Anatomy and Histology of the Breast

Dr.P.Karpagam Kiruba Rajeswari,M.B.B.S,D.C.P.,
Tutor in Pathology,
MAPIMS.

ANATOMY OF BREAST
 Modified apocrine sweat glands.

 Breast parenchyma  12 to 20
lobes.

 Within each lobe – Lactiferous duct
- branches repeatedly  leads to
no. of terminal ducts  each leads
to a lobule contains multiple
acini/alveoli  TDLU
(TERMINAL DUCT + LOBULE)

 Spaces around the lobules and
ducts and between the lobes are
filled with fatty tissue, ligaments
and connective tissue 
STROMA

LYMPHATIC DRAINAGE
OF BREAST

NORMAL HISTOLOGY OF THE BREAST
 2 cell types – line ducts &
lobules.

1. Contractile MYOEPITHELIAL
CELLS  lie on the BM 
assist in milk ejection during
lactation & provides structural
support to the lobules

2. EPITHELIAL CELLS 
Luminal – produce milk.

 Epithelial & Myoepithelial cells
lie on the basement
membrane.

NORMAL HISTOLOGY OF THE BREAST
2 types of breast
STROMA:

1. INTERLOBULAR
STROMA  Dense
fibrous connective tissue +
adipose tissue.

2. INTRALOBULAR
STROMA  Envelopes
the acini + hormonally
responsive fibroblast – like
cells + scattered
lymphocytes.

ACUTE MASTITIS
 First month of breast feeding.

 Cracks / fissures in the nipple 
portal of entry of bacteria.

 Breast 
erythematous,painful,fever +nt.

 MORPHOLOGY: Staph. Inf.
localized area of inflammation.
Strep. Inf.  Diffuse, spreading.

 HPE: Involved breast tissue –
necrotic, neutrophil infiltration.

 Treated with antibiotics,
continuous milk expression.
Rarely surgical drainage.

PERIDUCTAL MASTITIS
 Recurrent subareolar abscess/
Squamous metaplasia of lactiferous
ducts/ Zuska ds.
 Painful erythematous subareolar mass.
 90% cases – assoc. with smoking 
Vit.A def./toxic substances in smoke –
alters epithelial differentiation.
 Recurrent cases – fistula occurs.
 HPE : Keratinizing squamous
metaplasia of ducts. Keratin shed
from the cellsplugs the ductal
system  dilation & rupture of duct.
 Periductal tissue  keratin spill 
chronic granulomatous inflammatory
response.
 Treatment: En bloc surgical removal
of the involved duct, fistula.
Antibiotics for secondary bacterial
infection.

DUCT ECTASIA
 5th – 6th decade, multiparous women.

 Cl.features: Poorly palpable periareolar
mass, thick white secretions from
nipple, skin retraction.

 HPE: Dilated ducts filled by granular
debris  numerous lipid-laden
macrophages, inspissation of breast
secretions, marked periductal and
interductal ( dense )infiltrate of
lymphocytes and macrophages, and
variable numbers of plasma cells.

 Eventual fibrosis  skin & nipple
retraction. Principal significance
produces an irregular palpable mass -
mimics the mammographic appearance
of carcinoma.

DUCT ECTASIA
Dilated duct with
surrounding fibrosis and
chronic inflammation.
Lumen of the duct 
eosinophilic secretion &
markedly attenuated
epithelium.

FAT NECROSIS
 Cl.features: H/o breast trauma / prior
surgery.

 Painless palpable mass, skin thickening
or retraction, a mammographic
density, or calcifications.

 Acute lesions  hemorrhagic +
central areas of liquefactive fat
necrosis.
Subacute lesions - areas of fat
necrosis  ill-defined, firm, gray-
white nodules containing small chalky-
white foci or dark hemorrhagic debris.
Central region of necrotic fat cells
intense neutrophilic infiltrate +
macrophages.

 Proliferating fibroblasts + new vessels
+ chronic inflammatory cells surround
the injured area  Giant cells,
calcifications, and hemosiderin appear
 focus - replaced by scar tissue.

GRANULOMATOUS MASTITIS
 Rare.

 CAUSES:
1. Systemic granulomatous ds.
Sarcoidosis, Wegener’s.
2. Granulomatous inf. d/t
Mycobacteria, Fungi.

 GRANULOMATOUS LOBULAR
MASTITIS – Parous women,
confined to lobules, d/t
hypersensitivity reactions to the
antigens – expressed by the
lobular epithelium during
lactation.

Benign alterations – in ducts &
lobules:
Detected by mammography/incidental findings in
surgical specimens.
Based on the risk of developing Breast Cancer – 3
groups:

FIBROCYSTIC CHANGE
Most common benign  Morphology:
breast condition. ‘3 principle changes’
Primarily affects terminal
duct–lobular unit (TDLU).
 Pathogenesis Obscure
– hormones (estrogen)
-play a role.
Clinical features
Incidence: 10 – 20 % of
adult women.
Age : 25 – 45 yrs.
Usually bilateral.
Vague ‘lumpy’

FIBROCYSTIC CHANGE – CYSTS
 Dilation & unfolding of
lobules  small cysts – coalesce
 large cysts.
 Unopened cysts  turbid ,semi
translucent fluid  brown/blue
colour  BLUE – DOME CYSTS.
 Lined by flattened atrophic
epithelium/metaplastic apocrine
cells (Abundant granular
eosinophilic cytoplasm + round
nuclei).
 Calcification – common.
 “MILK OF CALCIUM” –
Mammographers
 Diagnosis – confirmed –
disappearance of the cyst after
FNAC.

