Paper - Cytology of the human spermatozoon
|Embryology - 9 Dec 2023 Expand to Translate|
|Google Translate - select your language from the list shown below (this will open a new external page)|
العربية | català | 中文 | 中國傳統的 | français | Deutsche | עִברִית | हिंदी | bahasa Indonesia | italiano | 日本語 | 한국어 | မြန်မာ | Pilipino | Polskie | português | ਪੰਜਾਬੀ ਦੇ | Română | русский | Español | Swahili | Svensk | ไทย | Türkçe | اردو | ייִדיש | Tiếng Việt These external translations are automated and may not be accurate. (More? About Translations)
|Historic Disclaimer - information about historic embryology pages|
|Embryology History | Historic Embryology Papers)|
Cytology of the Human Spermatozoon
Walter W. Williams, M.D.
Cytology of the Human Spermatozoon
Walter W. Williams, M.D.
Geneticist, Springﬁeld Hospital, Springﬁeld, Mass. (1950)
Male fertility depends not only upon the number of spermatozoa as determined by an actual sperm count, and their locomotive ability, but also upon normal sperm structure. Therefore, if a clinician plans to make a conscientious investigation of fertility he should be capable of differentiating between normal and abnormal sperm.
For the purpose of description, the spermatozoon may be divided into two parts, the head and the caudal appendage. The former is partly of nuclear and partly of cytoplasmic derivation. The latter is entirely of cytoplasmic origin. Variations in the anatomic components of the head and its caudal appendage produce bizarre forms which, according to the structure involved, the extent of deviation from normal, and the extent that the sperm population as a whole is involved in the morbid processes, serve to indicate impairment or destruction of fertility.” Various abnormalities arising from each of the anatomic components of the sperm may predominate in different individuals and possess widely different clinical signiﬁcance. Thus it is essential to become familiar with spermatic structure if one expects to evaluate male fertility. For instance, a little fragment of the undifferentiated extruded cytoplasm in the neck region is of no clinical signiﬁcance, but with improper methods of examination it is easily confused with centriolar or mitochondrial abnormalities which cause a marked reduction in fertility potential. The clinical signiﬁcance of asthenospermia and hyposperrnatogenesis is often clariﬁed if one knows the fundamental quality of the spermatozoa which are being produced.
The present paper deals with the recognition and deﬁnition of the anatomic evidences of spermatic disease. In the past, many ingenious terms have been devised to describe bizarre sperm conﬁgurations. It is more specific, accurate and informative, and therefore preferable to use the descriptive terminology of the cytologist, a practice which will here be followed.
(Figs. 1, 2)
When viewed ﬂatwise, the head of the normal spermatozoon is roughly oval in contour. However, when viewed sidewise, there is a marked narrowing of its anterior end, owing to the discoid acrosome which rests on the anterior pole of the rounded nucleus (Fig. 1). The posterior portion of the head is occupied by the nucleus, and lying in apposition to the posterior nuclear pole is the anterior centriolar body (anterior end knob). Variations in size or contour of the acrosome or nucleus provide the most frequent evidences of spermatic pathology. The normal sperm head is about 4.6 microns long.”
FIGURE 1. The structure of the human spermatozoon. A composite diagram, based principally on the studies of Meves (after Bonnet),1 the examination of stained specimens by Williams, and the studies with the electronic microscope by Tyler and Bretschneider. The proportions are essentially those of the average sperm cell.
- Photomicrographs illustrating the various spermatic abnormalities portrayed in the diagrams or alluded to in the text had to be deleted from this article because of lack of space. They will be published later in book form.
A sharp transverse line marks the junction of the nucleus and acrosome. The maximum width (about 2.6 microns) is at this line or slightly anterior to it. The longitudinal axis of the nucleus averages about 2.2 microns, that of the acrosome about 2.4 microns. Ordinarily the longitudinal axis of the nucleus is less than that of the acrosome. If the longitudinal axis of the nucleus is greater than that of the acrosome, the cell should be considered pathologic.
