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 An increased number or enlargement of
glandular components.
 Physiological/simple
 Sclerosing adenosis
 Radial scar and complex sclerosing lesion
 Tubular adenosis
 Microglandular adenosis
 Blunt duct adenosis/ ccc/cch
 Multiple nodules-rounded and well defined
 Retention of lobular architecture
 Numeric increase in the glandular elements
 Stromal proliferation
 Glandular compression and distortion-more
towards centre of lesion
 Tubules retain the two cell layers
 Microcalcification+/-
 Fibrous stroma dense ,hyalinized with elastic
tissue
 Lacks atypical features
 Apocrine metaplasia+/_
 Sclerosing adenosis lesion with superimposed
apocrine metaplasia
 Atypia may be moderately severe -
distinction from apocrine DCIS (with lobular
cancerisation) may be difficult
 Immunostaining will demonstrate an intact
myoepithelial layer and basement membrane
 Follow up of patients showed no greater
cancer risk than other atypical lesions
 Glands lined by a monolayer of bland epithelial
cells –no outer myoepithelial mantle.
 Tubules –haphazard, small, regular, rounded
without angulation.
 Lumens contain PAS positive,diastase resistant
secretory material .
 Myoepithelial layer absent but dense basement
membrane present
 Epithelial cells cuboidal or flattened without
apical snouts, cytologically benign.
 Cells- vacoulated and contain PAS positive
material.
 BM- PAS neg. reticulin –complete ring
 Type IV Collagen
 The cells show positive immuno staining with
S100, CK 8/18 & EGFR and negative staining
for ER, PGR & Her-2
 Immuno stains for Collagen IV or laminin are
usually positive indicating an intact bounding
basement membrane
 There is an association with atypical
proliferations and malignancy in up to 50% of
cases
 Histologically complex with adenosis
epithelial hyperplasia and frequent cyst
formation.
 Usually not palpable
 Often multiple
 Frequently bilateral
 Incidental findings in specimens and
mammography
 Usually detected as stellate shadows on
mammograms
 Therefore common in screening
 Radiologically very similar to cancers
 Note: both low grade cancers (especially tubular
cancers) and radial scars may remain unchanged
between screening rounds so a lack of growth is
no guarantee that the lesion is a radial scar
 > 10mm called "Complex sclerosing lesions
Gross:
 firm chalky white lesions with irregular outline
 like head of a flower
Microscopy :
 Lobular architecture is distorted
 Centre of lesion –sclerosis and elastosis
 Entrapped epithelial structure mimics carcinoma
 Surrounded by epithelial sructures showing
dilation ,adenosis, and epithelial hyperplasia.
 Haphazard arrangement of irregular small
tubules
 Two cell layers
 Apocrine metaplasia+/_
 Calcification+/-
 Associated sclerosing adenosis+/-
 Benign lesion.
 But associated with ADH,DCIS.-thus increased
risk of breast ca.
 pattern
BLUNT DUCT ADENOSIS,PRETUBULAR
HYPERPLASIA/COLUMNAR
ALTERATION OF
LOBULES/CAPSS/ELUCA
ATYPICAL CYSTIC LOBULES/ATYPICAL
CYSTIC DUCT/SMALL ECTATIC DUCTS LINED
BY ATYPICAL DUCTAL CELLS WITH
APOCRINE SNOUTS
DUCTAL INTRAEPITHELIAL NEOPLASIA 1 –
FLAT TYPE/ CLINGING
CARCINOMA,MONOMORPHIC TYPE/
CLINGING INSITU DUCT CARCINOMA FLAT
TYPE.
Schnitt and
vincent
salomon
Columnar cell
change
No atypia
With atypia
Columnar cell
hyperplasia
No atypia
With atypia
Simpson
CCC
CCH
CCH with
architectural
atypia
CCH with
cytological atypia
CCH with
cytological and
achitectural atypia
CCC with
cytological atypia
 ‘presumably neoplastic intraductal
alteration, characterised by the replacement
of native epithelial cells by a single layer or
three to five layers of mildly atypical cells’.
