Canities (overview) L67.1

(Diffuse) graying or whitening of the hair as a result of loss of melanin production by the melanocytes of individual or all hair bulbs. Depending on the cause, a distinction is made between:

• medicinal graying
• physiological gra ying
• Canities praecox
• symptomatic canities
• Canities subita (sudden graying - "overnight")

Ultimately, the etiopathogenesis of graying has not been fully elucidated to date. Premature graying may occur as an autosomal dominant primary disease. Graying may also occur in premature aging disorders such as progeria adultorum. An association with atopic diathesis and various autoimmune diseases has also been reported (Daulatabad D et al. 2016). The role of reactive oxygen species(ROS) in hair graying may be the best studied. During the active growth phase, i.e., the anagen phase, active melanogenesis occurs in the hair follicle, and the hair shaft is loaded with melanin. Melan production involves hydroxylation of tyrosine and oxidation of dihydroxyphenylalanine to melanin, which causes tremendous cumulative oxidative stress. Oxidative stress can be caused, for example, by ultraviolet radiation (UV), environmental pollution, by emotional factors, or by inflammatory processes. Oxidative stress can lead to increased graying of hair follicles (Arck PC et al. 2006).

Progeria syndromes are associated with defective DNA repair mechanisms. In this respect, DNA processes ebi these syndromes are more susceptible to oxidative stress. This may be associated with premature graying of the hair.

Vitamin B12 deficiency may also cause premature graying of hair via an unknown mechanism. Approximately 55% of patients with pernicious anemia graying before the age of 50 compared to 30% in the control group (Dawber RP (1970).

Furthermore, psychological stress also seems to induce increased oxidative stress. This could serve as an explanation that emotional factors are also thought to play a role in premature graying, even in canities subita(Epel ES et al. 2004).

Deficiency of thyroid hormones causes premature graying, alopecia, and changes in hair morphology. Thyroid hormones T3 and T4 act directly on hair follicles and increase melanogenesis (van Beek N et al 2008).

Furthermore, certain chemotherapeutic agents and antimalarials can cause premature graying. This is true for drugs that inhibit the receptor tyrosine kinase c-KIT , which is present in melanocytes. Chloroquine preferentially reduces pheomelanin production via an unknown mechanism (Hartmann JT et al 2008;Sideras K et al 2010); Di Giacomo TB et al 2009).

Apparently, cigarette smoking is also an etiological factor in premature graying. One possible explanation is the prooxidant effect of smoking on the body, leading to increased ROS damage to melanocytes of hair follicles ( Jo SJ et al. 2012). In a larger collective 10,000 respondents), the proportion of graying smokers was increased at 15.3% compared with the proportion of nonsmokers at 12.8% (Sabharwal R et al. 2014; Shin H et al. 2015).

Reversible hypopigmentation of hair can occur in nutritional deficiencies, protein-energy malnutrition, and diseases with chronic protein loss.

Copper and iron deficiencies can also cause hair graying. Zinc deficiency and premature graying have been reported sporadically(Vinay K et al 2014). Copper, iron, calcium and zinc are thought to affect melanogenesis and thus hair pigmentation.

The white of the hair is due to an optical illusion, because the pale yellow keratin appears white due to the reflection or refraction of the incident light. Gray hair is residually colored by only a few sparsely distributed melanosomes. Hair that appears completely white is free of melanosomes.

A rule of thumb states that by the age of 50, half of the hair in about 50% of the population has turned gray. In men, graying first occurs on the temples and sideburns. The graying spreads to the crown and the rest of the scalp, with the back of the head being the last to be affected. In women, graying is first noticeable on the edges of the scalp.

The progression of graying is determined by several factors, but they are mainly genetic. In addition, the rate of graying may vary in different areas of the scalp. A study of the Korean population showed that the temporal and occipital areas were more affected in men than in women. In addition, graying began in the frontal area in women, but in the temporal area in men. In those in whom graying began before age 40, the parietal and temporal areas were more affected. In those in whom graying began after age 40, the frontal area was more grayed. Interestingly, early onset of graying did not correlate with rapid progression. Regardless of age at onset of graying, rapid progression of graying occurred in this Korean population in the fifth decade of life (Jo SJ et al. (2012)

Gray hair is coarser, stiffer, and more difficult to tame than dark hair (Hollfelder B et al. 1995). Furthermore, the growth rate and thickness of non-pigmented hair is significantly higher than dark hair (Choi HI et al 2011; Nagl W 1995; Van Neste D 2004). Thus, gray beard hair can grow up to four times faster than pigmented hair (Nagl W 1995). Gray hair is also more difficult to comb.

Obesity: Apparently, there is a link between obesity and premature graying of the hair.

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