(Figs. 1, 2, 30)
The nucleus is roughly triangular in shape. Its anterior border ordinarily forms a shallow arc which arches into the base of the acrosome, while its sides are either straight or slightly rounded to form posteriorly an angle of 45 to 90 degrees, at the apex of which an intensely stained, ﬂattened granule marks the location of the anterior end knob. Because the chromosomes are dispersed and the nucleus condensed in the mature sperm, recognizable intranuclear morphology is absent, staining is homogeneous, and discrete chromatin material may not be observed. Abnormalities of the nucleus are indicated by differences in size and shape. Since the nucleus loses moisture and contracts to less than one—fourth its original size during spermiogenesis, one may observe considerable variation in its size. In many apparently normal specimens the nucleus appears unusually small in relation to the acrosome, occupying as little as one third of the longitudinal axis of the head. An excessive narrowing in the transverse nuclear axis may be accompanied by a corresponding increase in its longitudinal axis. Nuclear abnormalities are most frequently indicated by this narrowing of the transverse axis, which in different individuals or in the same individual assume various characteristics, such as:
- A nuclear angle of less than 45 degrees.
- A general narrowing of the nucleus.
- A sharp tapering of the posterior pole of the nucleus.
- A marked elongation of the nucleus, at times (Figs. 3a, 5) so narrow that it may be mistaken for the middlepiece excepting for difference in staining. An enlargement at the posterior end of this elongation may give the nucleus a dumb-belled appearance.
In other instances, the apparent enlargement of the caudal extension of the nucleus is an artifact resulting either from the caudalwards displacement of the nuclear shell or a small nondifferentiated cytoplasmic mass surrounding the distal end of the nucleus.
Various combinations of these different types may occur. Individuals with nuclear and other abnormalities tend to reproduce such speciﬁc abnormalities in a ﬁxed ratio. Indeed, it is often possible to identify a patient by the character of his spermatozoa, provided that there is a record of previous ﬁndings for comparison.
Cup-Like Shell of the Nucleus (Fig. 3d) According to Markus there is an outside border to the posterior aspect of the head measuring about $5 micron in thickness, forming a cup-like structure into which the real nucleus ﬁts, something like an acorn in its cup. If one studies stained spermatozoa, this cup-like shell may be readily discerned.14’ 15 Excepting for the anterior arch of the nucleus, its contour corresponds to that of the nucleus. This nuclear shell produces a sharp transverse line across the mid-portion of the sperm head and a slight lipping laterally on both sides where the transverse line meets the side wall of the shell (Fig. 2). Occasionally one may observe a sharp projection of the cup-like shell anterior to the nucleus, or it may be ruptured, exposing the underlying, more lightly stained nucleus beneath. This nuclear shell has considerable density and ﬁrmness and is apparently composed of a keratin-like substance which serves to maintain the contour peculiar to the mature spermatozoon.
The signiﬁcance of deviations in the nuclear shell as such is uncertain.
- It is resistant to the action of concentrated sulphuric acid.
FIGURE 2. Normal sperm populations. Top: Note uniformity in size and shape. In three cells, there is a double line transversely across the cell due to the partial separation of the galea capitis. In the lower cell of the group, a thickening of the anterior end of the middlepiece marks the site of the posterior end knob, and the mass at the distal pole of the head is caused by a mass of incompletely disintegrated cytoplasmic extrusion. Bottom: Note character of middlepiece, its common enlargement at the anterior end, the clear non-staining neckpiece anteriorly, and the small nick in the sheath just posterior to the distal end of the middlepiece. Three cells have small cytoplasmic masses adhering to the anterior end of the middlepiece.
