INFUNDIBULUM Extends from Skin surface (Ostium) above to the entry of Sebaceous duct below. Lining is similar to the surface epidermis.
ISTHMUS Extends from entry of Sebaceous duct above to attachment of Arrector muscle below. Narrow part of the hair follicle. Hair shaft is fully keratinized. Inner root sheath begins to disintegrate.
STEM Longest part of hair follicle. Extends from insertion of Arrector pili muscle above upto the keratogenous zone. Consists of 3 layers : Outer root sheath Inner root sheath Hair shaft
BULB Lower most part of hair follicle. Follicular papilla lies in the center of the follicular bulb. The bulk of the follicular bulb is formed of Epithelial matrix ( matrical cells ). Few melanocytes are interspersed.
ADAMSON’S FRINGE Upper part of the bulb. Keratogenous zone. Divided into 6 layers: Medulla Cortex Hair cuticle Cuticle of inner sheath Huxley’s layer Henle’s layer
FOLLICULAR PAPILLA Varies according to the phase of hair cycle. Composed of specialized fibroblast like cells embedded in extracellular matrix. Often contains a loop of capillary blood vessels. Volume of dermal papilla maybe responsible for controlling size of hair follicle.
HAIR SHAFT 3 layers : MEDULLA CORTEX HAIR CUTICLE Medulla is a variable structure. Maybe continuous, interrupted or absent. Contains few layers of rounded cells containing glycogen.
Cortex forms bulk of the hair shaft. Consists of numerous layers of flattened elongated cells packed together. Cell organelles and nuclei disappear as the cells keratinize.
Hair cuticle consists of 5 – 10 layers of flattened cells arranged in overlapping “roof – tile” pattern. The upwards pointing edges of the hair cuticle interlock with the downwards pointing edges of cuticle of inner sheath.
INNER ROOT SHEATH 3 layers : Cuticle Huxley’s layer Henle’s layer Henle’ s layer – 2 cells thick, keratinizes first Huxley’s layer – 4-6 cells thick At the Isthmus the IRS disintegrates .
OUTER ROOT SHEATH Most peripheral part of hair follicle. Single layered at lower tip of hair bulb and 4-6 layered at the isthmus. Keratinize at the level of Isthmus. Trichilemmal keratinization. Occasionally “companion layer” maybe seen in between IRS and ORS.
PERIFOLLICULAR FIBROUS SHEATH Thin layer of connective tissue which envelopes the hair follicle througout its length. PFS is variable: Early Anagen : Thin, containing collagen and fibroblasts Anagen : Thickened and trilayered Catagen : Hyalinization of PFS Telogen : Thinning of PFS
ULTRASTRUCTURE Hair is formed of hard keratin with high sulfur content. High sulfur content responsible for its extraordinary tensile strength. Fibrillar component consists of macrofibrils, 7 nm thick arranged in longitudinal lamellated form. S-H linkages of cysteine at the bulb are converted to S-S linkages of cysteine higher up.
HAIR FOLLICLE INNERVATION A plexus of longitudinally arranged sensory nerve fibres surrounds the isthmus region. Other nerve endings found are : Free nerve endings Pilo – Ruffini nerve endings Merkel nerve endings
HAIR CYCLE Hair follicles undergo a repetitive sequence of growth and rest known as hair cycle. Hair cycle varies between follicles in different regions of the skin in the same species . Hair growth occurs in 3 stages : Anagen Catagen Telogen
ANAGEN Period of active hair growth. Duration of this phase responible for final length of the hair. Usually lasts for 2 – 3 years. Duration of Anagen genetically determined. About 85% of all hairs are in this phase at any time.
Onset of mitotic activity in epithelial cells of Dermal papilla. Lower part of follicle elongates downwards along a preformed dermal tract ( stele ). Dermal papilla expands from a tightly packed ball of cells into a flask shaped structure. A network of capillary blood vessels develop around the lengthening follicle.
Epithelial cells in the hair bulb undergo vigorous proliferative activity. The melanocytes become active adding colour to this newly forming hair. Anagen consists of 6 substages. Differences in the length of hair is due to variable duration of the last stage ( VI ).
