Fibromas and Thecomas

Slide 1 · Fibromas and Thecomas

Ovarian sex cord–stromal tumors • morphology, clinical correlations, differential diagnosis

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Place fibromas and thecomas within ovarian sex cord–stromal neoplasia.

Recognize characteristic gross and microscopic patterns.

Explain endocrine activity, Meigs syndrome, and Gorlin syndrome association.

Apply morphology and selected ancillary tests to common diagnostic differentials.

Slide 3 · Ovarian tumor categories: Where do these fit?

Ovarian neoplasms

Epithelial

Serous, mucinous, endometrioid…

Germ cell

Teratoma, dysgerminoma…

Sex cord–stromal

Fibroma, thecoma, granulosa…

Schematic classification hierarchy

Slide 4 · Stromal and sex-cord differentiation

Embryonic gonadal mesenchyme

Stromal / sex-cord lineages

Fibroblastic or thecal tumor phenotype

The pathologic phenotype resembles a normal gonadal cell type.

Morphology and endocrine function reflect predominant differentiation.

Schematic — not a specimen

Slide 5 · A spectrum of ovarian stromal tumors

Fibroma

Fibroblastic cells predominate

Fibrothecoma

Mixed fibroblastic + thecal features

Thecoma

Lipid-containing theca-like cells predominate

Conceptual comparison — three linked properties

Slide 6 · Fibroma and thecoma are related—not identical

Fibroma

Well-differentiated fibroblasts

Firm, gray-white tumor

Generally hormonally inactive

Thecoma

Plump theca-like spindle cells

Intracytoplasmic lipid

May produce steroid hormones

Slide 7 · Frequency: A meaningful ovarian tumor subgroup

~4%

Of all ovarian tumors (fibromas and thecomas together)

The prevalence is not a malignancy probability.

Thecomas are less common than fibromas.

Use pathology and clinical features, not frequency alone.

Slide 8 · Benign behavior predominates

Most ovarian fibromas and thecomas are benign.

Tumors composed predominantly of theca cells are almost never malignant (Robbins).

Atypia, cellularity, and mitoses require careful interpretation—not an automatic malignant designation.

Slide 9 · The usual clinical entry point: Pelvic mass

Incidental / symptomatic pelvic mass

Imaging identifies solid adnexal lesion

Histology establishes subtype

Pain and abdominal distension may prompt assessment.

No single symptom identifies a fibroma or thecoma.

Schematic — not a specimen

Slide 10 · Laterality is a useful clue

~90%

Of ovarian fibromas are unilateral (Robbins)

Unilateral presentation is expected but not obligatory.

A bilateral or multifocal pattern should prompt careful contextual assessment.

Laterality alone does not establish histologic type.

Slide 11 · Fibroma: External gross appearance

Gross morphology schematic

Solid and spherical or slightly lobulated

Usually encapsulated and hard

Smooth, glistening, intact ovarian serosal surface

Slide 12 · Fibroma: Cut surface

Gross morphology schematic

Typically gray-white

Firm, fibrous character

Macroscopic appearance helps direct histologic sampling

Slide 13 · Why is the tumor firm and pale?

Fibroblastic differentiation

Fibrous tissue / collagenous matrix

Firm, gray-white gross appearance

This is a morphologic correlation, not proof of subtype.

Thecoma-rich areas may be more lipid-rich or yellow-tan.

Schematic — not a specimen

Slide 14 · Gross morphology: Diagnostic description

Document whether the lesion is solid, circumscribed, and unilateral.

Describe the cut-surface color, texture, hemorrhage, or degeneration if present.

Identify attached tube and residual ovarian tissue, if available.

Target unusual regions for additional sections.

Slide 15 · Fibroma on H&E: The constituent cells

Simplified stromal-cell diagram — NOT histology

Uniform spindle-shaped fibroblastic cells

Bland elongated or ovoid nuclei

Fibrous background, with generally little atypia

Slide 16 · Fibroma: An architectural reading

Simplified stromal-cell diagram — NOT histology

Interlacing spindle-cell fascicles / diffuse growth

Cellularity varies across lesions

Interpret distribution, cytology, and matrix together

Slide 17 · Collagen and cellularity are distinct axes

Cell-poor / fibrous

Prominent stromal matrix

More conspicuous collagen

Lower apparent nuclear density

More cellular

Closer-spaced tumor cells

Fibrous matrix less prominent

Still may represent a benign tumor

Slide 18 · Focal thecal differentiation in a fibroma

Simplified stromal-cell diagram — NOT histology

Plumper cells may appear focally

Lipid-rich cytoplasm suggests thecal differentiation

Small focal thecal component does not negate fibroma phenotype

Slide 19 · Thecoma on H&E: A plumper cell population

Simplified stromal-cell diagram — NOT histology

Plump, round-to-spindle stromal cells

Pale or vacuolated cytoplasm in lipid-containing cells

Less overtly fibrous appearance than classic fibroma

Slide 20 · Cytoplasmic lipid has functional relevance

Thecal differentiation

Steroidogenic capacity in some tumors

Clinical endocrine effects

Lipid morphology supports—but does not prove—hormone secretion.

