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Stratified Squamous Keratinized Epithelium

Stratified Squamous Keratinized Epithelium

Section titled “Stratified Squamous Keratinized Epithelium”

At a glance

Section titled “At a glance”
  • Multi-layered squamous epithelium culminating in anucleate keratin; maximal barrier for abrasion and water loss.
  • Classic sites: skin/epidermis, hard palate/gingiva (masticatory mucosa); thickness varies by site.
  • Layers to verify: basal (p63/p40+), spinous with intercellular bridges, granular with keratohyalin, cornified surface.
  • Pitfalls: physiologic hyperkeratosis vs dysplasia; rete ridge pattern differs by site; basal atypia is not normal.

Jump to sections

Section titled “Jump to sections”

Epidermis

Section titled “Epidermis”

Layers (deep → superficial):

  1. Stratum basale (germinativum): single layer, cuboidal/low columnar, p63+/p40+/CK5/6+, melanocytes, Merkel cells.
    • Why: stem/progenitor pool; attaches to BM via hemidesmosomes.
  2. Stratum spinosum: several layers of polygonal cells, prominent desmosomes → “spines.”
    • Why: main mechanical layer.
  3. Stratum granulosum: 1–3 layers, flattened, basophilic keratohyalin granules (profilaggrin, involucrin, loricrin), lamellar (Odland) bodies.
    • Why: aggregates keratin + extrudes lipids → barrier to water.
  4. Stratum corneum: anuclear, flattened keratin squames; thickness varies by site.
    • Why: abrasion + water loss protection.

Basement membrane / dermal papillae:

  • Wavy DE junction with rete ridges.
  • Why: increases adhesion and diffusion.

Junctions:

  • Desmosomes abundant in spinosum.
  • Hemidesmosomes basally.
  • Why: resist shear.

Function:

  • Barrier (water, microbes).
  • Mechanical protection.
  • UV/trauma interface.

Path relevance:

  • Loss of keratohyalin → ichthyosis-like.
  • Acantholysis (desmosome loss) → pemphigus.
  • Subepidermal split (hemidesmosome/BM) → bullous pemphigoid.

Generalities

Section titled “Generalities”
  1. Architecture

  • Multiple cell layers (basal → spinous → granular → keratin layer).

    Why: this is the “maximum protection” stratified epithelium — made to take friction, drying, and sometimes UV.

  • Basal layer: cuboidal/low columnar on a basement membrane.

    Why: stem/progenitor compartment that keeps renewing the surface.

  • Progressive maturation toward the surface (cells flatten, make more keratin, lose organelles).

    Why: cells are being “prepared to die” but to die in a useful way (as a barrier).

2. Basal layer
Section titled “2. Basal layer”

  • Small, basophilic cells, high N:C, p63+/p40+/CK5/6+.

    Why: actively cycling, squamous-programmed cells.

  • Hemidesmosomes to basement membrane.

    Why: whole sheet is pulled, stretched, rubbed — basal cells must stay fixed.

3. Spinous (prickle) layer
Section titled “3. Spinous (prickle) layer”

  • Polygonal cells with prominent desmosomes → intercellular bridges.

    Why: this is the mechanical “core” of the epithelium — resists shear.

  • Cytokeratin network (tonofilaments) becomes more abundant.

    Why: preps the cell to become a tough, keratin-filled squame.

4. Granular layer (key for keratinized)
Section titled “4. Granular layer (key for keratinized)”

  • Cells flatten, nuclei start to condense.

    Why: transition to nonviable surface.

  • Keratohyalin granules (profilaggrin, involucrin, loricrin, etc.).

    Why: these proteins help aggregate keratin filaments and form the cornified envelope → gives mechanical toughness and water resistance.

5. Keratin (cornified) layer
Section titled “5. Keratin (cornified) layer”

  • Most superficial layer: anuclear, eosinophilic, flattened squames.

