This document discusses non-neoplastic and neoplastic conditions of the female genital tract. It describes Bartholin's cyst and abscess, lichen sclerosus, and squamous hyperplasia as non-neoplastic epithelial disorders of the vulva. Benign tumors discussed include stromal polyps, papillary hidradenoma, and condyloma acuminatum. Vulvar intraepithelial neoplasia (VIN) and invasive carcinoma are also covered. For the vagina, vaginitis, tumors, and embryonal rhabdomyosarcoma are summarized. Finally, the document discusses cervicitis, cervical polyps, squamous intraepithelial

1. FEMALE GENITAL
SYSTEM - 2
DR. ROOPAM JAIN
PROFESSOR & HEAD, PATHOLOGY

2. MISCELLANEOUS
CONDITIONS

3. BARTHOLIN’S CYST & ABSCESS
• Inflammation of Bartholin’s vulvovaginal glands (Bartholin’s adenitis)
may occur due to bacterial infection, notably gonorrhoeal infection.
• Infection may be acute or chronic.
• Acute Bartholin’s adenitis occurs from obstruction and dilatation of the
duct by infection resulting in formation of a Bartholin’s abscess.
• Chronic Bartholin’s adenitis results from a less virulent infec tion so that
the process is slow and prolonged.

4. NON-NEOPLASTIC
EPITHELIAL
DISORDERS

5. • non-neoplastic epithelial disorders of the skin of vulva includes following
2 lesions:
• 1. Lichen sclerosus (older term: atrophic dystrophy).
• 2. Squamous hyperplasia or keratosis (older term: hyperplastic
dystrophy, or lichen simplex chronicus).
• The two types of lesions may coexist in the same patient called mixed
vulvar dystrophy.

6. Lichen Sclerosus
• more common and more extensive in the vulva in postmenopausal
women.
• Th e lesions appear as multiple, small, coalescent, yellowish-blue
macules or papules which produce thin and shiny parchment-like skin.
• The lesions may extend from vulva onto the perianal and perineal area.
• Clinically, the patient, usually a post-menopausal woman, complains of
intense pruritus which may produce excoriation of the affected skin.
• Eventually, there is progressive shrinkage and atrophy resulting in
narrowing of the introitus, clinically referred to as kraurosis vulvae

7. Lichen Sclerosus MORPHOLOGIC
FEATURES
• Microscopically, the follow - ing characteristics are seen (Fig. 22.1,A):
• 1. Hyperkeratosis of the surface layer.
• 2. Thinning of the epidermis with disappearance of rete ridges.
• 3. Amorphous homogeneous degenerative change in the dermal
collagen.
• 4. Chronic inflammatory infiltrate in the mid-dermis

8. Non-neoplastic epithelial
disorders of vulval skin
Lichen Sclerosus

9. Squamous Hyperplasia
• Squamous hyperplasia, or simply called keratosis, is characterised by
white, thickened vulvar lesions which are usually itchy.
• The cause is unknown
• symptomatic relief results from use of topical corticosteroids.

10. Non-neoplastic
epithelial disorders
of vulval skin
Squamous
Hyperplasia

11. VULVAL
TUMOUR

12. VULVAL TUMOUR
STROMAL POLYPS
• Stromal (fibroepithelial) polyps or acrochordons may form in the vulva or
vagina.
• There may be single or multiple polypoid masses.
• Histologically, they are covered by an orderly stratified squamous
epithelium. The stroma consists of loose fibrous and myxomatous
connective tissue with some adipose tissue and blood vessels.

13. PAPILLARY HIDRADENOMA
(HIDRADENOMA PAPILLIFERUM)
• This is a benign tumour arising from apocrine sweat glands of the vulva.
• Most commonly, it is located in the labia
Histologically
• the tumour lies in the dermis under a normal epidermis.
• The tumour consists of papillary structures
• covered by double layer of epithelial

14. CONDYLOMA ACUMINATUM
• Condyloma acuminata or anogenital warts are benign papillary lesions of
squamous epithelium
• transmitted venereally to male sex partner.
• They may be solitary but more frequently are multiple forming soft
warty masses.
• The common locations are the anus, perineum, vaginal wall, vulva and
vagina.
• They are induced by HPV, particularly types 6 and 11.

