ANATOMI OF THE BREAST

In the female, each mammary gland rests upon the fascia of the pectrolaris major muscle. The
peripheral limits of the gland are variable from one patient to another, but ordinarily breast
tissue extends almost to the midline over the sternum, to the anterior axillary line laterally,
and from the level of the second rib above to about the sixth rib inferiorly in a horizontal line
drawn through the nipple. The greatest variation in peripheral extension occurs in the axillary
area. Most often there is a blunted, narrow extension of the gland which may still lie on the
fascia over the converging fibers of the pectrolaris mayor, while in other instances this so-
called axillary tail of the breast is found below or posterior to the pectrolaris major muscle in
the lower third of the axilla. In unusual instances, the axillary tail may be a prolongation
extending in to the middle third of the axilla and lying in contact with the pectroralis minor
muscle or the intercostal muscle. In such abnormal axillary extensions, the indurative changes
of “cystic” disease may occur, as well as actual neoplasma, and in such instances their origin
in mammary tissue may be unrecognized. Still more unusual are the instances of
supernomerary foci of mammary glandular tissue, most often without corresponding nipples,
which may occur in the axillary area as well as in the anterior axillary line and also below and
medial to the normal breast.

Supernumerary foci of mammary tissue may exhibit the cyclic changes which
characterize the physiologic response of the breast to hormonal stimulation.

The superficial fascia of the breast is attached to the skin, a fact of extraordinary
clinical importance. A layer of fat surrounds the gland expect in the area of the nipple and
areola. The thickness of the subcutaneous fat is highly variable. In thin women with
underdevelop breasts, the subcutaneous fat layer may be almost nonexistent so that the
reflection of skin from the breast during radical mastectomy requires a meticulous peripheral
dissection of extremely thin skin skin flaps. With increasing obesity, or with fatty
replacement of mammary parenchyma, the thickness of the subcutaneous fatty layer
correspondingly increase. The anterior surface of the gland is irreguller owing to the
lobulations formed by the deep attachment of fibrous septa, the eponymic designation of
which is Cooper’s ligaments, which run between the superficial and deep fascia.

The mammary gland is made up of ten or twelve to twenty glandular lobes drained by en
equal number of tortuous ducts which dilate close to the nipple to form ampullae, and finally
divide into minute ducts ending in small openings in the nipple. Each of the orifices in the
nipple corresponds roughly to a truncated segment of breast which it drains, a fact of
importance in the investigation of bleeding or the other discharge from the nipple.

The parenchyma of the breast is composed of two types of epithelium, acinar or

secretory, and ductal. Both have a double fibrous convering, the inner periductal or periacinar
layer and an outer layer of perilobular connective tissue. The acinar components of the breast
are highly variable in quantity during puberty, the reproductive years and even after the
climacteric, conditioned upon response to hormonal stimulation. The ductal compenents are
less variable in quantity after maturation except in the instance of pregnancy and lactation.
The acinar epithelium is cuboidal in shape while the epithelium of the ducts is columnar.

In men and in prepubertal famales, the gland is rudimentary with only a few short
ducts and ordinarily without genuinely developed acini.

Cutaneous Lymphatics. There is a continuous intercommunicating network of lymphatics

over the entire surface of the chest, neck and abdomen. By this mechanism, the subcutaneous
lumphatics over one breast communicate with those of the opposite gland. There are even
some lymphatics originating under the skin which drain into the contralateral axillary nodes.
For each breast there is a collecting network of lymphatics under and adjacent to the areola.

Intramammary Lymphatics. The lymphatics originating within the breast drain by

the following pathways

1. A few will follow the ducts and terminate in the subareolar lymphatic network
mentioned above, mainly from the central area.
2. The principal route is the axillary pathway coming from all parts of the gland and
draining directly to the central axillary nodes, the nodes around the axillary vein or
the subscapular group. There is also drain age to intercostal nodes in the second and
third intercostal spaces
3. A transpectoral pathway penetrating the pectoralis major muscle and ending in the
supraclavicular nodes, althought some may drain into infraclavicular nodes behind the
pectoralis minor muscle.
4. The internal mammary pathway which passes through the pectoralis major and
intercostal muscles adjacent to the sternum and drains into the nodes of the internal
mammary chain, lying deep to the costal cartilages and surrounding the internal
mammary blood vessels.