 By Simpson’s classification, FEA would
pertain to categories 4 and 6
 Only low grade cytological atypia
 No architectural atypia
 No high grade atypia.
Simpson
CCC
CCH
CCH with
architectural
atypia
CCH with
cytological atypia
CCH with
cytological and
achitectural atypia
CCC with
cytological atypia
.
• CCLs with atypia are the early precursor
lesions in the low grade neoplasia pathway
• CCL WITH ATYPIA
• ADH/LOW GRADE DCIS
• LOW GRADE
CARCINOMAS[TUBULAR/CRIBRIFORM/LOBUL
AR/TUBULILOBULAR/]
 44-51 yrs
 Non palpable in 86%
 Intraluminal calcifications detected
mammogaraphically -74% cases of CCL
 TDLU
 Enlarged
 Epithelial proliferation and cystic dilatation
 Variably dilated acini at low power
 First terminal ductules are affected later acini
 Interlobular stroma diminished
 Simple columnar cell change
 1-2 layers of uniformly distibuted cuboidal to tall
columnar cells
 Apical snout
 Nucleus
 Large
 Crowded
 Perpendicular to BM
 No atypia
 calcification
 More than 2 layers of uniformly distibuted
cuboidal to tall columnar cells
 Tufts/ mounds can be seen
 No true papillae or cribriforn structures
 Apical snout+/- hobnailing
 Nucleus
 Large
 Crowded/ nucleus overlaps
 Perpendicular to BM
 No atypia
 calcification
 The earliest morphologically identifiable
neoplastic alteration among CCLs.
 Luminae-rigidly round [unlike irregular
outline in CCC and CCH without atypia.]
 Cells-atypical- larger, taller, uniform, high
N:C ratio, hyperchroamtic
 CCL s with low grade nuclear atypia= FLAT
EPITHELIAL ATYPIA
 CCLs with high grade nuclear atypia= high
grade DCIS
 CCLs with architectural atypia=ADH/ low
grade DCIS.
 Acute inflammation with abcess.
 Chronic granulomatous mastitis and its
differential diagnosis
 Periductal mastitis /duct ectasia
 Diabetic mastopathy and lymphocytic
mastopathy
 Usually occurs in the lactating breast
 Localised swelling/redness/tenderness
 Pus drained on aspiration
 Antibiotics effective
 Perilobular mastitis
 c/f:
 Breast mass in women of childbearing age
 Usually parous women
 Oten related to recent pregnancy
 Mimics carcinoma
 May be b/l
 Strong tendency for persistence or recurrence
in more than half the cases
The cause remains unknown (obstruction and
hypersensitivity reaction have been suggested).
Oral contraceptive use
Systemic lupus erythematosus
Hyperprolactinemia
Erythema nodosum
 Destructive granulomas.
 Lobulocentric disease pattern.
 Relative sparing of interlobular stroma
 Granulomatous infections
 Sarcoidosis
 Mammary duct ectasia
 Peurperal mastitis
 Vasculitis
 Foreign body reaction to polyvinyl plastic or silicone used for
mammaplasty can result in tumor-like masses, granulomas, and sinus
tracts
 Granulomatous angiopanniculitis
 Bacteria
 Bartonella henselae (cat scratch disease)
 Corynebacteria
 Fungi
 Actinomycosis
 Blastomycosis
 Cryptococcosis
 Histoplasmosis
 Mycobacterium tuberculosis
Granulomatous angiopanniculitis
This lesion contains multiple non-
necrotic,noncaseous granulomas with a
giant cell component and lymphocytic
angiitis, which involves predominantly
the subcutis but can extend into the
breast tissue without affecting lobules or
ducts.
