HAIR SHAFT DISORDERS

FRACTURES:
 TRICHOCLASIS: Green stick fracture of the shaft due to weathering and cosmetic defect.
 TRICHOPTILOSIS: (SPLIT HAIR) : Longitudinal fracture of hair shaft towards the tip. Occurs due to mechanical
and chemical trauma
 TRICHOTHIODYSTROPHY: (LOW CYSTEINE CONTENT IN HAIR--- POOR TENSILE STRENGTH) The hair breaks with
a clean cut (trichoschisis). Polarizing microscope shows alternating dark and bright zones showing a ‘tiger tail
pattern’. Scanning electron microscope reveals severe cuticular defects and secondary cortical degeneration.
The classification of trichothiodystrophy is :
A. Isolated hair defect
B. A+ nail dystrophy
C. B+ mental retardation
D. C+ growth retardation
E. D+ decreased fertility
F. E+ Icthyosis
G. F+ Photosensitivity
H. G+ neutropenia.

NODES:

 TRICHORRHEXIS NODOSA: These appear as minute grey nodes along the shaft where the cuticle is lost and
the frayed cortical fibres project out giving the appearance of two paint brushes thrust into one another. Hair
kink or break at the nodes. Causes are:
A. Acquired---- Mechanical and Chemical trauma(Most common cause). It affects the distal part of
the hair. It affects only the scalp hair.
B. Familial---- It is accompanied by nail and teeth defect. Here the process may involve the
proximal shafts and involve other body hairs other than the scalp hair.
C. In association with Menke’s kinky hair syndrome, Nethertons syndrome and trichothiodystrophy.

 PSUEDOMONELITHRIX: The hair shaft shows irregular flattened and expanded areas that have an indented
appearance. This results from--- TRAUMA OF FORCEPS, COMPRESSION BY OVERLAPPING HAIR.
 TRICHORHHEXIS INVAGINATA: ( bamboo hair) The hair shaft is invaginated into itself resulting in a ball and
socket type of defect. This is due softness in the cortex in the keratogenous zone resulting from incomplete
conversion of sulfhydryl (S-H) to disulfide(S-S) groups. The hairs become dry,brittle and short.
An autosomally recessive trait : NETHERTON’S SYNDROME is C/B :
• Trichorrhexis invaginata
• Atopic dermatitis
• Ichthyosis linearis circumflexa
• Recurrent infections and immunologic defects
• Growth retardation.

 TRICHONODOSIS(knotted hair): In curly hair persons , combing may produce knots in the hair where the shaft
may break.
 INFECTIVE: NITS, TRICHOMYCOSIS AXILLARIS, PIEDRA.
 HAIR CASTS: These probably are the remains of IRS that have failed to disintegrate properly. The appear grey.
They are seen commonly in inflammatory disease of the scalp.

MULTIPLE HAIR:

 PILI BIGEMINI: 2 hair bulbs with saperate shafts emerge from the same follicular opening.
 PILI MULTIGEMINI: 2-8 MATRICES AND PAPILLAE form hair with saperate IRS in the same follicular canal.
Commonest in the jawline.
 TRICHOSTASIS SPINULOSA: It resembles comedones nad present on the nose, forehead, cheeks, upper back,
shoulder and upper arms. On closer inspection the ‘Comedones’ show up as a tuft of tiny hairs projecting
through a keratotic plug. Microscopic examination shows 25-50 telogen vellus hairs embedded within the plug.
NARROWINGS:

 MONELITHRIX: (monile= necklace; thrix= hair)

• autosomal dominant.
• It is due to a mutation in the hair keratin type 1 controlling genes on chromosome 12q--------- defective
cortical keratinization.
• The affected hairs are beaded and brittle. The beaded appearance is due to alternate zones of spindle
like thickening and thinning placed about 1 mm apart. A break occurs commonly at the internodal
junction where the cortex is defective and medulla is absent.
• Hair loss is mild to severe due to hair fragility that results in 1-2cm long broken hair. Some of the
broken hair stubs project from the keratotic follicular papules especially on the occiput and nape of the
neck.
• It may be associated with trichorrhexis nodosa, nail and teeth defects, retarded growth and juvenile
cataracts.
 • Treatment includes: AVOIDANCE OF MECHANICAL AND CHEMICAL TRAUMA+ ORAL ETRITINATE.
 POHL-PINCUS MARK:
• This corresponds to the beau’s lines in case of hair. These are localized areas of shaft thinning
corresponding with area of severe systemic stress.
 TAPERED HAIR: The shaft shows gradual tapering to a point (pencil pointing) due to inhibition of matrix activity
as in anagen effluvium.
 EXCLAMATION MARK HAIR
 HYPOPLASIA

TWISTS AND CURLS:

