Cryptorchidism is the failure of one (unilateral)
or both (bilateral) testes to descend and be maintained in the
normal position in the scrotum. The retained testis may be in
the abdominal cavity, in the inguinal canal or just outside the
scrotum. When only one testis is present in the scrotum, the term
monorchid is sometimes used. This is incorrect – in a monorchid
only one testis exists in the body, a condition which, like anorchidism
(no testes), is extremely rare.
Cryptorchidism occurs in many species e.g. pigs, horses, goats,
sheep and other mammals, but is most common in the dog. In dogs
it is found more often in purebred dogs and small breeds are more
at risk than large breeds. In breeds with different sized varieties,
such as the poodle, schnauzer and dachshund, it occurs more frequently
in the smaller (miniature) variety than its larger relatives.
Breeds with short skulls have a higher incidence than normal and
the risk for Boxers has been found to be the highest of all large
breeds. Generally unilateral cryptorchidism occurs more often
than the bilateral form.
WHAT EFFECT DOES AN UNDESCENDED TESTIS
HAVE ON A MALE DOG?
Bilateral cryptorchids are sterile as spermatogenesis does not
occur due to the raised temperature and the abnormal size and
primitive morphology of the retained testes and epidydimus (coiled
segment of the spermatic ducts that serves to store, mature and
Some breeders argue that unilateral cryptorchids should not be
regarded as abnormal, as they are often fertile. However, Badinand
et al (1972) found that cryptorchidism results in lowered fertility
and a variably lowered ejaculation reflex. 47 cryptorchid dogs
were examined. Less than half of the unilateral cryptorchids ejaculated
and 27% of these had no sperm in the ejaculate. Only 8% of the
unilateral cryptorchids examined produced a normal volume of semen.
INCREASED RISK OF TESTICULAR TUMOURS
It is very well documented that the incidence of tumours (Sertoli
cell tumours) is significantly higher (about 13.6x) in retained
gonads than in normally descended testes. Further complications
of testicular tumours are feminization, hair loss, blood dyscrasias
and testicular torsion. Removal of the retained testes is therefore
recommended before 4 years of age.
OTHER ASSOCIATED PROBLEMS
Cryptorchidism has been linked to other defects such as penile/preputial
defects, umbilical hernia, inguinal hernia, hip dysplasia and
particularly subluxation of the patella. Although both cryptorchidism
and patellar subluxation are common in small breeds, there was
also a strong association in breeds not normally at high risk
for patellar subluxation. The association with inguinal hernia
could be due to a defect of the gubernaculum leading to an abnormally
large inguinal canal, combined with the absence of a spermatic
cord to act as a plug for the opening (Cox 1986).
NORMAL DESCENT OF THE TESTES IN THE
In mammals the sex of the individual is determined at fertilisation
by the sex chromosome present in the sperm. If a Y chromosome
is present, the embryo will develop into a male. An X chromosome
will result in a female. However, early development of the genital
system is indeterminate and similar in male and female embryos.
The differences between the sexes arise when the undifferentiated
gonads develop into ovaries in females, which remain in the abdominal
cavity, or testes in males, which then have to migrate from the
body cavity to their correct position in the scrotum.
About 53 days after conception the developing
testes are located at the rear end of the kidneys in the male
foetus. Each testis is attached to a cord of connective tissue,
(the gubernaculums), which causes the testis to descend into the
scrotum. During the first phase of descent, this cord grows through
the abdominal wall, with the inguinal canal forming around it,
and towards the future scrotal pouch. The gubernaculum contracts,
which pulls the testis into the inguinal canal. Several foetal
testicular hormones may be involved in the regulation of the first
phase of testicular descent. The part of the gubernaculum immediately
outside the abdominal wall forms a bulb. This outgrowth and swelling
of the gubernaculum has been observed to continue until about
five days after birth. The expansion of the bulb outside the abdominal
cavity might add traction on the portion inside and help to pull
the testes towards the inguinal ring. After the fifth day regression
of the gubernaculum starts. Its jelly-like composition gradually
becomes opaque and fibrous. The major part of the descent of the
testes – passage from the inguinal ring to the scrotum –
takes place during this regression phase of the gubernaculum.