“Infection should always be ruled
out”
 Often seen following conservation surgery for
breast cancer
 May occur at any time after about 6 months
following treatment
 Commonly presents as breast thickeneing
 Less commonly as a lump
 Changes include:
 Hyalinisation of collagen and necrosis
 Vascular changes
 Characteristic radiation fibroblasts
 30 year old female - 2 month history of firm
non-tender lump in breast deep to areola
 Inflammatory breast lesion
 Mimic carcinoma.
 It likely has an autoimmune cause.
 Association with diabetes, especially type 1
and less commonly type 2 (i.e., diabetic
mastopathy).
 Identical lesions occur in nondiabetic
patients, often with other evidence of
autoimmune disease (e.g., Hashimoto’s
thyroiditis) or circulating autoantibodies.
 Hard, painless, irregularly contoured,
movable masses.
 Occur in men and women
 Present as a solitary mass or bilateral
disease, and recur in either breast.
 Recognition of the potential for recurrence
is important because it can spare patients
with documented diabetic mastopathy from
repeated breast biopsies.
 Mammography reveals dense tissue
suggestive of malignant change.
 Lymphocytic lobulitis
 lymphocytic vasculitis
 Dense keloid-like fibrosis
 Peculiar epithelioid cells embedded in dense
fibrous tissue.
 Predominance of B lymphocytes
 Expression of HLA-DR antigen in involved
lobular epithelium.
 Frequent presence of circulating
autoantibodies associated with HLA DR3,
DR4, DR5.
 Resemble benign lymphoepithelial lesions of
the salivary gland and in Hashimoto’s
thyroiditis.
 The epithelioid stromal cells in sclerosing
lymphocytic lobulitis can sometimes be so
prominent and abundant that the possibility of
an infiltrating carcinoma or granular cell tumor
is seriously considered.
 Ashton and colleagues reported that the stromal
cells have features of Myofibroblasts, reacting
with antiactin.
 These cells were negative for antibodies to
keratin (AE1/3), S-100 protein, desmin, MAC-
387, factor XIIIa, CD20 (L26), and CD45RO, but
they reacted with anti-CD68, suggesting some
lysosome formation.
 Often involves the superficial subcutaneous
tissue rather than the breast parenchyma
itself.
 A history of trauma can be elicited in about
half the cases, usually 1 to 2 weeks before
diagnosis.
 Cases of mammary fat necrosis have also
been reported after radiation therapy and
as a local manifestation of Weber-Christian
disease
 The disease can simulate carcinoma because
of skin retraction and the scirrhous (stellate
scarlike) nature of the reparative response.
 Traumatic fat necrosis shows variable and
irregular stellate fibrosis around areas of
necrotic, variably vacuolated fat, with
abundant admixed foamy macrophages.
 varicocele tumor, comedomastitis, periductal
mastitis, plasma cell mastitis, stale milk
mastitis, chemical mastitis, granulomatous
mastitis, and mastitis obliterans.
 The earliest lesions are characterised by the
accumulation of foamy macrophages
between the basement membrane and the
epithelium and also within duct lumens.
Later lesions show periductal chronic
inflammation whilst the most advanced
lesions show marked periductal scarring.
Superimposed (dystrophic) calcification may
be seen.
 Most cases occur in premenopausal parous
women, possibly caused by duct obstruction
or triggered by different components of
stagnant colostrum.
 It may produce retraction or inversion of the
nipple, and nipple discharge is present in
about 20% of cases
 There is ectasia of the large ducts, with
accumulation of detritus in the lumen and
fibrous thickening of the wall, which contains an
increased amount of elastic fibers.
 Calcification is common, producing tubular,
annular, and linear shadows on the mammogram.
 There is no epithelial hyperplasia or apocrine
metaplasia.
 If there is epithelial denudation, the luminal
material may escape from the duct, resulting in
a florid inflammatory reaction that is rich in
macrophages and plasma cells
 In advanced stages, fibrous obliteration of
the ducts can occur.