15. CONDYLOMA ACUMINATUM
Histologically
• they are identical to their counterparts on male external genitalia.
• The features consist of a tree-like proliferation of stratified
squamous epithelium, showing marked acanthosis,
hyperkeratosis, parakeratosis, papillomatosis & perinuclear
vacuolisation of epithelium called koilocytosis, indicative of HPV
infection.
• The papillary projections consist of fibro vascular stoma.

16. VULVAL INTRAEPITHELIAL NEOPLASIA
& INVASIVE CARCINOMA
• Vulval intraepithelial neoplasia (VIN) and invasive squamous cell
carcinoma are morphologically similar to those in the cervix and vagina.
• viruses in carcinogenesis, particularly high-risk HPV types 16 and 18
• VIN is often multifocal within vulva and may be multicentric as well
• Vulval carcinoma constitutes 3% of all female genital tract cancers.
• VIN occurs in reproductive age

17. VULVAL INTRAEPITHELIAL NEOPLASIA
& INVASIVE CARCINOMA
• Grossly, VIN and vulval carcinoma in early stage is a ‘white’ lesion (leukoplakia)
while later the area develops an exophytic or endophytic (ulcerative) growth
pattern.
• The traditional VIN lesion, described as Bowen’s disease of the vulva, is
generally a slightly elevated, velvety, plaque lesion.

18. VULVAL INTRAEPITHELIAL NEOPLASIA &
INVASIVE CARCINOMA
Microscopically,
• VIN may also range from VIN I to VIN III, higher grade being also called
Bowen’s disease (in situ carcinoma).
• Vulvar cancer is squamous cell type with varying degree of anaplasia
and depth of invasion depending upon the stage (Fig.).
• HPV-positive tumours are more often poorly-differentiated squamous cell
carcinoma
• while HPV-negative are well-differentiated kerati nising type.
• Verrucous carcinoma is a rare variant which is a fungating tumour but is
locally malignant.

19. Vulval intraepithelial neoplasia (VIN) (Bowen’s disease)
There is hyperkeratosis, parakeratosis, acanthosis, koilocytosis and presence
of atypical anaplastic cells throughout the entire thickness of the epithelium.
Photomicrograph on right under higher magnification shows mitotic figures in
the layers of squamous epithelium.

20. • Clinical staging for vulval carcinoma based on tumour
size (< or > 2 cm) and extent of spread has been
described by International Federation of Gynaecology
and Obstetrics (FIGO staging)

21. FIGO staging of carcinoma of the vulva

22. VAGINA

23. VAGINITIS &
VULVOVAGINITIS
• Since vulva and vagina are anatomically close to each other, often
inflammation of one affects the other location.
• i) Bacterial e.g. streptococci, staphylococci, Escherichia coli,
Haemophilus vaginalis.
• ii) Fungal e.g. Candida albicans.
• iii) Protozoal e.g. Trichomonas vaginalis.
• iv) Viral e.g. Herpes simplex.

24. VAGINITIS &
VULVOVAGINITIS
• The most common causes of vaginitis are Candida (moniliasis) and
Trichomonas (trichomoniasis).
• The hyphae of Candida can be seen in the vaginal smears.
• Similarly, the protozoa, Trichomonas, can be identified in smears.
• These infections are particularly common in pregnant and diabetic
women and may involve both vulva and vagina.
• (adult vaginal mucosa is relatively resistant to gonococcal
infection because of its histology)

25. TUMOURS &
TUMOUR-LIKE
CONDITIONS

26. • Vaginal cysts such as Gartner’s duct (Wolffian) cyst lined by glandular
epithelium and vaginal inclusion cyst arising from inclusion of vaginal
epithelium are more common benign vaginal tumours
• Other uncommon benign tumours are papillomas, fi bromas, lipomas,
angiomas and leiomyomas
• Primary malignancies of the vagina are rare
• and include carcinoma (squamous cell carcinoma and adenocarcinoma)
• and embryonal rhabdomyosarcoma (sarcoma botryoides).

