women. Whether these differences con-
tribute to the different prevalence rates of PFD between
black women and white women remains unclear. Further
study is needed.
CONCLUSIONS
From an extensive search and critical appraisal of literature
pertaining to the role of racial background in the develop-
ment of PFD, the evidence, although sparse, suggests that
being white is a risk factor for stress urinary incontinence.
The evidence is even more sparse and unclear with respect
to pelvic organ prolapse. If racial differences do indeed
exist, they may arise from differences in pelvic morphology,
muscle mass bulk, and (or) inherent differences in collagen
quality.
Prevalence studies are necessary to better understand the
complex etiology of PFD in the general population. The
problem with collecting data only from women seen in
urogynaecology clinics is that racial differences may exist in
health care and referral patterns. Financial, geographic, and
language barriers may differ among racial groups, and these
may unequally influence access to specialized health care
and communication with the health care team. Culture is
also important because it determines the level of comfort
and acceptability that individuals feel with their symptoms
and their ability to report them.
Further research must address the role of racial background
in the development ofPFD, and these studies should make
every attempt to obtain a truly representative sample of the
general population. Ethnic rninotlnes are consistently
underrepresented as participants in medical research. Racial
differences in the willingness to participate in medical
research may be due to lower levels of trust or to the value
given to medical research by a given ethnic community.92
Racial differences in the prevalence of and risk factors for
PFD may provide important etiologic clues. Perhaps in the
future we will have enough information to recommend
appropriate preventative strategies for those groups at risk.
FUNDING AND SUPPORT
Funded by the Department of Obstetrics and Gynaecology,
Queen's University, Kingston ON
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