Pure thecomas are more often functional than fibromas.

Schematic — not a specimen

Slide 21 · Fibrothecoma: Overlapping morphologies

Fibroblastic component

Spindle-cell morphology

Fibrous matrix

Typically little endocrine activity

Thecal component

Plump, pale cells

Lipid-rich cytoplasm

Potential steroid production

Slide 22 · Contrast: Gross and microscopic clues

Feature

Fibroma

Thecoma

Typical cut surface

Firm / white–gray

Often more yellow-tan

Predominant cells

Bland fibroblasts

Plump theca-like cells

Cytoplasmic lipid

Limited / focal

More conspicuous

Hormonal activity

Generally absent

May be present

Slide 23 · Functional status: A spectrum, not a binary label

Fibroma usually inactive

Mixed differentiation

Thecoma may be functional

Do not infer estrogen production from the word “thecoma” alone.

Assess endocrine symptoms and endometrium when clinically indicated.

Schematic — not a specimen

Slide 24 · Estrogenic activity: Tissue consequences

Functional ovarian stromal tumor

Estrogenic stimulation

Endometrial response

Abnormal uterine bleeding can be a clinical clue.

Endometrial sampling is driven by symptoms, age, and clinical judgment.

Schematic — not a specimen

Slide 25 · Bleeding is a clinical clue, not a subtype label

A patient with a solid adnexal mass may report abnormal uterine bleeding.

A hormonally active thecoma is one possible contributor.

Other gynecologic causes remain common; Evaluate independently.

Neither bleeding nor estrogen effects establish the diagnosis without tissue.

Slide 26 · Diagnostic pathway for a suspected stromal mass

1

Clinical presentation

Pain, mass, distension, or bleeding

2

Anatomic evaluation

Identify adnexal origin and solid components

3

Pathologic assessment

Gross + H&E morphology

4

Selective ancillary tests

Resolve a genuine differential

Slide 27 · Ascites can complicate an otherwise benign tumor

~40%

Ascites among fibromas >6 cm

This is a size-selected group; Do not generalize to all fibromas.

Fluid plus an adnexal tumor is not equivalent to carcinoma.

Pleural effusion occurs less commonly.

Slide 28 · Meigs syndrome: The defining triad

Ovarian tumor

Classically a fibroma

Ascites

Peritoneal fluid

Pleural effusion

Often right-sided when present

Conceptual comparison — three linked properties

Slide 29 · Meigs syndrome: The pleural component

Pleural effusion is an uncommon additional feature of ovarian fibroma with ascites.

A frequent right-sided location.

Pleural fluid alone cannot prove ovarian tumor malignancy.

The mechanism of the syndrome is not established.

Slide 30 · The mechanism of Meigs syndrome is uncertain

Ovarian fibroma

Ascites ± pleural fluid

Clinical syndrome

Association is established; A single causal pathway is not.

Avoid drawing a speculative lymphatic or vascular mechanism as proven.

Schematic — not a specimen

Slide 31 · Ascites creates a diagnostic paradox

Initial concern

Solid adnexal mass

Abdominopelvic fluid

Possible pleural effusion

Pathologic resolution

May suggest advanced cancer

May instead accompany benign fibroma

Histologic confirmation remains essential

Slide 32 · Clinical interpretation of the fluid triad

1

Mass with fluid

Do not assign stage from fluid alone

2

Clinical and imaging assessment

Evaluate malignancy on its merits

3

Tissue diagnosis

Identify the actual ovarian lesion

4

Follow-up

Correlate pathology with clinical course

Slide 33 · Nevoid basal cell carcinoma syndrome association

Ovarian fibroma is one recognized tumor association of Gorlin syndrome.

The syndrome also involves multiple basal cell carcinomas and odontogenic keratocysts.

An unusual familial or multifocal presentation may raise clinical suspicion.

The association does not make every isolated fibroma hereditary.