27. CARCINOMA OF VAGINA
• Primary carcinoma of the vagina is an uncommon tumour.
• Squamous cell dysplasia or vaginal intra epithelial neoplasia occur less
frequently as compared to the cervix or vulva and can be detected by
Pap smears.
• Invasive carcinoma of the vagina includes two main types:
• 1. Squamous cell carcinoma of vagina constitutes less than 2% of all
gynaecologic malignancies. The role of HPV types 16 and 18 in its
etiology
• 2. Adenocarcinoma of the vagina is much less frequent than squamous
cell carcinoma of the vagina. It may be endometrioid or mucinous type.

28. FIGO clinical staging of
carcinoma of the vagina

29. EMBRYONAL RHABDOMYOSARCOMA
(SARCOMA BOTRYOIDES)
• This is an unusual and rare malignant tumour occurring in
infants and children
• under 5 years of age.
• The common location is anterior vaginal wall.

30. EMBRYONAL RHABDOMYOSARCOMA
(SARCOMA BOTRYOIDES)
MORPHOLOGIC FEATURES
Grossly
• The tumour is charac terised by bulky and polypoid grape-like mass
(botryoides = grape) that fills and projects out of the vagina.
Histologically:
• 1. Groups of round to fusiform tumour cells are characteristically lying
underneath the vaginal epithelium, called cambium layer of tumour cells.
• 2. The central core of polypoid masses is composed of loose and myxoid
stroma with many infl ammatory cells.

31. CERVIX

32. CERVICITIS
• Cervicitis may be specific or nonspecific, acute or chronic.
• Specific cervicitis may be caused by tuberculosis, syphilis, granuloma
inguinale, lymphogranuloma vene reum, chlamydia and chancroid.
• Nonspecific cervicitis is more frequent and is generally divided into
acute and chronic forms, the latter being quite common

33. ACUTE CERVICITIS
• Acute cervicitis is usually associated with puerperium or gonococcal
infection.
• Other causes are primary chancre and infection with herpes simplex.
• Grossly, the cervix shows everted endocervical mucosa which is red and
oedematous.
• Histologically, there is infiltration of the subepithelial and periglandular
tissue with neutrophils, and there is oedema and congestion.
• The mucosa may be ulcerated and haemorrhagic.

34. CHRONIC CERVICITIS
• encountered quite frequently and is the common cause of leucorrhoea.
• The most common organisms - normal mixed vaginal flora that
includes streptococci, enterococci (e.g. E. coli) & staphylococci.
• Other infecting organisms include gonococci, Trichomonas vaginalis,
Candida albicans and herpes simplex.
• Factors predisposing to chronic cervicitis are sexual intercourse,
trauma of childbirth, instrumentation and excess or defi ciency
of oestrogen

35. TUMOURS
• Both benign and malignant tumours are common in the cervix.
• In addition, cervix is the site of ‘shades of grey’ lesions that include
cervical dysplasia and carcinoma in situ (cervical intraepithelial
neoplasia, CIN), currently termed squamous intraepithelial lesions (SIL).
• Benign tumours of the cervix consist most commonly of cervical polyps.
• Uncommon benign cervical tumours are leiomyomas, papillomas and
condyloma acuminatum
• The most common malignant tumour is squamous carcinoma of the
cervix

36. CERVICAL POLYPS
• Cervical polyps are localised benign proliferations of endocervical
mucosa though they may protrude through the external os.
• They are found in 2-5% of adult women and produce irregular vaginal
spotting.
• MORPHOLOGIC FEATURES
• Grossly, cervical polyp is a small (up to 5 cm in size), bright red, fragile
growth which is frequently pedunculated but may be sessile.
• Microscopically,
• most cervical polyps are endo cervical polyps and are covered with
endocervical epithelium which may show squamous metaplasia.
• The stroma of the polyp is composed of loose and oedematous fibrous
tissue with variable degree of inflammatory infiltrate

37. Endocervical polyp
The surface is covered by endocervical mucosa with squamous
metaplasia. The stromal core is composed of dense fibrous tissue
which shows nonspecific inflammation.

