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Structure and Function of The Skin

»	Name the three layers of the skin. What composes them?
»	How many layers are there in the epidermis? How are they organized?
»	Do other types of cells normally occur in the epidermis?
»	What is apocopation?
»	Describe the structure of the basement membrane zone (BMZ).
»	How is the structure of the epidermis related to its functions?
»	What structural components of the epidermis are involved in blistering diseases?
»	Are there hereditary diseases of the BMZ and dermis that cause blistering and damage to the skin?
»	Are there acquired blistering diseases of the BMZ and dermis?
»	What abnormalities in structural components of the basement membrane are involved in bullous skin diseases?
»	What is the function of the sebaceous gland?
»	How do the eccrine sweat glands and apocrine sweat glands differ?
»	How is the dermis organized?
»	What are the components of the dermis?
»	What are the functions of the dermis?
»	Which structural component of the dermis is involved in congenital and autoimmune skin diseases?
»	How does the vasculature of the dermis function in temperature control?
»	How is the skin innervated?
»	Name the two main corpuscular (encapsulated) nerve receptors found in the skin.
»	Is loss of cutaneous sensation very serious?
»	How is the subcutis organized?

Are there hereditary diseases of the BMZ and dermis that cause blistering and damage to the skin?

Yes. There is a complex group of inherited diseases in which the skin is friable and bullous lesions occur, often with subsequent scarring. The two subgroups within this group are junctional epidermolysis bullosas (JEBs) and dystrophic epidermolysis bullosas (DEBs). Like the EBS diseases, which affect the epidermal layers, these diseases occur because the vital structural elements of the BMZ and dermis are missing, causing the skin to separate easily and blister.

In JEBs, the separation occurs within the lamina lucida (LL) of the BMZ. Decreased amounts or abnormalities in the LL components, such as laminins I and V, 19-DEJ-1 protein, XII collagen, plectin, XVII collagen (bullous pemphigoid antigen) and alpha 4 beta 6 integrin have been identified in this group.

Fig. 1.4 This diagram of the dermal epidermal junction illustrates the affected levels in the various types of epidermolysis bullosa (EB).

In the DEB group, separation occurs below the BMZ in the dermal layer, and a decreased amount or absence of type VII collagen has been noted. As a rule, the deeper in the skin the separation occurs, the more severe the clinical picture with increased scarring and loss of function. DEB patients typically have severe deforming scars and decreased life span (see Fig. 1-4).