 Mammary duct ectasia is probably unrelated
to fibrocystic disease, but duct ectasia may
be related to breast abscess, which usually
results from the rupture of mammary ducts.
 Abscesses occur most often during lactation
but can also occur independently of it.
 Abscesses may be located deep within the
parenchyma or periareolar region.
 Microscopic examination shows a central
cavity filled with neutrophils and secretion
surrounded by inflamed and eventually
fibrotic breast parenchyma, with obliteration
of the lobular pattern.
 Clinically, a localized abscess may simulate
carcinoma.
 Periareolar abscess associated with squamous
metaplasia of lactiferous ducts is referred to
as Zuska’s disease.
 Squamous metaplasia of lactiferous ducts
requires surgical excision for cure
 Very uncommon in the breast
 May be identified incidentally in a patient
with systemic amyloidosis
 May very rarely present as a mass lesion -
amyloid tumour
 THANKS……

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Benign breast disease

  • 1.
  • 2.  An increased number or enlargement of glandular components.  Physiological/simple  Sclerosing adenosis  Radial scar and complex sclerosing lesion  Tubular adenosis  Microglandular adenosis  Blunt duct adenosis/ ccc/cch
  • 3.
  • 4.
  • 5.
  • 6.
  • 7.
  • 8.
  • 9.
  • 10.
  • 11.
  • 12.  Multiple nodules-rounded and well defined  Retention of lobular architecture  Numeric increase in the glandular elements  Stromal proliferation  Glandular compression and distortion-more towards centre of lesion  Tubules retain the two cell layers  Microcalcification+/-
  • 13.  Fibrous stroma dense ,hyalinized with elastic tissue  Lacks atypical features  Apocrine metaplasia+/_
  • 14.  Sclerosing adenosis lesion with superimposed apocrine metaplasia  Atypia may be moderately severe - distinction from apocrine DCIS (with lobular cancerisation) may be difficult  Immunostaining will demonstrate an intact myoepithelial layer and basement membrane  Follow up of patients showed no greater cancer risk than other atypical lesions
  • 15.
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22.
  • 23.
  • 24.
  • 25.
  • 26.  Glands lined by a monolayer of bland epithelial cells –no outer myoepithelial mantle.  Tubules –haphazard, small, regular, rounded without angulation.  Lumens contain PAS positive,diastase resistant secretory material .  Myoepithelial layer absent but dense basement membrane present  Epithelial cells cuboidal or flattened without apical snouts, cytologically benign.  Cells- vacoulated and contain PAS positive material.  BM- PAS neg. reticulin –complete ring  Type IV Collagen
  • 27.  The cells show positive immuno staining with S100, CK 8/18 & EGFR and negative staining for ER, PGR & Her-2  Immuno stains for Collagen IV or laminin are usually positive indicating an intact bounding basement membrane  There is an association with atypical proliferations and malignancy in up to 50% of cases
  • 28.
  • 29.
  • 30.
  • 31.
  • 32.
  • 33.
  • 34.
  • 35.
  • 36.
  • 37.
  • 38.
  • 39.
  • 40.  Histologically complex with adenosis epithelial hyperplasia and frequent cyst formation.  Usually not palpable  Often multiple  Frequently bilateral  Incidental findings in specimens and mammography
  • 41.  Usually detected as stellate shadows on mammograms  Therefore common in screening  Radiologically very similar to cancers  Note: both low grade cancers (especially tubular cancers) and radial scars may remain unchanged between screening rounds so a lack of growth is no guarantee that the lesion is a radial scar  > 10mm called "Complex sclerosing lesions
  • 42. Gross:  firm chalky white lesions with irregular outline  like head of a flower Microscopy :  Lobular architecture is distorted  Centre of lesion –sclerosis and elastosis  Entrapped epithelial structure mimics carcinoma  Surrounded by epithelial sructures showing dilation ,adenosis, and epithelial hyperplasia.