FIGURE 3. Diagrammatic representation of spermatic abnormalities. Such abnormalities are commonly -observed in the semen of infertile individuals. a. Nuclear abnormalities. Some of the more common nuclear conformations commonly observed in the seminal ﬂuid of infertile individuals. b. Abnormalities of the acrosome. For the most part, abnormalities of the acrosome consist of Various stages of deﬁciency in its development. In some cases of male sterility, a large ratio of spermatozoa possess little or no acr-osome, causing the heads to assume a spherical contour, with concomitant gluing together of many such cells in pairs. In other instances, the acrosorne may be laterally situated in respect to the nucleus or tapered anteriorly instead of presenting the normal, full rounded contour of its anterior margin. c. Galea capitis. The galea capitis is more frequently discerned with the human sperm when it becomes partially loosened and produces in consequence a second line across the mid-portion of the sperm head just anterior to the nuclear line. d. Abnormalities of the nuclear shell. In many instances, there occurs a sharp protrusion of the nuclear shell over the acrosome, but when the acrosome is laterally situated with respect to the nucleus, the unusual contour of the nuclear shell may coincide faithfully with that of the nucleus. e. Incomplete disintegration of extruded cytoplasm. The disintegration of extruded cytoplasm at the base of the head or surrounding the middlepiece may be considered as signifying the terminal stage of spermiogenesis. Centrosomic abnormalities. Centrosomic abnormalities are generally indicated by an enlargement of the anterior or posterior end knob, or both. (A) Normal conformation. (B) Hypertrophy of the anterior end kn-ob, very common in association with mitochondrial disease. (C) Atrophy of the anterior end knob, often accompanied by a lengthening of the axial ﬁlament of the neck and a ﬁnely tapered nucleus. (D) Enlarged posterior end knob, usually not differentiated from the mitochondrial sheath. (E) May be an enlargement of both the anterior and posterior end knobs with consequential elimination of the neckpiece. (F) Enlargement of the endring. Rarely observed. (G) Enlargement of the anterior end knob with loss of the nucleus. Such cells have a small punctate head formed by the anterior end knob, with no nucleus or acrosome. They commonly migrate actively in the microscopic ﬁeld. g. Cytoplasmic envelope. Cells exhibiting homogeneous staining are very commonly -observed. Judging from the staining affinities of such cells, this abnormality is apparently due to a very thin cytoplasmic layer which surrounds the sperm head. In some instances, when this layer becomes partially loosened, the underlying nucleus may be observed. h. Abnormalities of the middlepiece. Abnormalities of the middlepiece consist principally of three types, (1) a moderate thickening but no great alteration in its length, (2) a bare axial ﬁlament due to loss of the mitochondrial sheath, and (8) a profound disorder of the mitochondrial sheath associated with a lack of development of the tailpiece. The latter usually affects the entire sperm populations and causes absolute sterility.
Such abnormalities are almost invariably associated with nuclear or acro somic pathology (usually the latter) and therefore are possibly of greater interest to the cytologist than to the clinician.
(Cytoplasmic Origin) (Figs. 3b, 5)?’ 3’ 5’ 1°’ 12
The acroso-me usually occupies slightly more than 50 per cent of the anterior portion of the normal sperm head. It ﬁts over the anterior curvature of the nucleus, producing a straight line transversely across the middle portion of the head as it contacts the nuclear shell, above which the nucleus projects to form a semi-elipse. With the cell lying ﬂatwise, its longest transverse axis lies a little anterior to the acrosomic-nuclear junction. The acrosome usually prescribes a full arc anteriorly but it may be slightly acute and still apparently within normal limits. Its surface area is commonly at least 50 per cent to 100 per cent greater than that of the nucleus. When viewed laterally, the acrosome narrows to a flat discoid structure above the arch of the nucleus. Vacuoles of various sizes are commonly observed at any location in the acrosome (in normally fertile as well as infertile individuals) and these often rupture through the surface of the cell, leaving a nick in the surface of the acrosome at the point of rupture (Fig. I Marked differences in both size and shape of the acrosome are common among infertile patients. In rare instances, the acrosome is enlarged, but in most instances it shows various degrees of deﬁcient development, changing the shape of its anterior contour and lessening to various degrees its visible surface area. In some semen specimens only a thin fringe of acrosome overlies the anterior nuclear pole, and in other instances the nucleus is entirely void of acrosome. With a deﬁciency in acrosomic development, the sperm head commonly becomes more rounded. When there is no acrosome, so that the head is formed only by the nucleus and its shell, the head is usually spherical.