The exact timing of the process of testicular
descent may vary in dogs, depending on breed, just as the age
at which puberty and enlargement of the testes starts, varies.
However, in the majority of dogs studied, progress of normal descent
of the testis occurred as follows:
• at birth the testis are about halfway between the kidney
and the internal inguinal ring;
• it passes through the inguinal ring by about the 3rd or
4th day after birth;
• by 15-17 days after birth it reaches the halfway mark
between the inguinal ring and the scrotum; and
• by 35-40 days after birth it attains its final position
at the lowest point of the scrotal pouch.
Initially the left testis always precedes the
right one during the descent; probably due to the fact that the
left kidney (and the accompanying developing testis) is situated
further back) in the body cavity. It is interesting to note that
in cryptorchid dogs the right testis is more frequently retained
than the left. (The ratio is about 2:1). This could reflect a
generally slower descent on the right side, due to the greater
distance that that testis has to travel. In normal dogs the right
testicle normally lies in front of the left in the scrotum.
In a week-old puppy the scrotum is filled with subcutaneous fat.
This fat should disappear by about 25 days of age to make room
for the testes. However, from 3-4 weeks of age onwards, “well-reared”
puppies lay down considerable deposits of fat in the scrotal area,
which may in some cases hinder the final descent of the testes.
Boxer pups conform to the “typical dog”
described above and the testes of normal pups are usually in the
scrotum by six weeks of age. If both testes are not fully descended
by the time a Boxer pup is eight weeks old, he must be regarded
as genetically suspect. Due to a highly effective reflex of the
cremaster muscle, puppies up to 10 or 12 weeks of age may retract
their testes into the groin area when picked up and examined.
In normal pups, the testes can be pushed back into the scrotum
easily, with light digital pressure. If a testicle tends to remain
at the entrance to the scrotum and requires a good deal of traction
to reach the correct position, particularly if it is then retracted
again when released, this should be regarded as a minor degree
CAUSES OF CRYPTORCHIDISM
Anything that impedes the initial outgrowth and swelling of the
gubernaculum and its subsequent regression, will lead to cryptorchidism.
Anatomic examination of unborn pups has shown
numerous abnormalities of the structures involved, eg underdevelopment
of the gubernaculum or defects where it passes through the abdominal
wall. Such abnormalities may cause some cases of cryptorchidism.
However, autopsies on 7 bilateral cryptorchid adult males in a
colony of research dogs (miniature schnauzers) revealed that a
well-defined cord-like gubernaculum was present on the left side
but indistinguishable on the right side in every case, although
both testes were undescended (Cox et al, 1978). It has also been
suggested that genetically influenced maldescent could be partly
related to the rate of growth of the involved structures - the
anatomy of the inguinal canal must permit the testis to pass through
unimpeded (Hayes et al 1985)
The importance of hypophyseal hormone is reported
in a study of mutant dogs, which showed a big variety of abnormalities,
which included cryptorchidism. Malfunctioning of the pituitary,
thyroid and adrenal glands have been mentioned, as has insufficient
production of the interstitial cell stimulating hormone (ISCH).
Histo-chemical analysis by Baumans, Dijkstra and Wensing (1981)
indicated that active steroid synthesis and secretion might be
important for the outgrowth of the gubernaculum.
Whatever the mechanisms involved, there is general agreement that
the defect is an inherited trait, as indicated by the following
evidence (Patterson 1983):
• It occurs more often in some breeds than in others.
• The frequency is higher in certain lines within breeds
and in these lines, it increases with inbreeding.
• Studies in other species (pigs, goats) have shown that
the incidence of cryptorchidism can be increased by using known
carriers as parents and reduced by eliminating them from the breeding
In the colony of miniature schnauzers referred
to above, deliberate inbreeding was practiced to increase the
incidence and severity of another defect. The observation of the
high incidence of cryptorchidism in the colony was coincidental
and the study of the condition was retrospective. It provided
good evidence for the hereditary nature of the condition, and
morphological observation suggested a multiple gene defect.
