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Stratum granulosum – The Granular Layer of the Skin

The stratum granulosum is a layer of the epidermis where keratinocytes form granules and initiate keratinization. It plays a key role in the skin barrier function.

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Things worth knowing about "Stratum granulosum"

The stratum granulosum is a layer of the epidermis where keratinocytes form granules and initiate keratinization. It plays a key role in the skin barrier function.

What is the Stratum granulosum?

The stratum granulosum (Latin for “granular layer”) is one of the five layers of the epidermis (outer skin). It is positioned between the stratum spinosum (spinous layer) below and the stratum lucidum or stratum corneum (horny layer) above. The layer consists of two to five rows of flattened keratinocytes that contain characteristic keratohyalin granules and are actively involved in forming the skin protective barrier.

Structure and Composition

Keratinocytes in the stratum granulosum are more flattened compared to the cells in deeper layers. They contain two key intracellular structures:

  • Keratohyalin granules: These basophilic granules contain profilaggrin, which is later converted into filaggrin. Filaggrin bundles keratin filaments into a dense network, contributing to the structural integrity of the skin.
  • Lamellar bodies (Odland bodies): These organelles secrete lipids (ceramides, cholesterol, fatty acids) into the intercellular space, forming the lipid barrier of the skin.

Functions

The stratum granulosum performs several essential functions:

  • Barrier function: Lipids secreted by lamellar bodies create a water-repellent barrier that minimizes transepidermal water loss (TEWL) and prevents the penetration of harmful substances, microorganisms, and allergens.
  • Initiation of keratinization: In the stratum granulosum, programmed cell death (apoptosis) of keratinocytes begins. Cell nuclei and organelles are broken down, the cells fill with keratin, and they eventually transform into the anucleate corneocytes of the horny layer.
  • Tight junctions: In the upper part of the stratum granulosum, tight junctions regulate the paracellular passage of substances and contribute significantly to barrier function.

Clinical Relevance

Alterations in the stratum granulosum are involved in a variety of skin conditions:

Psoriasis

In psoriasis, the stratum granulosum is often markedly reduced or entirely absent. This leads to disturbed keratinization and the characteristic silvery-white scales on inflamed skin.

Ichthyosis

Various forms of ichthyosis (fish scale disease) involve mutations in genes encoding proteins of the stratum granulosum, such as filaggrin or transglutaminase. These mutations result in severely impaired barrier function and excessive scaling.

Atopic Dermatitis

In atopic dermatitis (eczema), mutations in the filaggrin gene are commonly found. These mutations compromise the integrity of the skin barrier, facilitating the entry of allergens and triggering inflammatory responses.

Contact Dermatitis

A damaged stratum granulosum barrier facilitates the penetration of contact allergens and can contribute to the development of contact dermatitis.

Histological Examination

In histology (microscopic tissue examination), the stratum granulosum is readily identifiable by its characteristic dark keratohyalin granules. It stains darkly with hematoxylin-based methods and is a key feature when evaluating skin biopsies. The absence or thickening of this layer provides the pathologist with important diagnostic clues about underlying skin disorders.

References

  1. Proksch, E., Brandner, J. M., Jensen, J. M.: The skin: an indispensable barrier. In: Experimental Dermatology, 17(12), 2008, pp. 1063–1072.
  2. Elias, P. M.: Stratum corneum defensive functions: an integrated view. In: Journal of Investigative Dermatology, 125(2), 2005, pp. 183–200.
  3. Fleckman, P., Dale, B. A., Holbrook, K. A.: Profilaggrin, a high-molecular-weight precursor of filaggrin in human epidermis and cultured keratinocytes. In: Journal of Investigative Dermatology, 85(6), 1985, pp. 507–512.
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