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Trichorrhexis
nodosa
One of the most common hair shaft defects a dermatologist encounters
is trichorrhexis nodosa (also called trichonodosis). Trichorrhexis
nodosa is a focal defect in the hair fiber. When observed under
the microscope most of a hair shaft looks entirely normal. However,
in isolated spots along the length of a fiber swelling and/or fraying
can be seen. These focal defects develop where there is an absence
of cuticle.
The cuticle encases the hair cortex in a strong almost impenetrable
layer. It provides physical support and helps protect the cortex
of a hair shaft from environmental factors such as ultra violet
light, chemicals such as detergents and physical action such as
hair brushing. If the cuticle is absent then the cortex underneath
is directly exposed. The cortex is less resistant to the physical
and chemical factors in the environment compared to the cuticle.
Where the cortex is exposed its integrity is broken down. The chemical
bonds that maintain the hair structure can break down and the hair
becomes more flexible and weaker. The hair may split and fray into
minute strands at the point of cuticle break down. This focal disruption
of the hair fiber is a prime area for hair shaft breakage. As we
comb, brush, and generally manipulate our hair, these defective
nodes in the hair fiber may break.
Causes of trichorrhexis nodosa can be congenital or acquired.
Some people have naturally weak hair where the cuticle is not properly
produced. This influence is often hereditary and runs in families.
Congenital trichorrhexis nodosa is very rare and it often first
develops at a very young age. Abnormal production of hair fiber
that is irregular and brittle can occur in metabolic disorders such
as those that involve abnormal urea synthesis, abnormal copper or
zinc metabolism, or defective cysteine or sulfur incorporation into
hair fiber (trichothiodystrophy).
Trichorrhexis nodosa is more likely to be acquired through excessive
manipulation of hair. Too much brushing, hairstyles that put constant
stress on the hair, excessive washing, dying, and perming may disrupt
the cuticle in focal areas along a hair shaft. Trichorrhexis nodosa
is seen in people who repeatedly use hot combs or permanent waves
to style their hair. Once the cuticle is removed then the hair cortex
swiftly breaks down.
Trichorrhexis nodosa develops in association with a range of other
hair diseases. Any hair condition that weakens the hair shaft and/or
results in abnormal cuticle formation can result in Trichorrhexis
nodosa like hair breakage. Hair loss through breakage can be seen
in conditions such as alopecia areata as a secondary phenomenon.
Treatment depends on the considered cause of the focal defects.
If the hair production is believed to be abnormal then treatment
will focus on the hair follicle and improving the strength of hair
fiber. Where the defect is the result of excessive grooming the
obvious action is to reduce the amount of hair manipulation. People
are encouraged to stop using brushes, avoid hair styling that involves
chemicals and use only very mild shampoos. Once the integrity of
the hair fiber is broken down there is little that can be done to
repair it. Often the only answer is to choose a short hair style
and cut off the defective hair. It may take some time for hair to
recover from trichorrhexis nodosa. New, healthy hair has to grow
to replace the defective fibers. It may take several months or even
years before scalp hair completely recovers.
Trichorrhexis
nodosa references
- Lurie R,
Hodak E, Ginzburg A, David M. Trichorrhexis nodosa: a manifestation
of hypothyroidism. Cutis. 1996 May;57(5):358-9.
- Laude TA.
Approach to dermatologic disorders in black children. Semin Dermatol.
1995 Mar;14(1):15-20.
- Bhutto
AM, Taira K, Nagamine Y, Maruno M, Takamiyagi A, Nonaka S. A case
of trichorrhexis nodosa developed in winter. J Dermatol. 1995
Feb;22(2):107-10.
- Smith RA,
Ross JS, Bunker CB. Localized trichorrhexis nodosa. Clin Exp Dermatol.
1994 Sep;19(5):441-2.
- Slonim
AE, Sadick N, Pugliese M, Meyers-Seifer CH. Clinical response
of alopecia, trichorrhexis nodosa, and dry, scaly skin to zinc
supplementation. J Pediatr. 1992 Dec;121(6):890-5.
- Rushton
DH, Norris MJ, James KC. Amino-acid composition in trichorrhexis
nodosa. Clin Exp Dermatol. 1990 Jan;15(1):24-8.
- Venning
VA, Dawber RP, Ferguson DJ, Kanan MW. Weathering of hair in trichothiodystrophy.
Br J Dermatol. 1986 May;114(5):591-5.
- Weismann
K, Hagdrup HK. Hair changes due to zinc deficiency in a case of
sucrose malabsorption. Acta Derm Venereol. 1981;61(5):444-7.
- Rogers M. Hair shaft abnormalities: Part
I. Australas J Dermatol. 1995 Nov;36(4):179-84; quiz 185-6.
- Trueb RM. Trichonodosis neurotica and familial
trichonodosis. J Am Acad Dermatol. 1994 Dec;31(6):1077-8.
- Zhu WY, Xia MY. Trichonodosis. Pediatr
Dermatol. 1993 Dec;10(4):392-3.
- Leonard JN, Gummer CL, Dawber RP. Generalized
trichorrhexis nodosa. Br J Dermatol. 1980 Jul;103(1):85-90.
- English DT, Jones HE. Trichonodosis. Arch
Dermatol. 1973 Jan;107(1):77-9.
- Papa CM, Mills OH Jr, Hanshaw W. Seasonal
trichorrhexis nodosa. Role of cumulative damage in frayed hair.
Arch Dermatol. 1972 Dec;106(6):888-92.
- Pollitt RJ, Jenner FA, Davies M. Sibs with
mental and physical retardation and trichorrhexis nodosa with
abnormal amino acid composition of the hair. Arch Dis Child. 1968
Apr;43(228):211-6
- Rauschkolb EW, Chernosky ME, Knox JM, Owens
DW. Trichorrhexis nodsa--an error of amino acid metabolism? J
Invest Dermatol. 1967 Mar;48(3):260-3.
- Chernosky ME, Owens DW. Trichorrhexis nodosa.
Clinical and investigative studies. Arch Dermatol. 1966 Nov;94(5):577-85.
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