information on hair diseases and their remedies
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Home >> Hair shaft abnormalities >> Trichorrhexis Nodosa One of the most common hair shaft defects a dermatologist encounters is trichorrhexis nodosa (trichonodosis). Trichorrhexis nodosa is a focal defect in the hair fiber. When observed under microscope a large number of fraying and swelling nodes are evident in particular spots along the length of the hair fiber. These focal defects develop due to the absence of a cuticle layer. The function of the cuticle layer is to provide physical support, and protect the cortex of a hair shaft from ultra violet rays, harmful synthetic hair care products and harsh hair brushing. But if the cuticle is absent then the cortex underneath is directly exposed. The cortex is less resistant to the physical and chemical factors of the environment, when compared to the cuticle. The exposure of the cortex layer to chemicals in the environment leads to damage and reduction of the strength of the hair fiber. The chemical bonds that are present in the cortex 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. As we comb, brush or generally manipulate our hair, these defective nodes in the hair fiber may break. Types Trichorrhexis nodosa can be of two types:
Distal trichorrhexis nodosa occurs in straighter hair. In this shaft defect, only a few whitish colored nodules are seen in the hair fiber. The surface of hair may become dry, dull, or brittle. Distal trichorrhexis nodosa is more commonly seen in Caucasian and Asian populations. Causes The causes of this major hair shaft defect can be divided into two categories:
Natural growth of irregular and brittle hair fiber can also be due to metabolic disorders and conditions such as trichothiodystrophy. Metabolic disorders such as abnormal urea synthesis, abnormal copper or zinc metabolism, and defective cysteine or sulfur incorporation into hair fiber can result in defective hair shaft production. Acquired trichorrhexis nodosa is much more common than the congenital condition. Acquired trichorrhexis nodosa is the result of excessive hair manipulation and over-processing. Too much brushing or hairstyles that put constant stress on the hair can cause this hair shaft defect. Also, excessive cleansing, dying, and perming may disrupt the cuticle layer in focal areas along a hair shaft. Trichorrhexis nodosa is particularly seen in people who overuse hot combs or permanent waves to style their hair. Once the cuticle is removed from hair fiber due to excess styling, the cortex is exposed leading to severe damage. Effects This hair fiber defect damages the cuticle layer resulting in the disruption of the cortex. Also longitudinal and transverse fissures can occur in the fiber giving it a paintbrush-like look. Hair shaft abnormalities such as pili torti and monilethrix cause similar damage to the hair fiber as that of trichorrhexis nodosa. Pili torti is a twisting of hair fiber at focal points along its length leading to multiple fractures in a single strand. Treatment or hair care remedies for the defects Treatment or hair care remedy for this severe hair shaft defect depends on the cause which may vary from person to person. If the cause of the hair shaft defect is congenital then treatment will focus on improving the strength of hair fiber and follicle. But where the defect is the result of excessive grooming the obvious treatment or hair care remedies are to reduce the amount of hair manipulation. People are encouraged to reduce brush use, avoid hair styling that involves chemicals, and use only very mild shampoos and conditioners. Also, prior to styling it is recommended to have detailed information on safe styling agents. The styling procedures like straightening, coloring or curling if done in a proper way with the right products will not only give a trendy look but also take care of the hair. References: Shannon Harrison and Rodney Sinclair. “Optimal Management of Hair Loss (Alopecia) in Children”, 2003, Am J Clin Dermatol; 4 (11) |