  • 43.  Haphazard arrangement of irregular small tubules  Two cell layers  Apocrine metaplasia+/_  Calcification+/-  Associated sclerosing adenosis+/-
  • 44.  Benign lesion.  But associated with ADH,DCIS.-thus increased risk of breast ca.
  • 46.
  • 47.
  • 48.
  • 49.
  • 50.
  • 51.
  • 52.
  • 53.
  • 54.
  • 55.
  • 56.
  • 57.
  • 58.
  • 59.
  • 60.
  • 61.
  • 62.
  • 63.
  • 64.
  • 65.
  • 66. BLUNT DUCT ADENOSIS,PRETUBULAR HYPERPLASIA/COLUMNAR ALTERATION OF LOBULES/CAPSS/ELUCA ATYPICAL CYSTIC LOBULES/ATYPICAL CYSTIC DUCT/SMALL ECTATIC DUCTS LINED BY ATYPICAL DUCTAL CELLS WITH APOCRINE SNOUTS DUCTAL INTRAEPITHELIAL NEOPLASIA 1 – FLAT TYPE/ CLINGING CARCINOMA,MONOMORPHIC TYPE/ CLINGING INSITU DUCT CARCINOMA FLAT TYPE.
  • 67. Schnitt and vincent salomon Columnar cell change No atypia With atypia Columnar cell hyperplasia No atypia With atypia
  • 68.
  • 69.
  • 70. Simpson CCC CCH CCH with architectural atypia CCH with cytological atypia CCH with cytological and achitectural atypia CCC with cytological atypia
  • 71.
  • 72.  ‘presumably neoplastic intraductal alteration, characterised by the replacement of native epithelial cells by a single layer or three to five layers of mildly atypical cells’.  By Simpson’s classification, FEA would pertain to categories 4 and 6  Only low grade cytological atypia  No architectural atypia  No high grade atypia.
  • 73. Simpson CCC CCH CCH with architectural atypia CCH with cytological atypia CCH with cytological and achitectural atypia CCC with cytological atypia
  • 74.
  • 75.
  • 76.
  • 77.
  • 78.
  • 79.
  • 80.
  • 81.
  • 82.
  • 83.
  • 84.
  • 85.
  • 86.
  • 87.
  • 88. . • CCLs with atypia are the early precursor lesions in the low grade neoplasia pathway • CCL WITH ATYPIA • ADH/LOW GRADE DCIS • LOW GRADE CARCINOMAS[TUBULAR/CRIBRIFORM/LOBUL AR/TUBULILOBULAR/]
  • 89.  44-51 yrs  Non palpable in 86%  Intraluminal calcifications detected mammogaraphically -74% cases of CCL
  • 90.  TDLU  Enlarged  Epithelial proliferation and cystic dilatation  Variably dilated acini at low power  First terminal ductules are affected later acini  Interlobular stroma diminished
  • 91.  Simple columnar cell change  1-2 layers of uniformly distibuted cuboidal to tall columnar cells  Apical snout  Nucleus  Large  Crowded  Perpendicular to BM  No atypia  calcification
  • 92.  More than 2 layers of uniformly distibuted cuboidal to tall columnar cells  Tufts/ mounds can be seen  No true papillae or cribriforn structures  Apical snout+/- hobnailing  Nucleus  Large  Crowded/ nucleus overlaps  Perpendicular to BM  No atypia  calcification
  • 93.  The earliest morphologically identifiable neoplastic alteration among CCLs.  Luminae-rigidly round [unlike irregular outline in CCC and CCH without atypia.]  Cells-atypical- larger, taller, uniform, high N:C ratio, hyperchroamtic
  • 94.  CCL s with low grade nuclear atypia= FLAT EPITHELIAL ATYPIA  CCLs with high grade nuclear atypia= high grade DCIS  CCLs with architectural atypia=ADH/ low grade DCIS.
  • 95.
  • 96.