FIGURE 4. Immature spermatic cells. Immature forms, especially of the spermatid stage are occasionally observed in the ejaculated semen, as well as large cytoplasmic rests which may also be considered as evidence of immaturity, even in association with an otherwise fully mature spermatozoa. The immature cells are largely distinguished by means of the nuclear size. A: Normal sperm head. B: Spherical cell, nucleus protruding from posterior pole, with anterior portion of cell staining densely because of thick cytoplasmic envelope (see Figure 5). C: Large dense-staining cell, cytoplasmic bulge at posterior pole. D: Similar to B with undifferentiated cytoplasm fringing large nucleus. E: Spermatid, similar to D but with rudimentary caudal appendage. F: Large dense-staining nuclear—cytoplasmic mass with budding nondifferentiated cytoplasm at posterior pole. G: Dense staining head due to dense cytoplasmic envelope with nucleus visible posteriorly. H: Mature spermatozoon head surrounded by undifferentiated cytoplasm. Many cells appearing thus may be differentiated with diﬂiculty from a superimposition on a leukocyte. I : Loosened galea capitis and persistence of cytoplasm surrounding middlepiece. I: Same as I but with normal head associated with enlargement of mitochondrial sheath and abbreviated caudal appendage. K: Cytoplasmic extrusion associated with absence of acrosome.
As a rule, the size of the nucleus is not affected greatly by the loss of the acrosome, butthere may be a marked diminution in nuclear size as well. Occasionally the acrosome narrows to a point anteriorly or is situated laterally on the nucleus. There is a decided tendency for spermatozoa withcmarked acrosomic deﬁciencies to adhere in pairs in ejaculated semen. The greater the incidence of acrosomic deﬁciency, the greater is this tendency. The pairing of normally developed spermia is rarely observed and in most instances is merely coincidental and not indicative of any germinal disorder.
FIGURE 5. Sperm population from sterile man. All nuclei are abnormal. Defective acrosomia are common and there are a few cells with a disturbance of the mitochondrial sheath and abbreviated caudal extremities. The large, dense staining mass at the lower left is an immature cell.
The galea capitis is an exceedingly thin cap which fits over and entirely covers the acrosome. Its posterior margin lies in contact with the nuclear shell, forming, with the posterior margin of the acrosome and the anterior margin of the nuclear shell, a single transverse liner across the mid-portion of the sperm. The existence of this structure, although described by Meves many years ago, has been questioned by many. Blom, in 1945, amply demonstrated its existence with the spermia of the bull and stallion by presenting photomicrographs of free galea in the seminal ﬂuid, while Williams and Savage demonstrated the partially separated galea under the name of “spermatic veil” in 1925. A more careful examination of human spermatozoa not only reveals evidence of this structure but also by its recognition supplies an explanation of some hitherto unexplained abnormalities, or so called abnormalities, of the human sperm. If Blom’s conclusion is borne out that the shedding or loss of the galea capitis signiﬁes an aging of the sperm, and its consequent loss of fertilizing ability, the phenomenon of the loss of the galea should assume clinical signiﬁcance. Using ordinary sperm stains, it will be observed that although there is usually a single transverse line across the sperm head, one frequently sees a second line anterior to that of the nuclear shell (Fig. 2), and that the longitudinal axis is increased to the extent of the breadth of the band between the two lines. Thus, one may observe what appears to be an exceptionally long or large head which is due to the partial loosening of the galea rather than a head abnormality. In other instances in association with a somewhat tapered nucleus and apparently with a loss in ﬂuid of the acrosome, the cap becomes loosened and drops posteriorly over the nucleus so that the sperm head may be seen lying in a wide-mouthed bag. In rare instances, the writer has observed free galea in semen smears. Apparently they are not seen free in the human seminal ﬂuid more frequently either because of faulty laboratory technics or because of their rapid disintegration.
