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Alopecia and appendages final
Diseases of cutaneous appendages Nathan C. Walk, M.D. Overview – FOCUS on the hair follicle Scalp biopsy Hair anatomy Hair cycle…anagen, y g , catagen, g , telogen g Alopecias – Provide a basic algorithm Handout d hits hi highlights hi hli h Slide Unknowns – Rapid fire Why is examination of hair so tough?.... h? Equation with many variables…. variables A+B+C=X Epidermal appendages Pilosebaceous unit – Hair follicle – Sebaceous gland g – +/+/- Apocrine gland Eccrine sweat gland Hair follicle Scalp biopsy Valuable tool in the diagnosis of hair loss Id ll 2 deep Ideally, d 4 mm punch h biopsy bi should h ld be b obtained bt i d from f different diff t sites it – Healthy skin – Established lesion WITH inflammation 4 4mm punch h = 12.6 12 6 mm2 3mm punch = 7.07 mm2 Using 4mm punch, averages – – – – T:V Caucasians African Americans Korean – Telogen+Catagen 7:1, with 12 follicular units 35/5 (T:V) 20/3 (T:V) 15/2 Normal 00-15%, >20% definitely abnormal Hair anatomy Hair a follicles o c es – Found everywhere on the body, except palms and soles – Formation Intimate association between epithelial buds and mesenchymal elements Hair follicles in scalp – Grouped into follicular units 2-6 Terminal hairs + vellus hairs Sebaceous glands Arrector pili Hair anatomy Terminal hairs – – – – Larger than vellus hairs Descend to fat Pigmented Hair shaft diameter is > thickness of IRS Vellus hairs – Thin, short, nonnon-pigmented – Hair shaft diameter is <= thickness of IRS Indeterminate hairs – Intermediate in size Hair anatomy The hair follicle can be anatomically and functionally divided into 2 distinct segments – Upper portion Stable, not affected by maturation/shedding – Ostium u d bu u – Infundibulum – Isthmus – Lower portion Actively A ti l involved i l d in i hair h i growth th – Stem/suprabulbar region – Bulb Hair anatomy Transverse sectioning g allows all layers y of the anagen g follicle to be easily identified (@ suprabulbar zone) – Starting from center Æ out 1. Hair shaft – Medulla (not consistently present in humans) – Cortex – Cuticle 2 Internal root sheath 2. – Cuticle – Huxley’s layer – Henle’s layer 3. External root sheath 4. Vitreous layer 5. Fibrous root sheath Hair anatomy Changes C a ges as we e asce ascend d – Adamson’s fringe Nuclei dropout in IRS and hair shaft – [IRS shows tricholemmal keratinization] – At (about mid) Isthmus IRS abruptly desquamates Æ results in separation between hair shaft and follicular wall ERS begins to cornify without formation of a granular cell layer (tricholemmal keratinization) – Infundibulum (bounded inferiorly by sebaceous gland) ERS switches to epidermal type keratinization, WITH a granular layer Hair cycle Hair growth cycle cycle, whether terminal or vellus, is divided into three stages – Active growth = anagen 2-7 years – Involution = catagen 2-3 weeks – Rest = telogen 100 days Catagen hair anatomy At the end of anagen, g , catagen g begins… g – Hair matrix disappears, replaced by thin rim of epithelial cells surrounding the hair papilla – Epithelium of lower follicle undergoes disintegration by apoptosis – Vitreous layer markedly thickens – Fibrous root sheath thickens – As catagen progresses over 22-3 weeks, the hair papilla follows disintegrating epithelial column upwards into the dermis – Papilla eventually comes to rest just below bulge – As epithelial column moves upward, a collapsed fibrous root sheath is left behind – stela or streamer – Club hair begins to form Telogen At the end of catagen and the beginning of telogen, the hair papilla is a condensed ball of spindlespindle-shaped cells within a scanty stroma – Above papilla lies the secondary hair germ Epithelium has “asterisk– “asterisk–like” appearance on cross section – Below papilla lies the stela (collapsed fibrous root sheath) Above secondary hair germ, club hair is forming – Progressive cornification over 3 month period, after which the hair is shed At end of telogen, shortly before or after club hair is shed, stem cells of the follicular bulge are activated and form a population of rapidly idl proliferating lif i epithelium i h li – These cells descend into the vacant and collapsed fibrous root sheath – Thus begins formation of a new anagen hair! Alopecias Classification [Difficult – Great degree of overlap – Some variants are initially non non--scarring, but may become scarring with time] – Scarring S i Lymphocytic – Central centrifugal scarring alopecia – Lichen planopilaris – Lupus erythematosus Neutrophilic – Acne keloidalis – Dissecting cellulitis – NonNon-scarring Androgenic g alopecia p Alopecia areata Trichotillomania/Traction alopecia Tellogen effluvium Scalp biopsy in alopecia Evaluation 1 1. 