38. SQUAMOUS
INTRAEPITHELIAL LESION
(SIL)
(CERVICAL INTRAEPITHELIAL
NEOPLASIA, CIN)

39. • Presently, the terms dysplasia, CIN, carcinoma in situ,
and SIL are used synonymously as follows:

40. DYSPLASIA
• The term ‘dysplasia’ (meaning ‘bad moulding’) - atypical cytologic
changes in the layers of squamous epithelium, the changes being
progressive.
• Depending upon the thickness of squamous epithelium involved by
atypical cells, dysplasia is conventionally graded as mild, moderate and
severe.
• Carcinoma in situ is the full-thickness involvement by atypical cells, or in
other words carcinoma confined to layers above the basement
membrane.
• It is well accepted that invasive cervical cancer evolves through
progressive stages of dysplasia and carcinoma in situ.

41. CIN
• An alternative classification is to group various grades of dysplasia and
carcinoma in situ together into cervical intraepithelial neoplasia (CIN)
which is similarly graded from grade I to III.
• According to this concept, the criteria are as under:
• CIN-1 represents less than one-third involvement of the thickness of
epithelium (mild dysplasia).
• CIN-2 is one-third to two-third involvement (moderate dysplasia).
• CIN-3 is full-thickness involvement or equivalent to carcinoma in situ
(severe dysplasia and carcinoma in situ).

42. SIL
• 3 grades of CIN are readjusted into two grades of squamous
intraepithelial lesions (SIL)—low-grade SIL (L-SIL) & high-grade SIL (H-
SIL):
• L-SIL corresponds to CIN-1 and is a flat condyloma, having koilocytic
atypia, usually related to HPV 6 and 11 infection
• About 10% cases of L-SIL may progress to H-SIL.
• H-SIL corresponds to CIN-2 and 3 and has abnormal pleomorphic
atypical squamous cells.
• HPV 16 and 18 are implicated in the etiology of H-SIL (i.e. includes
moderate dysplasia, severe dysplasia, and carcinoma in situ).
• Approximately, 10% cases of H-SIL may progress to invasive cervical
cancer over a period of about two years

43. Etiopathogenesis
• The biology of CIN/SIL and its relationship to invasive carcinoma
of the cervix is well understood by epidemiologic, virologic,
molecular, immunologic and ultrastructural studies
• 1. Epidemiologic studies
• 2. Virologic studies
• 3. Molecular studies
• 4. Immunologic studies
• 5. Ultrastructural studies

44. Etiopathogenesis
Role of human
papillomavirus
(HPV) in the
pathogenesis of
cervical neoplasia

45. Classifi cation of cervical
intraepithelial neoplasia/squamous
intraepithelial lesion (CIN/SIL).

46. MORPHOLOGIC FEATURES
Grossly
• no specific picture is associated with cellular atypia found in
dysplasias or carcinoma in situ
• The diagnosis can be suspected clinically on the basis of Schiller’s
test

47. MORPHOLOGIC FEATURES
Histologically
• in general dysplastic cells are distri buted in the layers of squamous
epithelium for varying thickness, and accordingly graded as mild, moderate
and severe dysplasia, and carcinoma in situ (Fig.).
• In mild dysplasia (CIN-1), the abnormal cells extend up to one-third
thickness from the basal to the surface layer
• In moderate dysplasia (CIN-2) up to two-thirds
• In severe dysplasia (CIN-3), these cells extend from 75- 90% thickness of
epithelium
• In carcinoma in situ (included in CIN-3), the entire thickness from the
basement membrane to the surface shows dysplastic cells.

48. MORPHOLOGIC FEATURES
Histologically
• The atypical cells migrate to the surface layers from where they are shed
off (exfoliated) into vaginal secretions in Pap smear.
• The individual dysplastic or abnormal cells in these grades of atypia
show various cytologic changes such as: crowding of cells,
pleomorphism, high nucleocytoplasmic ratio, coarse and irregular
nuclear chromatin, numerous mitoses and scattered dyskaryotic cells

49. Cervical intraepithelial neoplasia (CIN) and squamous intraepithelial lesions (SIL). A, Exfoliative
cytologic studies in various grades of cellular changes (upper part of fi gure). B, Schematic
representation of histologic changes (lower part of fi gure). The grades of CIN-1 or mild dysplasia
(L-SIL), CIN-2 (moderate dysplasia) and CIN-3 (severe dysplasia and carcinoma in situ) (together
grouped as H-SIL) show progressive increase in the number of abnormal cells parallel to the
increasing severity of grades.