This is a summary of the pathology of the breast.after going through the slide you will have a general concept of Breast

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

2. 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

3. LYMPHATIC DRAINAGE
OF BREAST

4. 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.

6. 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.

10. 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.

12. 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.

13. 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.

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

15. 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.

16. FAT NECROSIS

17. 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.

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

20. 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’

21. 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.

22. FIBROCYSTIC CHANGE - FIBROSIS
Cysts rupture
Secretory material
Adjacent stroma
Chronic inflammation,
Fibrosis
Palpable firmness of the
breast

23. 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

24. 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

26. 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.

27. 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.

28. 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.

29. 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)

30. 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

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

32. 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.

33. 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.