Slide 34 · Gorlin syndrome: Mechanistic context

Germline PTCH-pathway abnormality

Hedgehog signaling dysregulation

Predisposition to characteristic lesions

PTCH as a tumor-suppressor gene.

Association should trigger clinical pattern recognition, not universal germline testing.

Schematic — not a specimen

Slide 35 · When to consider a syndromic context

Finding

Interpretive significance

Young patient / multifocal ovarian lesions

Assess broader clinical history

Multiple basal cell carcinomas

Gorlin syndrome clue

Odontogenic keratocysts

Additional syndrome clue

Isolated unilateral fibroma

Syndrome cannot be inferred

Slide 36 · Solid spindle-cell ovarian lesions: Differential

Spindle-cell ovarian mass

Fibroma / thecoma

Bland stromal phenotype

Leiomyoma

Smooth-muscle differentiation

Other stromal tumors

Specific architecture or cell types

Schematic classification hierarchy

Slide 37 · Fibroma versus ovarian leiomyoma

Fibroma

Ovarian fibroblastic stromal tumor

Bland spindle cells + fibrous matrix

Sex cord–stromal context

Leiomyoma

Smooth-muscle tumor

Intersecting eosinophilic fascicles may be prominent

Muscle marker panel may support distinction

Slide 38 · Fibroma versus granulosa cell tumor

Fibroma

Predominantly fibroblastic cells

Fibrous stroma

Usually benign

Granulosa tumor

Follicular / sex-cord differentiation

Nuclear grooves or Call–Exner bodies may occur

Potentially malignant behavior

Slide 39 · Thecoma versus granulosa–theca tumor

Predominant thecal cells

Lipid-rich plump cells

Often endocrine phenotype

Pure thecoma almost always benign

Granulosa component present

Look for follicular-cell architecture

Adult granulosa tumors may be FOXL2-mutated

Behavior differs from a pure thecoma

Slide 40 · Sclerosing stromal tumor as a mimic

Consider when vascular, pseudolobular, or heterogeneous stromal patterns predominate.

A focal vascular area does not by itself reclassify a fibroma.

Seek the global growth pattern and characteristic cell populations.

Use ancillary studies only if routine morphology leaves genuine ambiguity.

Slide 41 · Atypical areas: Avoid automatic overclassification

Degeneration, sclerosis, calcification, and focal increased cellularity may occur.

Isolated mitoses do not by themselves establish an aggressive stromal malignancy.

Interpret cytologic atypia and proliferation in context.

Defer precise malignant classification until adequate sampling and review.

Slide 42 · Cellular fibroma: A diagnostic problem

Typical fibroma

Low to moderate cellularity

Bland fibroblastic morphology

Usually little proliferative activity

Cellular fibroma pattern

Higher cell density

May show mitotic activity

Needs assessment for severe atypia / necrosis

Slide 43 · Fibrosarcoma is not defined by size alone

A highly atypical, proliferative malignant spindle-cell process raises a different differential.

Do not apply an unverified mitotic threshold to label fibrosarcoma.

Necrosis, destructive features, and cytology require integrated interpretation.

Expert review may be appropriate in equivocal cases.

Slide 44 · Reticulin: An architectural adjunct

Identify diagnostic uncertainty

Assess reticulin framework

Integrate with H&E + immunostains

Reticulin can help characterize stromal patterns and highlight nested sex-cord elements.

A reticulin stain is not a stand-alone classifier.

Schematic — not a specimen

Slide 45 · Immunophenotype: Purpose and limits

Inhibin and calretinin support sex cord–stromal differentiation in context.

Fibromas may show absent, focal, or weaker staining than thecomas.

Expression varies; A negative individual marker does not automatically exclude fibroma.

Interpret phenotype together with the microscopic pattern.

Slide 46 · A focused stain panel answers a question

Question

Potential approach

Caution

Stromal lineage?

Inhibin, calretinin ± others

Variable expression

Smooth muscle?

Desmin / SMA as indicated

Overlap exists

Epithelial lesion?

Cytokeratin / EMA as indicated

Use morphology first

Mixed sex-cord elements?

H&E ± reticulin

Cannot decide from one stain

Slide 47 · Do not turn biomarkers into unsupported cutoffs

Stain extent and intensity are interpreted with morphology.

No single percentage of inhibin positivity defines fibroma versus thecoma here.

Avoid assigning a FOXL2 mutation to a tumor based on FOXL2 protein expression.

Tests should resolve a specific alternative diagnosis.

Slide 48 · Molecular findings: The appropriate scope

Fibroma/thecoma diagnosis is primarily morphologic.

Molecular testing can help in selected difficult sex cord–stromal differentials.