  • 97.  Acute inflammation with abcess.  Chronic granulomatous mastitis and its differential diagnosis  Periductal mastitis /duct ectasia  Diabetic mastopathy and lymphocytic mastopathy
  • 98.  Usually occurs in the lactating breast  Localised swelling/redness/tenderness  Pus drained on aspiration  Antibiotics effective
  • 99.
  • 100.
  • 101.
  • 102.
  • 103.
  • 104.  Perilobular mastitis  c/f:  Breast mass in women of childbearing age  Usually parous women  Oten related to recent pregnancy  Mimics carcinoma  May be b/l  Strong tendency for persistence or recurrence in more than half the cases The cause remains unknown (obstruction and hypersensitivity reaction have been suggested).
  • 105. Oral contraceptive use Systemic lupus erythematosus Hyperprolactinemia Erythema nodosum
  • 106.  Destructive granulomas.  Lobulocentric disease pattern.  Relative sparing of interlobular stroma
  • 107.  Granulomatous infections  Sarcoidosis  Mammary duct ectasia  Peurperal mastitis  Vasculitis  Foreign body reaction to polyvinyl plastic or silicone used for mammaplasty can result in tumor-like masses, granulomas, and sinus tracts  Granulomatous angiopanniculitis  Bacteria  Bartonella henselae (cat scratch disease)  Corynebacteria  Fungi  Actinomycosis  Blastomycosis  Cryptococcosis  Histoplasmosis  Mycobacterium tuberculosis
  • 108.
  • 109. Granulomatous angiopanniculitis This lesion contains multiple non- necrotic,noncaseous granulomas with a giant cell component and lymphocytic angiitis, which involves predominantly the subcutis but can extend into the breast tissue without affecting lobules or ducts.
  • 110. “Infection should always be ruled out”
  • 111.
  • 112.
  • 113.
  • 114.
  • 115.  Often seen following conservation surgery for breast cancer  May occur at any time after about 6 months following treatment  Commonly presents as breast thickeneing  Less commonly as a lump  Changes include:  Hyalinisation of collagen and necrosis  Vascular changes  Characteristic radiation fibroblasts
  • 116.  30 year old female - 2 month history of firm non-tender lump in breast deep to areola
  • 117.
  • 118.
  • 119.
  • 120.
  • 121.
  • 122.  Inflammatory breast lesion  Mimic carcinoma.  It likely has an autoimmune cause.  Association with diabetes, especially type 1 and less commonly type 2 (i.e., diabetic mastopathy).  Identical lesions occur in nondiabetic patients, often with other evidence of autoimmune disease (e.g., Hashimoto’s thyroiditis) or circulating autoantibodies.
  • 123.  Hard, painless, irregularly contoured, movable masses.  Occur in men and women  Present as a solitary mass or bilateral disease, and recur in either breast.  Recognition of the potential for recurrence is important because it can spare patients with documented diabetic mastopathy from repeated breast biopsies.  Mammography reveals dense tissue suggestive of malignant change.
  • 124.  Lymphocytic lobulitis  lymphocytic vasculitis  Dense keloid-like fibrosis  Peculiar epithelioid cells embedded in dense fibrous tissue.
  • 125.  Predominance of B lymphocytes  Expression of HLA-DR antigen in involved lobular epithelium.  Frequent presence of circulating autoantibodies associated with HLA DR3, DR4, DR5.  Resemble benign lymphoepithelial lesions of the salivary gland and in Hashimoto’s thyroiditis.
  • 126.  The epithelioid stromal cells in sclerosing lymphocytic lobulitis can sometimes be so prominent and abundant that the possibility of an infiltrating carcinoma or granular cell tumor is seriously considered.  Ashton and colleagues reported that the stromal cells have features of Myofibroblasts, reacting with antiactin.  These cells were negative for antibodies to keratin (AE1/3), S-100 protein, desmin, MAC- 387, factor XIIIa, CD20 (L26), and CD45RO, but they reacted with anti-CD68, suggesting some lysosome formation.
