Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
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Alopecia (hair loss) is one of the categories of hair abnormalities. Rather than count the hairs in a biopsy, we pathologists must presume that there is clinical alopecia when we get a scalp biopsy to categorize the alopecia. Though aware of it, our pathology group has never really used (as of 2011) the technique of sectioning the punch biopsies en face to the epidermis, continuing the classical stepcuts along the length of 3-4mm punch biopsies. If any hairs are grossly visible, it can be an advantage to orient the core and agar pre-embed so that one has a chance at getting hairs to show as full-length on a slide. A decent layman-like overview is HERE and good questions for patient at Wrong Diagnosis website.

Normally, about 90% of scalp hair follicles are in the growing anagen (long follicle with vascular root) phase, and about 10% to 15% are in the resting catagen (long follicle with withering vascular root) and telogen (short follicle with defunct vascular root) phases.

Classification:
Non-scarring alopecias:
  • alopecia areata (AA): common autoimmune process; [clinical patches of alopecia] (inflammatory...tending to orient at hair bulb).
  • dermatophyte (tinea capitis) alopecia: patchy hair loss.
  • androgenetic alopecia (AGA): common; [diffuse male pattern alopecia in males or females] (non-inflammatory). Increased proportion of hairs atrophy (miniaturized anagen follicles) and express/manifest toward morphology of short vellus-like (infant) hairs. On biopsy, hair follicles short & more superficial in dermis than normal.
  • traction alopecia: common; [trichotillomania; hair abuse; hot comb alopecia: clinical patches to almost diffuse] (non-inflammatory...maybe the slightest follicular scarring; might see bent hair structures/follicles &/or streaks of follicular tract pigment in longitudinal histology).
  • telogen effluvium: common (reflects stress or shock to your system = surgery, giving birth, some medications, crash diets, severe stress, thyroid problems...these can push hair into its resting, or telogen, state); there are both (1) classical acute TE (ATE) & (2) chronic TE (CTE2) cases. Idiopathic ATE appears to have no inciting event. Postpartum ATE is an entity. The big DDX with CTE is vs. AGA. CTE is diffuse generalized thinning of abrupt onset but remains cyclically or steadily chronic because of recurring "triggers" delaying/preventing recovery.
    • nutritional deficit or excess: reduced anagen component by prematurely entering a resting, telogen phase. Sort of a CTE. Nutritional deficits usually include protein lack but may be due to lack of iron (iron deficiency). In the USA, this cause tends to show up in those struggling hard to lose weight. May be due to toxic, excessive vitamin A (check your A intake from all vitamin suppliments, hair loss prevention suppliments, and diet [is it heavy on raw vegetables?]. Blood tests for iron and thyroid are readily available (maybe even without a doctors order). Treatment is to correct any vitamin A problem and/or be moderate, calm, and lon-term (moderation) in weight-control efforts.
    • hormonal deprivation or changes: May be due to stopping and starting or changing and re-changing birth control pills. May be due to thyroid hormone deficiency.
    • stress alopecia: stress causes growing anagen hairs to convert prematurely into resting telogen hairs, which means that more than the normal number of hairs are in the telogen phase and ready to shed & easily combed out. Akin to idiopathic acute telogen effluvium (ATE) when happens once and CTE when a series of major stresses come in a series over a number of years. This might affect "high-strung" individuals more than "laid back" individuals. In the USA between 2008-2012, a time of major job loss and home foreclosure...events in a prolonged series, I wonder if dermatologists saw more ATE & CTE than usual.
    • RULE OF THUMB: when the dermatologist examines you and thinks you likely have a form of TE and did not uncover too much dieting zeal or excess vitamin A, they might (1) check iron & thyroid status, (2) ask you to analyze your dietary suppliments carefully, (3) have some sort of stress analysis done. If iron and thyroid status is normal and no vitamin A problem, then the cause is likely "between the ears" (stress)6. It may take some short term counseling and/or anti-stress medication to break the pattern of serial stress triggers.
    • COMPLEX causes: it is not too uncommon for a patient to get wrapped up in a combination series of the above in which the various individual causes come in and come in again, off and on, to result in an ongoing series of "triggers" that feed on themselves in a continuing, chronic state whose cycle has to be broken.
  • toxic alopecia: (non-inflammatory); affects the anagen phase & due to chemo and some other toxins & even vitamin A overdose (see above, telogen effulvium causes). Follicular production of the anagen stage hair shaft peters out within the follicle & hair "breaks" loose...shedding as if broken hairs.
  • alopecia neoplastica: patchy loss...metastatic (lobular breast cancer) carcinoma causing an AA-like alopecia.
  • seborrheic dermatitis: (inflammatory); usually scaley & obvious as to cause, clinically; wouldn't expect a biopsy of this.

Scarring (cicatricial) alopecias1:

  • folliculitis decalvans: also known as alopecia folliculitis or acne decalvans, is an inflammatory reaction in hair follicles on the scalp that causes hair loss by micro-abscessing the air structure out. Akin to groin & axillary hidradenitis suppurativa. It leads to scarring and permanent hair loss. Maybe akin are "acne keloidalis" and "dissecting cellulitis of the scalp".
  • tinea capitis: ring worm dermatophytic kerions (crusts of broken fungus, hairs, & ooze) can heal and leave alopecia patches due to follicular scarring.
  • lichen planopilaris (LPP):  (usually inflammatory [interface lichenoid]...superficially folliculocentric). [S-05-9178?].Clinical correlation1: various patterns of hair loss are seen, but most commonly there are scattered foci of partial hair loss. Perifollicular erythema and scaling are common to all cases. Lichen planus lesions elsewhere on the body support the diagnosis of LPP on the scalp. "Frontal fibrosing alopecia" appears to be just one of several clinical patterns of hair loss that can be seen in lichen planopilaris. However, lesions of lichen planus are not usually found in these patients, and the lichenoid inflammation does not affect the interfollicular epidermis.
  • chronic cutaneous lupus (CCLE): [clinical patches of alopecia] (usually inflammatory...folliculitis/perifolliculitis, vacuolar basal epidermal change with underlying melanophages, thickened basement membranes).
  • central, centrifugal scarring or cicatricial alopecia (CCSA or CCCA):clinically is an adult, most often a black woman, with a progressive, permanent loss of scalp hair starting on the central crown or vertex.... synonyms = FDS, folliculitis decalvans, tufted folliculitis, pseudopelade, hot comb alopecia.
  • Brocq's alopecia (pseudopelade of Brocq): end stage scarring alopecia from many starting-point etiologies...too far gone (too close to end stage) for good clues as to etiology but maybe not so far as " burnt out scarring alopecia " (decreased total number of hairs, especially terminal hairs; loss of the sebaceous glands; residual, naked hair shafts surrounded by mild, granulomatous inflammation; follicular stelae without overlying follicles; and cylindrical columns of connective tissue at the sites of former follicles).
  • keratosis follicularis spinulosa decalvans:

References:

  1. Len Sperling's web notes PDF on working classification from the NAHRS workshop (2001).
  2. Publication on-line about histologic DDX chronic telogen effluvium vs. androgenetic alopecia.
  3. PhD imunodermatologist, Kevin ?'s Keratin.com website...huge amount of detail.
  4. American Hair Loss Council (AHLC).
  5. The International Society of Hair Restoration Surgery (ISHRS).
  6. various colleagues.

(posted 26 May 2005; latest addition 9 February 2012)
 
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