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term ''acephalic spermatozoa'' (Chemes et al.
1999
) and, in agreement with Perotti
and Gioria (
1981
), proposed that abnormal head-midpiece alignments originated in
the testis because centrioles failed to attach normally to spermatid nuclei. This failure
could also result from a nuclear defect that interferes with the formation of the
implantation fossa, normal lodging site for the sperm proximal centriole. Nuclei and
flagella develop independently and become separated within the seminiferous
tubules or in the seminal pathway as a consequence of increased instability of the
head-midpiece junction. This interpretation is supported by observations that the
separation or abnormal relations between heads and tails increase due to mechanical
stress in centrifugation or sperm in vitro manipulation (Chemes et al.
1999
; Kamal
et al.
1999
). The admixture of acephalic spermatozoa and abnormal head-middle
piece connections expresses different degrees of abnormalities of the head-neck
junction with acephalic forms representing the most extreme situation. In most cases
the sperm neck was the preferred region where cleavage between heads and mid-
pieces took place. In occasional reports separation resulted from dissociation
between proximal and distal centrioles (Holstein et al.
1986
) or due to other sperm
defects at more distal locations. The study of a testicular biopsy in one of our patients
confirmed that alterations started very early during testicular spermiogenesis with
abnormal relations between spermatid nuclei and tails (Fig.
2.4
) that resulted in
abnormal lateral implantations or completely independent development. When
present, heads implanted at abnormal angles on the middle piece. The caudal nuclear
pole of elongating spermatids appeared as a protruding area without an implantation
fossa to lodge the proximal centriole.
We had previously shown (Chemes et al.
1978
) that in early human spermio-
genesis the spermatid nucleus differentiates a cranial pole where the Golgi com-
plex attaches to form the acrosome. Shortly after, the centriole-flagellum complex
approaches the opposite pole of the nucleus and attaches to it. Acephalic sper-
matozoa derive from the failure of this caudal migration, while some acrosomeless
spermatozoa result from the lack of proper attachment of the Golgi complex to the
cranial pole of the spermatid nucleus (Zamboni
1992
). The unusual case described
by Aughey and Orr (
1978
), with round acrosomeless heads and acephalic sper-
matozoa in the same patient indicate that these two abnormal mechanisms have
combined, suggesting that there are different pathologies derived from an abnor-
mal differentiation of the bipolar nature of spermatid nuclei. In very recent studies
(Alvarez Sedo et al.
2012
) we have found that failures of proper Golgi attachment
to nuclei are indeed accompanied by frequent failures in head-tail connections.
In one of the reported patients, that had around 1 % normal spermatozoa in his
ejaculate, it was possible to follow the evolution of seminal profiles over an
extended period, before, during, and after pharmacologic suppression of sper-
matogenesis. Testosterone propionate treatment was instituted to achieve oligo-
azoospermia in an attempt to promote expansion of the clone of normal sperma-
tozoa during spermatogenic recovery that follows testosterone administration.
However, sperm morphology did not change along the course of spermatogenic
regression-recovery, the percentage of normal spermatozoa remained very low,
and about 99 % of all newly formed spermatozoa were again acephalic.