    Why: dead cells = no water loss from them, no easy microbial entry, and they can be shed without pain.

  • Thickness of keratin varies by site (thin in some oral masticatory mucosa, very thick in skin/palms/soles).

    Why: the body adds more keratin where friction/drying is highest.

6. No surface nuclei (orthokeratosis)
Section titled “6. No surface nuclei (orthokeratosis)”

  • In classic keratinized epithelium, nuclei are lost.

    Why: fully keratinized cells are dead, better as a dry shield.

  • If nuclei are retained (parakeratosis), it’s either normal for that site (gingiva, hard palate sometimes) or a sign of increased turnover.

    Why: fast turnover doesn’t leave time to lose the nucleus.

7. Junctions
Section titled “7. Junctions”

  • Desmosomes very prominent in spinous and suprabasal layers.

    Why: need strong lateral cohesion to transmit forces to the BM.

  • Hemidesmosomes basally.

    Why: anchor to BM so the whole stack doesn’t slide.

8. Basement membrane
Section titled “8. Basement membrane”

  • Continuous BM with dermal/lamina propria papillae interdigitating.

    Why: increases surface area for nutrition and makes the dermo-epidermal junction mechanically stronger (resists shearing).

9. Vascularity / nutrition
Section titled “9. Vascularity / nutrition”

  • Epithelium itself is avascular.

    Why: like all epithelia.

  • Nourished from dermal/lamina propria capillaries in the papillae.

    Why: upper layers are dead — lower viable layers need short diffusion distance.

10. Function
Section titled “10. Function”

  1. Barrier to water loss

    Why: keratin + lipid envelope ↓ transepidermal water loss.

  2. Barrier to microbes and chemicals

    Why: dead, tightly packed squames are hard to penetrate.

  3. Mechanical protection

    Why: thick stratified stack + desmosomes + keratin cap = abrasion-resistant.

  4. UV and environmental protection (skin)

    Why: upper dead layer + melanin in basal/suprabasal help protect deeper cells.

11. Immuno (generic squamous keratinized)
Section titled “11. Immuno (generic squamous keratinized)”

  • Basal/suprabasal: p63+, p40+, CK5/6+, HMWK+.

    Why: confirms stratified squamous origin.

  • Differentiating SCCs often keep this pattern.

    Why: helps match tumor to its surface epithelium of origin.

12. Typical anatomic sites
Section titled “12. Typical anatomic sites”

  • Epidermis (skin) — classic example.

  • Masticatory oral mucosa (gingiva, hard palate) — often orthokeratinized or para-keratinized.

    Why: these areas take chewing forces directly.

  • Vermilion border — keratinized but modified.

Oral Masticatory Mucosa (gingiva, hard palate)

Section titled “Oral Masticatory Mucosa (gingiva, hard palate)”

Location:

  • Attached gingiva, hard palate.

Epithelium:

  • Stratified squamous keratinized OR parakeratinized.
    • Orthokeratinized: clear granular layer + anuclear surface.
    • Parakeratinized: surface squames keep small pyknotic nuclei; granular layer reduced.
    • Why: chronic mechanical load from mastication → needs tougher surface, but oral cavity is still moist, so parakeratin is acceptable.

Layers:

  1. Basal: cuboidal, p63+/CK5/6+, firmly attached.
  2. Spinous: thick, desmosome rich.
  3. Granular: present but sometimes thin.
  4. Keratin/parakeratin: variable thickness depending on chewing stress.

Lamina propria:

  • Dense collagen, often with long CT papillae.
  • In gingiva: blends with periosteum (mucoperiosteum).
  • Why: strong anchorage to bone/teeth.

Function:

  • Resist mastication/shear.
  • Maintain oral seal at gingival margin.

Path relevance:

  • Frictional keratosis → thickened para/orthokeratin.
  • Must distinguish from leukoplakia/dysplasia → look for atypia, disordered maturation.