FIBROCYSTIC CHANGE - FIBROSIS
Cysts rupture

Secretory material

Adjacent stroma

Chronic inflammation,
Fibrosis

Palpable firmness of the
breast

FIBROCYSTIC CHANGE - ADENOSIS
Increase in the number of
acini per lobule.
Pregnancy Normal
physiologic adenosis.
Nonpregnant women 
adenosis - focal change.
Acini – enlarged,not
distorted (blunt-duct
adenosis).
Calcifications – occasionally -
within the lumens.
 Acini - lined by columnar
cells  benign / atypical
features (“flat epithelial
atypia”)  Earliest
recognizable precursor of
epithelial neoplasia

LACTATIONAL ADENOMAS
 Palpable masses –
pregnant/lactating women.

 Normal appearing breast tissue +
physiological adenosis +
lactational changes.

 Exagerrated focal response to
hormones.

 Gross appearance: Well
circumscribed mass - distinct
lobular configuration, yellowish
color, and marked vascularization.
C/s: Gray / tan. Necrotic changes
frequent.

 HPE:Proliferated glands lined by
actively secreting cuboidal cells

PROLIFERATIVE BREAST DISEASE
WITHOUT ATYPIA
Mammographic densities, calcifications, or as
incidental findings in specimens from biopsies.

Found alone/assoc. with non prolif. breast
changes.

Lesions  proliferation of ductal epithelium and/or
stroma without cytologic or architectural features
suggestive of carcinoma in situ.

MORPHOLOGY –
Epithelial hyperplasia
Normal breast ducts &
lobules – double layer of
epithelial cells  luminal &
myoepithelial layers.

Epith.hyperplasia
Incidental finding - > 2
layers – luminal &
myoepithelial cells 
fill,distend ducts & lobules.

Irregular lumens – periphery
of the cellular masses.

Sclerosing Adenosis
 Palpable mass, a radiologic
density, or calcifications.

 No. of acini per terminal duct -
increased to double the number NORMAL
found in uninvolved lobules.

 Normal lobular arrangement -
maintained.

 Acini - compressed and distorted
in the central portions of the
lesion & characteristically dilated
ADENOSIS
at the periphery.

 Myoepithelial cells - prominent.

Complex sclerosing lesion
 Radial sclerosing lesion (“radial
scar”) - commonly occurring
benign lesion  forms - irregular
masses (mimic invasive
carcinoma)mammographically,
grossly, and histologically.

 Central nidus of entrapped glands
in a hyalinized stroma with long
radiating projections into stroma.

 Radial scar – misnomer (lesions -
not assoc. with prior trauma or
surgery)

Papillomas
 Multiple branching fibro vascular cores, each with
a connective tissue axis lined by luminal and
myoepithelial cells.

 Growth - within a dilated duct.

 Epithelial hyperplasia and apocrine metaplasia -
frequently present.

 Large duct papillomas - solitary, situated in the
lactiferous sinuses of the nipple.

 Small duct papillomas - multiple - located deeper
within the ductal system.

 > 80% of large duct papillomas  nipple discharge.

 Large papillomas  torsion of stalk  infarction
bloody discharge.

 Intermittent blockage and release of normal breast
secretions or irritation of the duct by the papilloma
 Non bloody discharge.

 Others  + nt as small palpable masses, or as
densities or calcifications seen on mammograms

Atypical ductal/lobular hyperplasia  Cellular proliferation -
resembles carcinoma in situ - but lacks sufficient qualitative or
quantitative features for diagnosis as carcinoma.

ATYPICAL DUCTAL
HYPERPLASIA
 Found in Bx specimens – done for
calcifications,mammographic
densities,palpable masses.

 Relatively monomorphic
proliferation of regularly spaced
cells, sometimes with cribriform
spaces.Limited in extent, only
partially filling ducts.

Duct is filled with a mixed population of
cells  oriented columnar cells at the
periphery and more rounded cells within
the central portion. Some of the spaces -
round and regular, the peripheral spaces -
irregular and slitlike  Highly Atypical.

ATYPICAL LOBULAR HYPERPLASIA
 Proliferation of cells  the cells
do not fill or distend more than
50% of the acini within a lobule.

 Atypical lobular hyperplasia 
also involves contiguous ducts
through pagetoid
spread( discrete intraepidermal
proliferation of cells occurring
singly/ nests at all levels of the
epidermis) in which atypical
A population of monomorphic small,
lobular cells lie between the ductal
round, loosely cohesive cells partially fill
basement membrane and a lobule. Some intracellular lumens can
overlying normal ductal epithelial be seen
cells.

Anatomy and Histology of the Breast

Anatomy and Histology of the Breast

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (11)

Similar to Anatomy and Histology of the Breast

Similar to Anatomy and Histology of the Breast (20)

Recently uploaded

Recently uploaded (20)

Anatomy and Histology of the Breast