When only a portion of the lesion can be removed due to its size or location, the biopsy should sample tissue from the thickest area of the lesion, as SCCs are most likely to be detected in that area. If a shave biopsy is performed, it should extend through to the level of the dermis in order to provide sufficient tissue for diagnosis; ideally, it would extend to the mid-reticular dermis. Punch biopsy usually extends to the subcutaneous fat when the entire length of the punch blade is utilized. Histopathology
On histologic examination, actinic keratoses usually show a collection of atypical keratinocytes with hyperpigmented or pleomorphic nuclei, extending to the basal layer of the epidermis. A "flag sign" is often described, referring to alternating areas of orthokeratosis and parakeratosis. Epidermal thickening and surrounding areas of sun-damaged skin are often seen. The normal ordered maturation of the keratinocytes is disordered to varying degrees: there may be widening of the intracellular spaces, cytologic atypia such as abnormally large nuclei, and a mild chronic inflammatory infiltrate.Specific findings depend on the clinical variant and particular lesion characteristics. The seven major histopathologic variants are all characterized by atypical keratinocytic proliferation beginning in the basal layer and confined to the epidermis; they include:
Hypertrophic: Notable for marked hyperkeratosis, often with evident parakeratosis. Keratinocytes in the stratum malphigii may show a loss of polarity, pleomorphism, and anaplasia. Some irregular downward proliferation into the uppermost dermis may be observed, but does not represent frank invasion.
Telogen effluvium is a scalp disorder characterized by the thinning or shedding of hair resulting from the early entry of hair in the telogen phase (the resting phase of the hair follicle). It is in this phase that telogen hairs begin to shed at an increased rate, where normally the approximate rate of hair loss (having no effect on ones appearance) is 125 hairs per day.There are 5 potential alterations in the hair cycle that could lead to this shedding: immediate anagen release, delayed anagen release, short anagen syndrome, immediate telogen release, and delayed telogen release. Immediate anagen release occurs when follicles leave anagen and are stimulated to enter telogen prematurely. The effects become visible 2–3 months later with increased telogen effluvium. Delayed anagen release, most commonly associated with pregnancy, involves the prolongation of anagen under the effect of pregnancy hormones, resulting in delayed but synchronous and heavy postpartum hair shedding. Short anagen syndrome is characterized by an idiopathic and persistent telogen hair shedding, as well as the inability to grow hair long. This is a result of the shortening of the duration of anagen, meaning a greater number of telogen hairs at any given time, and is responsible for the majority of chronic TE cases. Immediate telogen release generally occurs with drug-induced shortening of telogen leading to the premature reentrance of follicles to anagen, which causes a massive release of club (telogen) hairs. Drugs such as minoxidil can precipitate immediate telogen release.