Hair Loss (Alopecia) Alopecia. Anatomy and Physiology of Hair. The Active Follicle

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1 Dr. Sahni BS DHMS Hons, PGRT (BOM), FF Hom Deputy Chief Medical Officer (H), ONGC Hospital Panvel , Navi Mumbai, INDIA Hair Loss (Alopecia) Website: Alopecia Alopecia partial or complete loss of hair that results from aging, hormone defects, drug allergy, anticancer treatment, or skin disease. Anatomy and Physiology of Hair Hair grows from follicle, which are stocking like in pushing of the superficial epithelium, each of which encloses at its base, a small stud of dermis known as the dermal papilla. The cylinder of hair may be regarded as a holocrine secretion arising by division of cells surrounding the papilla, in a region known as the bulb. The follicles are slanted in the dermis, and the longer ones extent into the adipose layer. An oblique muscle, the arrector pilli, runs from the point in the mid region in the follicle wall to the dermo epidermal junction. Above the muscle one or more sebaceous glands, and in some regions of the body an aprocrine gland open into the follicle. The Active Follicle The bulk of any hair is formed by a thick cortex made up of elongated keratinized cells cemented together, which in pigmented hairs contains granules of melanin. The cortex is surrounded by a cuticle and may have a continuous or discontinuous core or medulla. Although the cuticle is formed as a single layer, the cells become progressively imbricated as they move peripherally. The outer cells overlap, their free edges directed towards the tip, and they interlock with the cuticle of the surrounding inner root sheath. The inner root sheath consists, in addition to its cuticle of Henle s and Huxley s layers; it is formed in pace with the hair and its keratinized cells are ultimately desquamated. Investing it is the outer root sheath, which is continuous with the superficial epithelial and this is itself enclosed in a non-cellular partition known as the vitreous or glassy membrane. The entire follicle is surrounded by a connective-tissue sheath formed of collagenous fibers, a new elastic fibers and fibroblasts. (See Fig 1 below)

2 Figure 1: The Human hair cycle (a) an active follicle, (b) early catagen, (c) late catagen, showing ascent of the presumptive club, (d) tellogen, (e) early anagem Hormonal Influences It is important to make a clear distinction between the effects of a range of hormones on the follicular cycle, in evolutionary terms related to the adaptive function of moulting, and the particular role of androgens in the induction of sexual and other adult hair which is an adaptation for delaying until puberty the associated socio sexual signals. Most dermatological problems center around androgen dependent hair. Knowledge of other hormonal mechanisms is however relevant not only to understand the control of the moult cycle but also to the problems of human hair loss in thyroid disorder and following pregnancy. Human hair is profoundly affected by thyroid hormones. In a study carried out by Sheffield, 16 out of 150 women who complaint of hair loss were diagnosed as hypothyroid on the basis of serum protein bound iodine level confirmed by radio iodine tracer studies.

3 The phenomena of post partum hair loss also appear to result from a hormonally mediated change in the cycles of scalp follicles. A loss of hairs at about 2 to 3 times the normal rate gives rise to transit alopecia about 4 to 6 months after parturition. Changes with Age At puberty, terminal hair gradually replaces vellus, starting in the pubic regions. In both boys and girls, the first pubic hair is sparse, long, downy, slightly pigmented and almost straight. It later become s darker, coarser, and more curled and extends in area to form an inverse triangle. The boys have the first recognizable pubic hair at an average age of 13.4 years and the full adult female pattern at 14.2 years, about 3 ½ year after the start of development of the genetalia. The corresponding mean ages for girls were considerably earlier, mainly 11.7 years and 13.5 years. In about 80% of men and 10% of women, the pubic hair continues spreading until the mid 20 s or later; there is no absolute distinction between male and female pattern. Axillary hair first appears about 2 years after the start of pubic hair growth. The amount as measured by the fully-grown mass; continuous to increase until late 20 s in males as well as in females, in whom, however it is less at any age. The mean amounts grown per day increase from late puberty until the mid 20 s and thereafter decrease steadily. Facial hair in boys first appear at about the same time as the axillary hair, starting at the corner of the upper lip, and spreading medially to complete the mustache and then the cheeks and beard. Terminal hair development is continued in regular sequence on the legs, thighs, forearms, abdomen, buttocks, back, arms and shoulders. The extent of terminal hair tends to increase throughout the ears of sexual maturity, but most patterns occur over a vide age range. The adult pattern is not achieved until the forth decayed; when the androgen level is already somewhat lower than the early adult life. Moreover, aural hairs do not appear until late middle age. Certain follicles of the scalp may regress with age to produce only fine, short vellus hair. The condition of patterned baldness is inherited and requires male hormone; it is prevented by castration before puberty, though not substantially reversed by castration in maturity.

4 Androgenetic Alopecia (Common Baldness, Male Pattern Alopecia) Hair Patterns: Hamilton produced the first useful grading scale after examining 312 white males and 214 white females aged years (See Figure 2). This classification was modified by Norwood, who added grades III a, III vertex, IV a and V a to the Hamilton scale. Hamilton described the natural progression of the normal pre pubertal scalp pattern (Type I) in both sexes to type II in 96% of men and 79% of women after puberty. He also observed patterns type V to VIII (See Figure 3) in 58% of men aged over 50 years with the extent of baldness tending to increase to the 70. About 25% of women developed type IV scalps by the age of 50, after which there were no further increase in balding. Indeed, after 50, some women who have developed type II at puberty revert to type I. Types V to VIII were not found in any women. Although, as these figure shows, androgenetic alopecia occurs in females with some frequency androgenetic alopecia in women more often assumes a diffused form (See Figure 4 & 5) Fig 2: Hamilton Classification of Androgenetic Alopecia (Type II to IV overlapped) Fig 3: Grade VIII in a normal man. Fig 4: Androgenetic Alopecia Ludvig Grades, most typically seen in women. Fig 5: Ludvig Grade III in a normal postmenopausal woman.