(Fig. 3e)5’ 7
Extrusion of undifferentiated cytoplasm marks the ﬁnal stage of spermiogenesis and signiﬁes in general that the various intracellular changes of spermiogenesis affecting the nucleus, acroblast, mitochondria, or centrosomes, together with the budding out of the caudal appendage, have already transpired and that the cell has reached its adult stage. Small cytoplasmic rests, the remnants of these extrusions, are so common with spermatozoa from fertile individuals that they can hardly be considered as pathologic. Cytoplasmic masses of various sizes are commonly seen adhering to the neck region or the mass may be roughly the size of the sperm head, ovoid or globular and surrounding the entire middlepiece. One may at times observe what are apparently the fragments of the cell membrane about this cytoplasmic mass. It is quite likely that when the cytoplasmic masses are large, surround the entire middlepiece, and show no evidence of disintegration, they should be considered as pathologic. A high incidence of such cells is uncommon and its clinical signiﬁcance unknown.
Cytoplasmic Covering of Sperm Head
One frequently observes spermatozoal heads which exhibit homogenous staining with a cytoplasmic stain. This is apparently due to an extremely thin layer of undifferentiated cytoplasm completely surrounding the nucleus and acrosome, which interferes with the staining and visualization of these structures. In most instances the general contour of the cell gives evidence of the presence of the nucleus and acrosome. The speciﬁc clinical signiﬁcance of such cells, if any, is not entirely clear, but they are- observed somewhat more frequently in connection with coiled caudal appendages, and immature cells.
Anterior End Knob
(Anterior Centriolor Body) (Figs. 1, 3f)
The anterior end knob is ordinarily observed as a small flattened granule closely applied to the caudal end of the nucleus and, in normal cells, causes a slight ﬂattening of this area. It is of cytoplasmic origin and is best revealed with a cytoplasmic stain. Its transverse diameter is ordinarily slightly greater than that of the middlepiece. VV hen pathologic, the anterior end knob may be either hypertrophied or atrophied. A shortening of the neck may cause the anterior and posterior end knob to appear as one. The axial ﬁlament apparently arises from the anterior end knob and passes posteriorly to form the inner core of the caudal appendage of the spermatozoonf“ Bretschneider” 18 reveals with the electronic microscope in the case of the bovine sperm that the ﬁbrillae which are demonstrated so readily in the endpiece continue throughout the length of the tailpiece, middlepiece and neckpiece.
- It is claimed by most cytologists that the axial ﬁlament arises from the posterior end knob. This belief seems hardly tenable in View of the clear visualization of the neckpiece when the distance between the anterior and posterior end knob is abnormally increased. In the more normal appearing spermatozoa, the clear, nonstaining area of the neck and the lack of visualization of the central filament is apparently the result of refractoriness of the sheath to the stains employed.
When dismemberment of the sperm occurs mechanically, the break often occurs in the neckpiece. In some instances, however, the nucleus becomes loosened from the anterior end knob and one observes the small punctate head (anterior end knob only) attached to the anterior end of the neck. Such caudal appendages, without nuclei but possessing the punctate anterior centriolar body, are commonly highly motile. Since this anomaly occurs most frequently in connection with other cytoplasmic pathology, rather than nuclear, it is probably of centriolar etiology.
Occasionally there is a doubling of the centriolar bodies and from each a caudal appendage arises; or the caudal appendage may arise from only one of the centriolar bodies and in consequence have an abaxial insertion. In one instance observed by the writer in bovine semen, in which doubling of the centriolar bodies was a common feature, a vestigial middlepiece developed on one side and an apparently normal appendage on the other. A double head with a single caudal appendage never occurs, nor is such possible, since the caudal appendage always arises as an outgrowth from the anterior centriolar body (Fig. 8f).