 PILI TORTI: The shaft is flattened and twisted at angles of about 180 with 4-5 twists at irregular intervals giving
it a spangled appearance in the reflected light. The affected hair is unable to resist stretching forces and
breaks at the twists. The abnormality is most evident over the occipital and temporal regions. The inheritance
is AUTOSOMAL DOMINANT. Starts in childhood and tends to improve after puberty. Associations include-------
KP, Icthyosis, nail dystrophy, widely spaced teeth, enamel hypoplasia, corneal opacities, MR, Hypogonadism
and deafness.
 WOLLY HAIR: These are thightly coiled markedly curly hairs that do not form locks. The hairs are usually short
probably due to shortened growth cycle. Hereditary wooly hair is a autosomal dominant trait that presents at
birth and improves with age(sometimes associated with pili torti, teeth and eye defect, deafness, ichthyosis,
KP ). A localized patch of wooly hair , wooly hair nevus has a linear epidermal nevus associated with it.
 CIRCLE HAIR: A tightly coiled hair shaft gets embedded in the statum corneum. The condition is seen in middle
aged over abdomen and bony prominence.
In KP and SCURVY, the coiled and corkscrew hairs are associated with follicular keratoses.
 CORKSCREW HAIR: The hair are thick and coiled into a double spiral that resembles a corkscrew.

UNRULY HAIR: These are hairs that are difficult to manage by combing. Causes are:
 CONGENITAL: Normal infants, Cornelia de lange syndrome, Down’s syndrome. Mental retardation, wooly hair,
pili torti.
 ACQUIRED: drug induced(etretinate, spironolactone), as a forrunner of androgenetic alopecia.

BANDS:

 PILI ANNULATI: The hairs are fragile and appear banded in reflected light giving a sandy appearance. Scanning
electron microscope reveals air filled spaces in the cortical portion .
 BUBBLE HAIR: This a cosmetic abnormality caused by brief but rapid and focal heating of damp hair by a blow
dryer. The affected hair breaks easily. Light microscope reveals bubbles within the hair shaft. Severe affection
gives a banded appearance.

MENKES KINKY HAIR DISEASE:

 XLR
 Defect in copper metabolism. Copper is required in the formation of both melanin and cystine------- results in
alteration of keratinization and pigmentation of hair.
 The hair is normal at birth but after the shedding of first hair in infancy, the new hair that grow are light
colored, twisted and fragile with a STEEL HAIR APPEARANCE.
 The plasma copper and ceruloplasmin levels are reduced+ hair copper content is reduced.
 Other features:
• mental and physical retardation
• progresive psychomotor retardation and hypotonia from the third month. Convulsions esp. myoclonic
jerks are common.
• Prone to hypothermia and infection
• Aneurysm and hemorrhage in
internal organs Waardenburg syndrome: perceptive deafness+ broad
• Metaphysic of long bones have nasal root+ confluent eyebrows+ lateral displacement of
changes similar to scurvy. medial canthi+ heterochromia irides+ poliosis+
hypopigmented macules.
POLIO
SIS Woolf’s syndrome: white forelock+ piebaldism +
deafness
It refers to circumscribed whitening of
hair affecting a group of neighbouring hair
follicles. Causes are:

GENETIC
Isolated(autosomal dominant)
Peibaldism
Tuberous sclerosis
Waardenburg syndrome
Woolf’s syndrome
AUTOIMMUNE
Vitiligo
Alopecia areata
Vogt- Koyanagi Harada syndrome
INFLAMMATORY
X-rays
Herpes zoster
EXOGENOUS CAUSES
Hydroquinone
Hydrogen peroxide
Monobenzyl ether of hydroquinone.

PREMATURE CANITIS

CAUSES: Autoimmune
GENETIC------- pernicious anemia
Isolated Hypothyroidism
Progeria Hyperthyroidism
Werner’s syndrome infective
Myotonic dystrophy HIV infection
Rothmund Thomson syndrome Drugs
Ataxia telangiectasia Mephenesin,Flurobutyrophenon
Chloroquin
CUTIS VERTICIS GYRATA

It is a term applied to the hypertrophy and parallel or gyrate folds of the skin of the scalp. Biopsy findings
include hypertrophy of the sebaceous glands but no excess collagen. Causes are----------

ISOLATED(AUTOSOMAL DOMINANT)
HEREDITARY
 Pachydermoperiostosis
 Neurofibromatosis
 Tuberous sclerosis
 Darier’s disease
ENDOCRINE

 Acromegaly
 Myxedema
 Cretinism

INFLAMMATORY
 Dissecting cellulites of the scalp
 Chronic folliculitis

TRAUMATIC
 Traction

TUMOROUS
 Congenital melanocytic nevus
 Neurofibroma