PHYSIOLOGI

The hormonal control of the parenchyma of the breast has become well established, both by
experimental studies in animals and biopsies form human mammary glands during various
phases of the menstrual cycle and during pregnancy and lactation. The estrogenic hormones
during the first half of each menstrual cycle produce ductal hyperplasia, and at the same
sensitize the acinar epithelium for the action of progresterone during the second half of the
cycle the latter hormone producing acinar hyperplasia. In the absence of preliminary
sensitization of the acinar components by estrogens, there is very littlr hyperplastic response
form the administration of progesterone alone, as shown in oophorectomized animals.

The cyclic changes of ductal and acinar hyperplasia, with some hypertrophy, occur in
irregular focal fashion, although the degree and extent of response each month is highly
variable from one woman to another. With the onset of menstruation, there normally occur
involutionary changes in the areas which have been so stimulated to hyperplasia, only to be
succeeded promptly by the same cycle of hyperplasia of ducts and then of acini in other
segments of the breast. If these repetitive cycles of response in the parenchymal (target)
tissue are unttended by abnormalities throughout the reprocdutive years, there is little in the
way of sympatomology except a feeling of premenstrual fullnes or, at the most, a slight
soreness ussualy limited to small areas in the breast. Distinct abnormalities in this
hyperplasia-involution cycle are interpreted as the basic mechanism in the production of so-
called cystic disease.

During pregnancy steroids and progesterone concerned in the cycle changes are the
same as those during a menstrual cycle except on a grandiose scale. During the first four to
five months of pregnancy, the changes are largely in the ductal system, while in the latter part
of pregnancy, particularly in the last three months, the dominant response is that of
tremendous acinar overgrowth. The final phase is that of secretory response by the acinar
epithelium, with prelacteal exudate draining into the ducts and constituting the material
known as colostrum. After delivery, and principally under the ifluence of a hormone from the
anterior pituitary, prolactin, the acinar components rapidly reach a peak of secretory activity
and distention to produce the fully lactating breast.

The estrogenic steroids and progesterone concerned in the cyclic changes are, of
course, elaborated by the ovaries, under the control of tge corresponding gonadotropic
hormones of the anterior pituitary. Following the climacteric, there is evidence that in some
women the adrenal cortices take over the function of production of estrogenic steroids and, in
occasional in stances, such levels of estrogen production may approach those of the woman
with an active follicular-luteal mechanism. This evidence seems to account satisfactorily for
the occasional postmenopausal woman whio continues to have symptoms of mammary
congestion and soreness and objective findings similiar to those patients who suffer from
abnormalities of the hyperplasia-involution cycle in earlier years.

With these unusual exceptions, the parenchyma of the breast undergoes a slow
progressive involution over a period of five or more years following the onset of the
climacteric, with atrophy and replacement of parenchyma by fatty infiltration.

The preceding description of interplay of centain steroid hormones on the mammary

epithelium is, of course, a working skeletonization of existing knowledge and is dependent
upon a considerably more complex endocrine background involving the pituitary-thyroid-
adrenal axis. Some experimental work, for example, indicates that in hypothyroidism
estrogenic stimulation of the breast produces a cystic type of hyperplasia. In some species of
animals, after castration, stimulation with estrogen alone will produce considerable acinar
hyperplasia which frequent papillomatous epithelial lesions of hyperplasia occur, while with
the concomitant administration of progesterone such cystic and papillary changes do not
occur. Although experimental, these are findings which one may relate by inference to some
of the abnormalities of hyperplasia-involution in the human being.