(Fig. 1) The caudal appendage may be divided into the neckpiece, middlepiece, tailpiece, and endpiece or terminal ﬁlament. l 5 6
The neck of the human spermatozoon as seen in most stained preparations is represented by a lucid interval of about 0.5 micron between the head and the middlepiece where the axial ﬁlament appears as if devoid of sheath. With a microscope of high resolving power the central axial ﬁlament comes in view. Electron microscope photomicrographs suggest that a sheath is present in this area. In many instances the neckpiece is obscured either because it is obliterated by the close proximity of the anterior and posterior end knob, or because the presence of a residual cytoplasmic extrusion hides it. Because of its minute size and simple structure, very little of a pathologic nature can ordinarily be observed in the neck. It is so minute that inability of resolution can hardly be considered as an abnormality. Occasionally, however, one observes an excessive lengthening of the neckpiece, increasing the distance between the anterior and posterior end knobs to as much as 8 to 5 microns (Fig. 3f). The head, in consequence of the lengthening of the axial ﬁlament of the neck, is poorly supported and under the impetus or drive of the motile caudal extremity becomes doubled back against the middlepiece which drags rather than pushes it across the microscopic ﬁeld. The presence of this defect, therefore, can be easily recognized under a magniﬁcation so low that the basic defect itself cannot possibly be deﬁned. With this type of abnormality, it is common to observe a very ﬁne tapering of the posterior pole of the nucleus and an exceedingly small anterior end knob. Apparently the structure of the head and the anterior end knob exert very little inﬂuence upon motility. If interference with motility is attributed to a cytologic defect (in contrast to exhaustion or abnormal physiology) the cause must lie in the middlepiece.
(Figs. 1, 3h)
The middlepiece is that portion of the caudal appendage lying between the neck anteriorly and the tailpiece posteriorly. It is about the same length as the head. Its diameter is about one-tenth that of the transverse diameter of the head (about 0.8 microns) and is slightly greater than that of the tailpiece. At its anterior end lies the posterior end knob (the anterior division of the posterior centriolar body) and at its posterior end, the end ring (posterior division of the posterior centriolar body). In ordinary sperm staining, the former is commonly indicated by a slight enlargement or clubbing of the proximal end of the middlepiece or infrequently by a small granule in this region, while the latter is not visible unless pathologically increased in size.
The central core is formed by the axillary ﬁlament, a continuation of the axillary ﬁlament of the neck, arising from the anterior centriolar body and continuing to the tip of the tailpiece. The axillary sheath immediately surrounds the axillary ﬁlament; and outside of this is the mitochondrial sheath in which is located the spiral ﬁlament. With the staining methods which I have employed in the clinical analysis of human sperm populations, it has not been possible to visualize the spiral ﬁlament clearly, but. in bovine spermatozoa stained with carbol fuschin, 9 turns of the spiral ﬁlament may occasionally be visualized. Occasionally when the spiral ﬁlament of the human sperm could be partially visualized, there seemed to be 5 or 6 turns.
Abnormalities of the middlepiece are frequent in infertile men and may be of considerable clinical signiﬁcance. These abnormalities fall into 8 principal groups.
a. Centriolar origin (Fig. 8f), indicated by an enlargement of the middlepiece at its anterior end (posterior end knob) or at its posterior end (end ring). Such abnormalities may be differentiated from cytoplasmic extrusion 212 WILLIAMS [Fertility 3. Sterility
masses by their denser staining and a more even contour. Undifferentiated cytoplasmic extrusion masses are common in normally developed spermatozoa and have no proven clinical import, Whereas centriolar disease interferes with a vital component of the sperm and cannot occur in a high incidence without reducing fertility.
b. A simple deformity of the middlepiece (Fig. 3b) occurs either as a slight thickening, or a variation in length, with an otherwise normal development of the caudal appendage. In some instances, the middlepiece is decidedly shorter than normal. In other instances, the sheath becomes loosened from the axial ﬁlament anteriorly and bunches up in the region of the end ring leaving a bare axial ﬁlament or there may be no vestige of the sheath present. Such anatomic variations seem to have no clinical signiﬁcance when their incidence is low.
c. Mitochondrial sheath (Fig. Sh). In some cases of sterility a profound disturbance in the formation of the mitochondrial sheath occurs, often involving the entire sperm population. The accompanying sterility is, as far as is known, absolute and incurable. The disorder is characterized by a clubbing of the caudal appendage and by immotility. There is an abnormal distribution of the mitochondrial sheath, usually over a very much longer area than ordinary, together with a lack of development of the tailpiece. The caudal appendage may be represented in some spermia by a small knob at the base of the head; or a thickened middlepiece of unusual density which may be several times its ordinary length and thickness with the mitochondrial sheath often very unevenly distributed. Frequently the tailpiece is completely absent and the endpiece protrudes from the distal end of the hypertrophied middlepiece. Wide variations occur in the length and thickness of the caudal appendage in these cases, but its general foreshortening, increased diameter, and primary immobility, associated with a head of fairly normal size and contour, make it fairly easy to render a prompt and accurate diagnosis and prognosis in these particularly grave cases. Although the principal defect concerns the mitochondrial sheath, it is quite evident that the posterior centriolar body must also be involved and interfere in some manner with the distribution of mitochondria and the normal outgrowth of the axillary ﬁlament.