CATAGEN Short transition stage that occurs at the end of the anagen phase. Signals the end of active growth of hair. Usually lasts about 2 – 3 weeks.
At the end of Anagen, epithelial division declines and ceases. Proximal end of the hair shaft keratinizes to form a club shaped structure. Lower part of the follicle involutes by apoptosis. Basement membrane surrounding the follicle becomes thickened to form “glassy membrane”. Base of the follicle along with dermal papilla moves upwards to lie below the level of Arrector muscle attachment.
TELOGEN Resting phase of the hair follicle. Usually lasts for about 3 months. About 10 – 15% of all hairs are in this phase at any time.
Quiscient period between completion of follicular regression and onset of next anagen phase. Resting club hair lies within an epithelial sac. Streak of fibrous tissue extends from base of follicle to quiscient papilla beneath – fibrous tract
EXOGEN / TELOPTOSIS Active process of shedding of club hair. Defective Exogen gives rise to Trichostasis spinulosa.
KENOGEN / LAG PHASE Latent phase in the hair cycle where hair follicle is empty after hair shedding and persists in this stage for a variable duration. Seen in patients with AGA and prepubertal children.
Approx. 100000 follicles are present on the average scalp. About 70 – 100 hairs in telogen are shed daily. Hair on the scalp grows at an average rate of 0.45 mm daily. It grows faster on the crown > vertex > temple.
FUNCTIONS OF HAIR Tactile perception Protection of scalp from sunlight and trauma. Protection of eyes from foreign bodies. Screening nasal passages. Reduce friction in intertriginous areas.
ANDROGENS Follicles that respond to androgen are grouped as androgen dependent hair. Converts axillary and pubic follicles into terminal follicles. Similar course in beard, moustache, abdomen, chest area in men. Increases the duration of anagen hence thickness of hair shaft. Increases size of hair follicle.
However, Scalp hair respond in a regressive manner to androgens. Pubertal recession of frontal hair in boys and are resposible for AGA. Enzyme 5α reductase is responsible for conversion of weaker androgens into more potent form. Finasteride inhibits 5α reductase type 2 and prevents AGA.
Growth Hormone - synergistic effect on androgen dependent hair. Estrogen - retains club hair in follicle. Prolactin - androgen like effect. Throid hormone - Both hypo and hypersecretion can cause alopecia. Retards the rate of hair growth. Retains club hair in the follicle.
IGF – I : promotes hair growth and proliferation. Insulin - acts through IGF – I and promotes hair growth. Cortisol - enhances proliferative actions of IGF – I Shaving has no effect on the rate of hair growth.
DURING PREGNANCY Increase in proportion of follicles in anagen. Reduction in hair density. Post partum - large number of follicles enter into telogen, leading to increased shedding - Postpartum telogen effluvium
MOLECULAR CONTROL OF HAIRCYCLING ANAGEN Activation of various mediators - IGF – 1, HGF, SHH, Whn, beta catenin IGF – 1 plays an important role. It promotes hair growth and proliferation. IGF – 1 receptors are located in dermal papilla and ORS. Insulin acts through IGF – 1 and promote hair growth.
CATAGEN It is marked by down regulation of IGF – 1 receptors and HGF expression in hair bulb. TGF – β, IL – α1, TNF – α are the mediators of catagen activation. Stress, trauma, dexamethasone, ACTH, es tradiol also initiate catagen phase.
TELOGEN Bone morphogenetic protein – 4 plays an important role in suppressing follicular growth and differentiation. BMP – 4 acts on BMPR – IA expressed by keratinocytes. BMP – 4 antagonist Noggin accelerates the onset of anagen.
COMMON CAUSES OF HAIRFALL Androgenetic Alopecia Alopecia areata Infection Postpartum Hypothyroidism Hyperthyroidism Stress
Inadequate diet Low serum iron Major surgery / chronic illness Fungal infection of scalp Trichotillomania Oral contraceptives Chemotherapy Other drugs – Vit. A, β blockers, Antidepressants, Anticoagulants, etc.