The colony consisted mainly of the offspring
of an inbred littermate pair. Over a span of four generations
12 cases of cryptorchidism (5 unilateral and 7 bilateral) were
found in the colony. The degree of inbreeding was greater for
the bilateral cases than the unilateral cases. The greater than
normal incidence of bilateral over unilateral cryptorchids suggests
that the severity of the condition increases with inbreeding.
Increased severity was based on the following four criteria:
• The high incidence of bilateral cryptorchids.
• The more primitive structure of the epididymus found in
the bilateral cryptorchids.
• The location of the testes in the bilateral cryptorchids
– all the bilaterally retained testes were near the kidneys,
while the unilaterally ectopic testes were lower down next to
the bladder and one was in a prescrotal position.
• Abdominal retention rather than an inguinal or prescrotal
position of the retained testes.
Regardless of the exact mode of inheritance,
it must be accepted that both parents of a cryptorchid male are
carriers, and that male and female siblings may also carry the
genes responsible for the defect.
A heritability of 40% has been established for
cryptorchidism in the Boxer, as well as a polygenic mode of inheritance.
This signifies that environmental factors (which have not been
identified) may be responsible for the remaining 60%.
HOW CAN THE INCIDENCE OF CRYPTORCHIDISM
Unfortunately the only way to entirely eradicate the problem would
be not to use for breeding the cryptorchid dog, its parents, their
parents and any of its siblings. Regrettably this would probably
also eradicate the Boxer as a breed.
The main problem that breeders face in respect
of genetic defects is the fact that the genetic base of the entire
Boxer breed as it exists worldwide is quite limited. There is
probably not a Boxer alive today which does not trace back to
the four great German stud dogs – Sigurd von Dom and his
three grandsons Utz von Dom, Dorian von Marienhof and Lustig von
Dom. These dogs were widely used in Europe and thereafter exported
to the USA. Unfortunately all four had cryptorchid progeny. The
tight linebreeding to these dogs both in Europe and North America
is probably why the incidence of cryptorchidism is such a problem
in the breed today.
While there is evidence that inbreeding can increase
the incidence of cryptorchidism, (Cox et al, 1978), with a defect
as widespread as this is in the Boxer, Padgett (1998) has postulated
that the risk is as high with outcrossed as with inbred pedigrees.
Unilateral cryptorchid males have been excluded
entirely from breeding in Germany from as early as 1942. This
did not reduce the incidence at all. In fact there was an increase
in the incidence from 6.39% in 1941 to 10.21% in 1981 in East
Germany. In West Germany it increased from 7.4% in 1959 to 14.2%
in 1985. Breeders were encouraged to try and increase the heterozygosity
of the breed by not only using the popular, top-winning stud dogs,
but by breeding to lesser known males and to males in neighbouring
countries. The results were disappointing. Some of the widely
used stud dogs had percentages of above 20% and as high as 30%.
After the reunification of Germany, the incidence increased further
to 17.0% in 1995. In 1996 various quite severe measures to address
the problem were instituted in Germany. A bitch was excluded completely
from breeding if she produced cryptorchids in two litters, and
the further use of males with more than 15% cryptorchids produced
in a total of more than 20 male offspring, was restricted. This
resulted in the prevalence of cryptorchidism coming down to 11.1%
in 1998. This however had to be weighed up against the alarming
fact that these and the numerous other existing breeding restrictions
had further limited the genetic base of the Boxer in Germany to
the extent that only 16% of the population could still be used
for breeding. The initial reduction in cryptorchidism also did
not last and slowly started rising again. In addition breeding
activities lessened dramatically with the number of matings recorded
falling from 597 in 1998 to 483 in 1999.
As a result all previous restrictions in respect
of cryptorchidism and certain other inherited traits were revoked
in Germany after the year 2000. The method already in operation
for curtailing HD (Breed Value Assessment) was extended to include
cryptorchidism. Breeding partners are selected on the basis of
a system where the risk of producing affected offspring is calculated
for every dog and bitch to be used for breeding, based on all
available information for that animal, its parents, siblings,
halfsibs, as well as its progeny. The combined figure for a proposed
breeding pair may not exceed a specified threshold value (105
for cryptorchidism). Breeding prohibition was replaced by breeding
recommendations. In this way they hoped to gradually improve the
incidence of the inherited defects without further restricting
the genetic base of the breed. By 2002 breeding activities had
shown a slight increase and the incidence of cryptorchidism had
gone down to 10%. Unfortunately the gene pool remains very limited
and the degree of inbreeding very high.