The tailpiece is that part of the caudal appendage lying between the middlepiece anteriorly and the terminal filament posteriorly (endpiece). It is normally about eight to ten times the length of the head and consists of an axial ﬁlament centrally, which is surrounded by a thin cytoplasmic sheath (axial sheath). At the proximal end, there is commonly a constriction or nick of the sheath leaving at this point little or no covering to the axillary ﬁlament. Cytoplasmic extrusion masses do not extend beyond this nick.
Very little pathology has been discerned in the tailpiece excepting in those cases in which its lack of development is associated with a disturbance of the mitochondrial sheath and in those instances where an coiling of the tailpiece and middlepiece portends a disorder of the appendage. The signiﬁcance of coiling of an otherwise normal appendage when sperm are smeared on a microscope slide has not been established, and its clinical appraisal, as with many other types of anomalies, must await the results of more critical observations.
The endpiece is the terminal portion of the caudal appendage. It is usually about the same length as the head, but may be twice its length, and consists of an unsheathed axillary filament. Although small in diameter, it may be readily observed with a magniﬁcation of about 1500 ><. At its distal end, as revealed by the electron microscope, the axillary ﬁlament frays out into nine ﬁbrillae, forming a tassel.’“ 17’ 18 It seems very likely, therefore, that the axillary ﬁlament from its point of origin consists of a bundle of ﬁne ﬁbrillae which are closely bound together as in a cable, excepting at its ter .minal portion. The caudal appendage is ordinarily at least 10 times the length of the head, but the length of its different segments vary considerably. The clinical signiﬁcance of these variations is not apparent excepting in those individuals whose semen contains many spermatozoa with short ened or absent appendages.
(Figs. 1, 4)
It is seldom that a desquamation of the germinal epithelium causes immature germinal cells to appear in ejaculated semen. Cells resembling spermatogonia or spermatocytes are almost never observed and thus play little or no part in the clinical evaluation of semen. Transitional cells of spermiogenesis are, however, occasionally observed, especially in association with a high incidence of pathologic mature cells.
- Electronic microscopic studies of the human sperm by Albert Tyler, California Institute of Technology, Pasadena, California, reveals, as does the study of Bretschneider with his study on the bull sperm, that there are 9 ﬁbrillae in the endpiece. Tyler also shows very distinctly the cupping at the lateral aspects of the head, caused by the cup—like shell of the nucleus. The latter may also be observed in stained preparations at comparatively low magnifications.
The characteristics of the immature cell (spermatid stage) depends upon the stage of its development. The most important evidence of immaturity consists of a large dense staining spheroid cell, having a large nucleus surrounded by a cytoplasmic envelope. A caudal appendage of different lengths may be present, depending upon the stage of immaturity. During spermiogenesis, all the nuclear and cytoplasmic elements of the cell undergo striking and important changes, which if abnormal, result in a wide variation of cell types. Often, the large spheroid cells of spermiogenesis present at some point on their surface a point of budding of undifferentiated cytoplasm which stains lighter than the rest of the cell mass, and protruding from this site one occasionally observes the tailpiece of a spermatozoon. The more immature types will show no evidence of a caudal appendage, but a rather large, dense nucleus surrounded by a layer of cytoplasm as is observed in testicular biopsy specimens, excepting that the cytoplasmic layer is commonly thinner and more densely stained.