5 Inheritance: The very high frequency of common baldness has complicated the many attempts to establish its mode of inheritance. Moreover, it is by no means clear that common baldness is genetically homogenous and some authorities differentiate between early on set (before the age of 30 in men) and the same pattern 20 years latter. Some think that baldness is determined by a single pair of sex-influenced factors. Both gene frequency studies and families history support this hypothesis. There is no association between baldness and dense hair patterns on the trunk and limbs; nor there is an association between hair loss and increased fertility. Pathology: The earliest histological change is focal perivascular basophilic degeneration in the lower third of the connective tissue sheath of otherwise normal anagen follicles. This is followed by a perifollicular lymphohistiocytic infiltrate at the level of the sebaceous duct. The basophilic sclerotic remains of the connective tissue sheath can be seen in the process as 'streamers'. The destruction of the connective tissue sheath may account for the irreversibility of hair loss. In about a third of biopsies, multinucleate giant cells are seen surrounding fragments of hair. The erector pili muscle decreases in size more slowly than the follicle. In the scalp, which appears totally bald, most of the follicles are short and small, with some quiescent terminal follicles. As the balding scalp loses its protective covering of hair, so solar degenerative changes may be seen. The reduction of blood supply has been confirmed by modern methods, but whether it follows or precedes baldness is unknown. The development of baldness is associated with shortening of the anagen phase of the hair cycle and consequently with an increase in the proportion of telogen hairs, which may be, detected m trichograms of the frontovertical region before baldness is evident. The reduction in the size of the affected follicles, which is the essential histological feature of ordinary baldness necessarily results in a reduction in the diameter of the hairs they, produce. This reduction is said to be greater in women than in men. Clinical Features: The essential clinical feature of androgenetic alopecia in both sexes is the replacement of terminal hairs by progressively finer hairs, which are eventually short and virtually un-pigmented. This process may begin at any age after puberty and may become clinically apparent by the age of 17 in the normal male and by in the endocrinologically normal female. The reduction in the size of the follicles is accompanied by shortening of anagen and by increased shedding of telogen hairs. Males: The replacement of terminal by smaller hairs occurs characteristically in a distinctive pattern, which spares the posterior and lateral scalp margins, even in the most advanced cases, and even in old age.

6 The sequence of patterns in the male has been described by Hamilton (Figures 2 & 3). Bitemporal recession is followed by balding of the vertex. Variations in the pattern are governed at least in part by genetic factors. The rate of progression is probably determined by heredity. Females: The use of the term 'male pattern alopecia' must be held partly responsible for the frequent failure to appreciate that in its earlier stages androgenetic alopecia in women need not conform to the 'male pattern' (See Figures 4 & 5 above). As in the male, increased shedding of telogen hairs accompanies the reduction of shaft diameter, but the follicles first affected are more widely distributed over the frontovertical region. As a result, many secondary vellus hairs are interspersed with hairs, which are still normal, and others only slightly reduced in diameter. Partial baldness is sometimes first apparent on the vertex, but the most frequent presentation of androgenetic alopecia in women is as a diffuse alopecia. Ludwig has classified the succession of patterns, which occur in women to produce the distinctive clinical features of 'female pattern alopecia'. However, Venning and Dawber have shown that all women display a change of scalp hair pattern after puberty. The rate of change of patterning is very slow but accelerates during and after the menopause. These workers also showed that hair patterns of the classical 'male type' shown by Hamilton (See Figures 2 & 3) occur with increasing frequency after the menopause. The occurrence of Ludwig pattern III or Hamilton pattern V or greater in a pre-menopausal woman is unlikely. Androgens also stimulate sebaceous gland activity. A full medical history and examination are essential, and in many cases endocrinological investigation is desirable in all women with androgenetic alopecia of rapid onset, even if it be an isolated abnormality, and in women with baldness of gradual onset but accompanied by menstrual disturbance, hirsutism or recrudescence of acne. Hair loss of Hamilton type IV may occur in women without hirsutism but extensive baldness (types VI-VII) is always accompanied by hirsutism. Homoeopathic Repertory: Hair Falling In Handfuls: Phosphorous From forehead: Heper Sulph, Merc Sol, Nat Mur, Phos From Sides: Graphites From Occipit: Carbo Veg., Chellidonium, Petroleum From Temples: Kali Carb, Nat Mur From Vertex: Lycopodium, Bryta Carb, Sulphur, Zinc Met From Grief: Ignatia, Staphisgaria, Acid Phos From Shock: Ignatia, Rescue Remedy (Bach Flower Remedy) During Pregnancy: Lachesis After Delivery: Cal Carb, Carbo Veg, Cantharis, Lycopodium, Nat Mur, Nitric Acid, Sepia, Sulphur Young Age: Acid Phos, Phosphorous, Kali Phos, Bryta Carb, Silicea

7 Old Age Male: Lycopodium, Selenium Old Age Female: Sepia, Sulphur Thyroid Disorders: Thyrodinum, Thallium,Jaborandi, Sepia, Silicea, Sulphur Due to Anemia: Ferrum Phos, Cal Phos, Nat Mur Tension: Kali Phos, Calming*, Tension* * Vibronic Remedies References Text Book of Dermatology Vol. 4 Fifth Edt. By R H Champion, J.L Burton & F.J.G Ebling Materia Medica, Murphy Materia Medica, Kent

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