  • 127.
  • 128.
  • 129.  Often involves the superficial subcutaneous tissue rather than the breast parenchyma itself.  A history of trauma can be elicited in about half the cases, usually 1 to 2 weeks before diagnosis.  Cases of mammary fat necrosis have also been reported after radiation therapy and as a local manifestation of Weber-Christian disease
  • 130.  The disease can simulate carcinoma because of skin retraction and the scirrhous (stellate scarlike) nature of the reparative response.  Traumatic fat necrosis shows variable and irregular stellate fibrosis around areas of necrotic, variably vacuolated fat, with abundant admixed foamy macrophages.
  • 131.
  • 132.
  • 133.
  • 134.
  • 135.
  • 136.
  • 137.
  • 138.
  • 139.
  • 140.
  • 141.
  • 142.  varicocele tumor, comedomastitis, periductal mastitis, plasma cell mastitis, stale milk mastitis, chemical mastitis, granulomatous mastitis, and mastitis obliterans.
  • 143.  The earliest lesions are characterised by the accumulation of foamy macrophages between the basement membrane and the epithelium and also within duct lumens. Later lesions show periductal chronic inflammation whilst the most advanced lesions show marked periductal scarring. Superimposed (dystrophic) calcification may be seen.
  • 144.  Most cases occur in premenopausal parous women, possibly caused by duct obstruction or triggered by different components of stagnant colostrum.  It may produce retraction or inversion of the nipple, and nipple discharge is present in about 20% of cases
  • 145.  There is ectasia of the large ducts, with accumulation of detritus in the lumen and fibrous thickening of the wall, which contains an increased amount of elastic fibers.  Calcification is common, producing tubular, annular, and linear shadows on the mammogram.  There is no epithelial hyperplasia or apocrine metaplasia.  If there is epithelial denudation, the luminal material may escape from the duct, resulting in a florid inflammatory reaction that is rich in macrophages and plasma cells
  • 146.  In advanced stages, fibrous obliteration of the ducts can occur.  Mammary duct ectasia is probably unrelated to fibrocystic disease, but duct ectasia may be related to breast abscess, which usually results from the rupture of mammary ducts.  Abscesses occur most often during lactation but can also occur independently of it.  Abscesses may be located deep within the parenchyma or periareolar region.
  • 147.  Microscopic examination shows a central cavity filled with neutrophils and secretion surrounded by inflamed and eventually fibrotic breast parenchyma, with obliteration of the lobular pattern.  Clinically, a localized abscess may simulate carcinoma.  Periareolar abscess associated with squamous metaplasia of lactiferous ducts is referred to as Zuska’s disease.  Squamous metaplasia of lactiferous ducts requires surgical excision for cure
  • 148.
  • 149.
  • 150.
  • 151.
  • 152.
  • 153.  Very uncommon in the breast  May be identified incidentally in a patient with systemic amyloidosis  May very rarely present as a mass lesion - amyloid tumour

Editor's Notes

  1. Mimics carcinoma mammographically as well as histologically Usually incidental but may be a mass lesion Often associated calcs - picked up on screening May be confused with cancers histologically Low power view critical to make correct diagnosis..... note the nodular arrangement of crowded acini The edge of a focus may be apparently infiltrative but less so than many low grade carcinomas At high power the glands are very crowded and may be cytologically atypical Around some glands at least you should be able to see a compressed myoepithelial layer Immunostaining shows an intact myoepithelial layer e.g. with CK 5/6