It is unnecessary to describe here the wide variety of cell types resulting from arrest at various stages of spermiogenesis, since presumably all such cells are infertile; but for the guidance of those presuming to evaluate semen from the viewpoint of fertility, some of the fundamental characteristics of maturity and immaturity may be mentioned. Of these, the most striking concerns the loss in moisture by the nucleus and its consequent reduction in size, a phenomenon so evident on routine microscopic examination of semen that a micrometer is not in the least necessary for its detection. The nuclei of the spermatogonia measure about 4.5 microns, or a little more than twice the size of the nuclei of the mature cells. With the increased mitotic activity associated with the spermatocyte stage, the size of the nucleus increases to about 9 microns. Thereafter, during the spermatid stage, as the gamete metamorphoses to the mature type, the nuclear size diminishes very rapidly so that in the mature cell its diameter becomes about one-ﬁfth that of the spermatocyte. The nuclei of most immature cells that are observed in the ejaculated semen measure not more than 2 to 8 times the size of the mature nucleus, and may be considered as transitional cells of the spermatid series. The reduction of nuclear size to that of the normal mature gamete furnishes a rough though practical index to the attainment of maturity. As the metamorphosis of the gamete nears completion, the differentiation of maturity and immaturity becomes more difficult since it depends upon the recognition of the ﬁner intracellular changes which are a little too technical for routine clinical consideration.
It is hoped that a consideration of spermatic cytology such as here outlined may lead to a better, more reliable evaluation of a sperm population in relation to potential fertility. Whether the enumeration of spermatozoa according to their general conﬁguration as is usually done in most spermicgrams constitutes a satisfactory substitute for a knowledge of spermatic cytology, or to what extent various motility and postcoital examinations reflect the incidence of signiﬁcant spermatic disease, can only be answered if cytologic studies are conducted in connection with other phases of the semen analysis and these various items correlated with demonstrated fertility. Unfortunately, studies on the infertile couple too frequently fail to include a full investigation of existing spermatic pathology and consequently we know too little about the clinical signiﬁcance of basic pathology of the sperm.
. Bonnet, R.: Lehrbuch der Entwicklungsgeschichte, Berlin, Verlag von Paul Parey, 1907, pp. 4-7.
. Bowen, R. H.: Anat. Record 28:1-18, 1924.
Bowen, R. H.: Anat. Record 81:8, 201.
Blom, E.: Scandinavish Veterinzirtidskrift, pp. 779-789, 1945.
Cowdry, E. V.: Special Cytology. New York, Paul B. Hoeber, Inc., 1928, p. 1758.
Furzet, 0.: Compt. rend. Soc. de biol. 102:88, 747, 1929.
. Hammen, R.: Studies on Impaired Fertility in Man, with Special Reference to the Male. Copenhagen, Einar Munksgaard, 1944.
8. Lagerl-'o'f, N.: Morphologische Untersuchen iiber veranderungen im Spermabild und in den Hoden bei Bullen mit Verminderter oder Aufgehobener Fertilitat. Uppsala, Almquist 8: Wiksells Boktyrckeri, 1984.
9. Markus, H.: Arch. f. Zellforsch. 15:445-448, 1919-21.
10. Maximow, A. A., and Bloom, W.: A Textbook of Histology. (ed. 8) Philadelphia, 1988, pp. 490-508, 524.
11. Popa, C. T.: Biol. Bul. 52:288-257, 1927.
12. Stieve, H.: Handbuch der Mikrospischen Anatomie des Menschen, Berlin, SpringerVerlag, 1980, p. 87-148.
18. Williams, W. W., McCugan, A., and Carpenter, H. D.: ]. Urol. 82:201-212, 1984.
14. Williams, W. W., and Savage, A.: Cornell Veterinarian 15:858, 1925.
15. Williams, W. W.: New Eng. Med. 217:946-951, 1987.
16. Wilson, E.: The Cell in the Development of Heredity. (ed. 8) New York, Macmillan, 1925, pp. 279-885.
17. Bretschneider, L. H.: Proc. Konin Klinjke Nederlandsche, Akademie van Wetenschappen, 52:801-809, 1949.
18. Ibid.: 52:526—584, 1949.
Cite this page: Hill, M.A. (2023, December 9) Embryology Paper - Cytology of the human spermatozoon. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Paper_-_Cytology_of_the_human_spermatozoon
- © Dr Mark Hill 2023, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G