Just to complicate matters further, a study carried
out in the Netherlands (Janneke et al 2009) using data of 11 230
litters in 12 purebred dog breeds, found that litters produced
by two parents who were both cryptorchidism carriers had an increased
number of males (all breeds), a reduced number of females (8 breeds)
and an increased litter size (11 breeds) when compared to litters
from non-carrier or mixed parents. They concluded that a mechanism
exists in the dog species which causes both cryptorchidism as
well as increased male/female ratios and increased litter sizes.
A consequence would be that selection for bigger litters frustrates
selective efforts to eliminate cryptorchidism.
In South Africa with its small Boxer population, it would obviously
be very dangerous and foolish to base the selection of breeding
partners entirely on one or two aspects. A Boxer does not consist
of testes or hips or a fawn coat only. Most knowledgeable breeders
would list correct type, sound conformation and a steady disposition
as their main concerns. The absence of serious health problems,
such as heart defects and hip dysplasia, are also regarded as
important, with some breeders placing a premium on working ability.
Genetic defects, while a problem, can however never be the only
selection criterion for our Boxers.
In respect of cryptorchidism, perhaps in our
circumstances we should heed the advice of Fred Lanting (2001):
“At any rate, the unilateral condition at least is so widespread
in many families and breeds that an all-out effort to combat it
would take our minds and efforts away from more serious disorders,
which would consequently increase. It’s just a minor thing
we have to put up with. Simply remove the affected ones from the
gene pool and shift your preference away from breeding any (including
females) that come from litters in which the defect occurred.
Since cryptorchidism is sex-limited (only affected
males, not carrier females, show it) it is likely to persist at
about the same prevalence in the breed for a long, long time.”
BADINAND F., SZUMOWSKI P., BRETON A. 1972. Etude morphobiologique
et biochemique de sperme de chien cryptorchide. Rec Med. Vet.,
BAUMANS V., DIJKSTRA G., WENSING C.J.B. 1981. Testicular descent
in the dog. Zbl Vet Med C Anat. Histol Embryol. 10:97.
COX V.S. 1986. Cryptorchidism in the Dog. In D A Morrow (Ed) Current
Therapy in Theriogenolgy: Diagnosis, Treatment and Prevention
of Reproductive Diseases in Small and Large Animals. 2nd Edition.
COX V.S., WALLACE L.J., JESSEN C.R. 1978. An Anatomic and Genetic
Study of Canine Cryptorchidism. Teratology 18:233-240.
HAYES H.M., WILSON G.P.,PENDERGRASS T.W. COX V.S. 1985. Canine
cryptorchidism and subsequent testicular neoplasia: Case-controlled
study with epidemiologic update. Teratology 32:51.
JANNEKE S., JANSS L., ROTHUIZEN J. 2009. Relationship of cryptorchidism
with sex ratios and litter sizes in 12 dog breeds. Animal Reproduction
Science Volume 113:187-195.
LANTING F. 2001. Cryptorchidism. http://www.dogstuff.info/cryptorchidism.html
LüERSSEN D. 1990. Möglichkeiten und Probleme therapeutischer
Massnamen beim gestörten Descensus testis. Kleintierpraxis
PADGETT G.A. 1998. Control of canine genetic disease. New York:
PATTERSON D.F. 1983. Disorders of Sexual Development. AAHA’s
50th Annual Meeting Proceedings.
PENDERGRASS T.W., HAYES H.M. 1975. Cryptorchidism and related
defects in dogs: Epidemiological comparisons with man. Teratolgy
SITTMANN K. 1980. Cryptorchidism in dogs: Genetic assessment of
published data. Ninth International Congress of Animal Reproduction
and Artificial Insemination, Madrid.
WERNER U. 2004. Zuchtwertschätzung für Kryptorchismus
seit 2000 – Was hat sie bewirkt? http://www.bk-muenchen.de/cms/archiv/werner.htm