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trichorrhexis nodosa

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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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