2. 3. 4. 5. 6. ?4mm Evenly spaced follicles? Are most units 22-6 follicles w/ LARGE > small >85% telogen Do any follicles show distorted features Inflammation? 7. 8. Fibrosis? Total number of 1. At what level? 1. 2. 3. Follicular structures Terminal hairs Vellus hairs Using 4mm punch, averages – – – T:V Caucasians African Americans 7:1, 7:1 with 12 follicular units 33/5 (T:V) 21/3 (T:V) – Tellogen+Catagen Normal 00-15%, >20% definitely abnormal Androgenic alopecia Variation in follicle size – “miniaturization” – i.e. increased number vellus hairs Normal # follicles at top (decreased deep) Increased number of telogen/catagen hairs NO inflammation Telogen effluvium INCREASED terminal telogen and catagen hairs Normal # follicles at top (d (decreased d deep) d ) Normal Terminal:vellus Streamers Alopecia areata Peribulbar mononuclear inflammation INCREASED miniaturized h i hairs INCREASED telogen/catagen hairs Normal # follicles early, decreased late Trichotillomania INCREASED telogen/catagen Pigmented casts Traumatized hair follicles – Bizarre morphology Normal # follicles (may be decreased late) Scarring alopecias – Scarring g Lymphocytic – Central centrifugal scarring alopecia – Lichen planopilaris – Lupus erythematosus Neutrophilic – Acne keloidalis – Dissecting cellulitis – NonNon-scarring Androgenic alopecia Alopecia areata Trichotillomania/Traction alopecia Telogen g effluvium Pathophysiology of scarring alopecias obviously varies…. – Inflammation in upper ½ of hair follicle is CRUCIAL to the development of permanent damage da age Stem cells located at bulge Remember in alopecia areata, although there IS intense inflammation around the hair bulb…. – This leads to involution of follicle but not its permanent loss…until veryy late… Neutrophilic scarring alopecias – Acne keloidalis nuchae – Dissecting cellulitis Scarring alopecias – Scarring Lymphocytic – Central centrifugal scarring alopecia Follicular degeneration syndrome Pseudopelade (not Brocq’s) Folliculitis decalvans Tufted folliculitis – Lichen planopilaris – Lupus erythematosus Scarring alopecias Central centrifugal scarring alopecia – – – – F lli l d Follicular degeneration ti syndrome d Pseudopelade (not Brocq’s) Folliculitis decalvans Tufted folliculitis “CCSA” groups several variants of inflammatory, scarring alopecia. – Difference between these variants may be due to racial differences or variability in immune responses. responses Have in common: – – – – Chronic and progressive, with eventual burn out. Centered on crown, vertex Progress symmetrically Show clinical and histologic evidence of inflammation in active peripheral zone Scarring – Lymphocytic Central centrifugal scarring alopecia – Lymphocytic infiltrate – infundibulum/isthmus + NO basal vacuolar change g – Eccentric epithelial atrophy + Onion skin fibrosis – Premature desquamation of IRS Lichen planopilaris – Lymphocytic infiltrate – infundibulum/isthmus + basal vacuolar change – Colloid bodies + Some interface changes away from follicles – Onion skin fibrosis Lupus erythematosus – INTERFACE dermatitis – lots away from follicles + basal vacuolar change – S+D perivascular lymphocytic infiltrate – Interstitial mucin CCSA versus LPP CCSA Lichen p planopilaris p – Lymphs IN epidermis, follicular epithelium – Asymmetry of follicles – < 16 follicles – > 16 follicles CCSA – Note a few lymphs in follicular epithelium. – Medicine is a continuum…. continuum LPP Case 98 HSV folliculitis Case 99 A Case 99 B Fungal folliculitis Dermatophytes – Endothrix Invasion of hair shaft – Ectothrix Confined to surface of hair shaft – 3 major genera Epidermophyton Microsporum Trichophyton p y Case 100 Pitysporum folliculitis Case 101 Hidradenitis suppurativa Follicular occlusion triad 1. Hidradenitis suppurativa 2 Dissecting cellulitis of the scalp 2. 3. Acne conglobata Deep scarring folliculitides Presumed common pathogenesis of pore occlusion followed by bacterial infection Draining sinuses Case 102 A & B Trichotillomania Case 103 Rosacea Case 104 Folliculitis keloidalis nuchae Aka Acne keloidalis nuchae D Deep scarring i foliculitides f li litid 1. Folliculitis keloidalis nuchae – Folliculitis w/ rupture, liberation of hair shafts into dermis… – More severe scarring than #2 2. Folliculitis decalvans Case 105 Demodex Folliculitis Case 106 A & B Lichen planopilaris Case 107 Central centrifugal scarring alopecia Case 108 Alopecia areata Selected pictures for this lecture taken from: – Leonard C. C Sperling An Atlas of Hair Pathology with Clinical Correlations – Phillip McKee, McKee et al Pathology of the Skin
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