FOXL2 mutation is strongly associated with adult granulosa cell tumors, not a default fibroma test.

Syndromic PTCH-pathway testing is a separate clinical genetics question.

Slide 49 · Specimen sampling: Answer the highest-value questions

1

Map the tumor

Capsule, size, cut-surface heterogeneity

2

Sample representative tissue

Fibrous and atypical-looking regions

3

Microscopic integration

Cell shape, stroma, atypia, architecture

4

Classify cautiously

Correlate with clinical context

Slide 50 · Pathology report: Core narrative elements

State the tumor entity and ovarian location.

Describe the dominant morphology and meaningful variant features.

Note unusual atypia or proliferative findings if present.

Avoid inferring endocrine secretion without a clinical basis.

Slide 51 · Clinical behavior guides communication

Most benign

Typical fibromas/thecomas

Function may vary

Assess hormone-related symptoms

Fluid may mislead

Meigs syndrome can mimic malignancy

Conceptual comparison — three linked properties

Slide 52 · Clinical vignette 1: Solid mass with effusions

Illustrative case • A patient has a unilateral solid ovarian mass, ascites, and a right pleural effusion. No histology is yet available.

What named syndrome is suggested?

Does this triad establish ovarian carcinoma?

Which finding is needed for tumor classification?

Illustrative vignette — not a patient record

Slide 53 · Vignette 1: Reasoned interpretation

The triad suggests Meigs syndrome in the appropriate setting.

The findings are compatible with an ovarian fibroma but not pathognomonic.

Clinical assessment still must exclude alternative etiologies.

Tissue diagnosis determines the actual ovarian neoplasm.

Slide 54 · Clinical vignette 2: Endocrine symptoms

Illustrative case • An adult with abnormal uterine bleeding has a solid ovarian lesion. Histology shows bland, plump stromal cells with pale cytoplasm.

What stromal differentiation is suggested?

Which clinical phenomenon could connect the mass and bleeding?

What must not be inferred from cytoplasm alone?

Illustrative vignette — not a patient record

Slide 55 · Vignette 2: Pathologic interpretation

Plump, pale theca-like cells favor thecoma differentiation.

Steroidogenic activity may explain estrogenic manifestations.

Lipid-containing cells do not prove clinically significant estrogen secretion.

Evaluate other causes of abnormal bleeding independently.

Slide 56 · Clinical vignette 3: Spindle-cell ambiguity

Illustrative case • A solid ovarian tumor contains bland spindled cells; A small zone is more cellular and shows focal mitotic activity.

Should it automatically be labeled fibrosarcoma?

Which tissue findings deserve additional sampling?

How should stains be selected?

Illustrative vignette — not a patient record

Slide 57 · Vignette 3: Avoid the mitotic trap

No: Some fibromas may be relatively cellular and mitotically active.

Review atypia, necrosis, global architecture, and tumor interface.

Sample suspicious areas adequately.

Order immunostains to distinguish concrete morphologic alternatives.

Slide 58 · Six discriminators that matter

Question

Most useful observation

Predominant lineage?

Fibroblastic versus theca-like cells

Stromal matrix?

Fibrous versus lipid-rich morphology

Gross pattern?

Solid, hard, pale, usually circumscribed

Clinical function?

Bleeding / endocrine context

Fluid phenotype?

Ascites with or without pleural effusion

Syndrome clues?

Gorlin-associated manifestations

Slide 59 · Synthesis: Classification from evidence

Clinical context

Gross + microscopic phenotype

Targeted differential / ancillary workup

Most ovarian fibromas/thecomas are benign.

Separate established morphology from unverified mechanisms or thresholds.

Schematic — not a specimen

Slide 60 · Core principles for examination and practice

Fibroma: Usually unilateral, firm gray-white, fibroblastic, and hormonally inactive.

Thecoma: Plump lipid-containing stromal cells; May be hormonally active.

Meigs syndrome combines ovarian tumor, ascites, and pleural effusion; Mechanism uncertain.

Gorlin syndrome is an important uncommon association of ovarian fibroma.

Slide 61 · References and source boundaries

Robbins, Cotran & Kumar. Pathologic Basis of Disease, 11th ed. (2026), Ch. 22, p. 932 (primary text).

Trecourt A et al. Cancers. 2023;15:5864. doi:10.3390/cancers15245864 (diagnostic details).

Mobarki M et al. Pathol Res Pract. 2024;256:155236 (morphologic variability).

Robbins, Ch. 25 (Gorlin syndrome); Parwate NS et al., PMCID: PMC5080219 (clinical context).