  2. Radial scar/complex sclerosing lesion/radial sclerosing lesion/scleroelastotic scar/stellate scar/etc..
  3. Awareness of this condition is important, because surgical therapy is suboptimal for recurrent disease, which requires antibiotics and even corticosteroids before resolution occurs. In fact, resolution may require several years of therapy
  4. Destructive, necrotizing, granulomatous inflammation involving numerous polymorphonuclear leukocytes, multinucleated giant cells,lymphocytes ,plasma cells and focal lipogranuloma-like changes. Centered on the segmental ducts and attached lobules, yielding a lobulocentric disease pattern. Lobulocentric abscesses develop in adjacent segmental ducts and TDLUs, with relative sparing of interlobular stroma
  5. Granulomatous lobular mastitis is distinct from variants of duct ectasia or periductal mastitis, which involve dilated large ducts rather than lobules. Infection must always be considered with necrotizing granulomatous disease. Indeed, histoplasmosis can cause a granulomatous lobular mastitis–like pattern of inflammation. Mycobacterial, fungaland parasitic diseases and cat-scratch disease should also be considered and ruled out with appropriate stains
  6. Lymphocytic lobulitis (i.e., mature lymphocytes and plasma cells surrounding acini and invading across basement membranes), “lymphocytic vasculitis” (mature lymphocytes surrounding small venules), and dense keloid-like fibrosis, which in 75% of cases is characterized by peculiar epithelioid cells embedded in dense fibrous tissue. According to some reports, the lobulitis and vasculitis can be found in nondiabetic patients, but the epithelioid fibroblasts appear to be much better developed, and possibly unique, in those with diabetes. However, others question the specificity of this feature because of identical findings in both patients with type 2 diabetes and nondiabetic patients
  7. predominance of B lymphocytes in most cases and expression of HLA-DR antigen in involved lobular epithelium. These immunologic features closely resemble those found in benign lymphoepithelial lesions of the salivary gland and in Hashimoto’s thyroiditis. Schwartz and Strauchen speculated about an association between sclerosing lymphocytic lobulitis and an increased incidence of lymphoma development, much like that observed with Sjögren’s syndrome and Hashimoto’s thyroiditis. The resulting lymphomas are thought to be related to mucosaassociated lymphoid tissue (MALT). However, with insufficient follow-up, these authors were unable to reach a conclusion. Other investigators have concluded that primary breast lymphomas may show features characteristicof MALT lymphoma (e.g., presence of lymphoepithelial lesions, tendency to remain localized or recur at other MALT sites, low-grade cytology, indolent behavior) arising from other organs such as the stomach, salivary glands, and thyroid. Moreover, Aozasa and colleagues found enough histologic and immunologic evidence to suggest that most mammary lymphomas are B-cell tumors and are associated with coexisting or antecedent lymphocytic mastopathy. In fact, histologic evidence of lymphocytic mastopathy in mammary tissue apart from lymphoma was found in 11of 19 patients, and evidence of lymphocytic mastopathy was confirmed in 10 of the 11. The so-called lymphoepithelial lesion, a characteristic finding of MALT lymphoma, was observed in 42% of their breast lymphomas. Others, however, dispute the existence of MALT features in breast lymphoma. A variety of pseudolymphomas (lymphoid hyperplasias) of the breast have been reported, but they may actually represent either florid cases of sclerosing lymphocytic lobulitis or undetected early, low-grade (B-cell) MALT lymphomas. The epithelioid stromal cells in sclerosing lymphocytic lobulitis can sometimes be so prominent and abundant that the possibility of an infiltrating carcinoma or granular cell tumor is seriously considered. Ashton and colleagues reported that the stromal cells have features of Myofibroblasts, reacting with antiactin. These cells were negative for antibodies to keratin (AE1/3), S-100 protein, desmin, MAC- 387, factor XIIIa, CD20 (L26), and CD45RO, but they reacted with anti-CD68, suggesting some lysosome formation. These stains are important because lymphoepithelioma- like carcinoma of the breast can occur (rarely), and the lymphoid infiltrate could simulate lymphocytic lobulitis and obscure the underlying carcinoma
  8. Duct ectasia with a central calcified keratin plug and associated giant cell inflammatory response