Trichorrhexis may have a genetic basis but appears to be precipitated by environmental factors. Among Caucasians the defect often appears at the ends of the hair shaft with splitting of the ends, thinning and whitish discoloration.

These conditions are directly related to environmental causes such as "perming", blow drying, aggressive hair brushing, and excessive chemical exposure.

In some cases, trichorrhexis nodosa may be caused by an underlying disorder such as argininosuccinic aciduria, Menkes' kinky hair syndrome, Netherton's syndrome, hypothyroidism, or trichothiodystrophy.

This condition is self-limiting. Improvements in grooming techniques and in environmental conditions will correct the abnormality.

Genetic forms of localized autosomal recessive hypotrichosis include:

Acquired hypertrichosis lanuginosa is commonly present with cancer. This condition is also linked to metabolic disorders, such as anorexia, hormone imbalances, such as hyperthyroidism, or as a side effect of certain drugs.

Acquired generalized hypertrichosis may be caused by cancer. The resulting hair growth is known as malignant down. The mechanism behind cancer induced hypertrichosis is unknown. Oral and topical minoxidil treatments are also known to cause acquired generalized hypertrichosis.

The exact genetic mutation that causes congenital circumscribed, localized, and nevoid hypertrichosis is unknown.

Woolly hair nevus (alternatively spelled "Wooly hair nevus") is a congenital condition in which hair in a circumscribed area of the scalp is kinked or woolly.

Hypotrichosis ("" + "" + "") is a condition of abnormal hair patterns, predominantly loss or reduction. It occurs, most frequently, by the growth of vellus hair in areas of the body that normally produce terminal hair. Typically, the individual's hair growth is normal after birth, but shortly thereafter the hair is shed and replaced with sparse, abnormal hair growth. The new hair is typically fine, short and brittle, and may lack pigmentation. Baldness may be present by the time the subject is 25 years old.

Hypotrichosis is a common feature of Hallermann–Streiff syndrome as well as others. It can also be used to describe the lack of hair growth due to chemotherapy.

The opposite of hypotrichosis is hypertrichosis, where terminal hair (thick) grows in areas that would otherwise normally have vellus hair (thin), for example abnormally thick facial hair growth in women.

Oil production in the sebaceous glands increases during puberty, causing comedones and acne to be common in adolescents. Acne is also found premenstrually and in women with polycystic ovarian syndrome. Smoking may worsen acne.

Oxidation rather than poor hygiene or dirt causes blackheads to be black. Washing or scrubbing the skin too much could make it worse, by irritating the skin. Touching and picking at comedones might cause irritation and spread infection. It is not clear what effect shaving has on the development of comedones or acne.

Some, but not all, skin products might increase comedones by blocking pores, and greasy hair products (like pomades) can worsen acne. Skin products that claim to not clog pores may be labeled noncomedogenic or non-acnegenic. Make-up and skin products that are oil-free and water-based may be less likely to cause acne. It is not known whether dietary factors or sun exposure make comedones better, worse or have no effect.

A hair that does not emerge normally can also block the pore and cause a bulge or lead to infection (causing inflammation and pus).

Genes may play a role in the chances of developing acne. Comedones may be more common in some ethnic groups. People of recent African descent may experience more inflammation in comedones, more comedonal acne, and earlier onset of inflammation.

"Bamboo hair" is a rare autosomal recessive genodermatosis characterized by congenital ichthyosiform erythroderma, trichorrhexis invaginata, and atopic diathesis with failure to thrive. Chronic skin inflammation results in scaling and exfoliation, predisposing these patients to life-threatening infections, sepsis, and dehydration. The Netherton syndrome Mendelian Inheritance in Man is inherited as an autosomal recessive disorder due to mutations of both copies of the "SPINK5" gene (localized to band 5q31-32), which encodes the serine protease inhibitor LEKTI (lymphoepithelial Kazal-type-related inhibitor). LEKTI is expressed in epithelial and mucosal surfaces and in the thymus. Each "SPINK5" mutation leads to a different length of LEKTI protein, resulting in genotype/phenotype correlations in cutaneous severity, susceptibility to atopic dermatitis, growth retardation, skin infection, increased stratum corneum protease activities, and elevated kallikrein levels in the stratum corneum.

Trichorrhexis invaginata, or bamboo hair, is a hair shaft abnormality that occurs as a result of an intermittent keratinizing defect of the hair cortex. Incomplete conversion of the sulfhydryl –SH group onto S-S disulfide bonds in the protein of the cortical fibers leads to cortical softness and subsequent invagination of the fully keratinized distal hair shaft into the softer, abnormally keratinized proximal hair shaft. Intussusception of the distal hair shaft into the proximal hair shaft results in a distinctive ball-and-socket hair shaft deformity. The affected hairs are brittle and breakage is common, resulting in short hairs.

Migratory lesions of ichthyosis linearis circumflexa may be caused by a dermal influx of inflammatory cells that undergo phagocytosis and digestion by keratinocytes, resulting in disruption of keratinization.

Increased transepidermal water loss resulting from the disturbance of corneocyte barrier function in erythroderma may cause profound metabolic abnormalities and hypernatremia, particularly in neonates.

Approximately 200 cases of trichorrhexis invaginata (bamboo hair) have been reported in the literature, but the true incidence is not known. The incidence of trichorrhexis invaginata (bamboo hair) may be as high as 1 case in 50,000 population.

Girls are affected more often by trichorrhexis invaginata (bamboo hair) than boys, but is present in all races.

Trichorrhexis invaginata (also known as "Bamboo hair" ) is a distinctive hair shaft abnormality that may occur sporadically, either in normal hair or with other hair shaft abnormalities, or regularly as a marker for Netherton's syndrome. The primary defect appears to be abnormal keratinization of the hair shaft in the keratogenous zone, allowing for intussusception of the fully keratinized and hard distal shaft into the incompletely keratinized and soft proximal portion of the shaft.

Treatment of manifestations: special hair care products to help manage dry and sparse hair; wigs; artificial nails; emollients to relieve palmoplantar hyperkeratosis.

Favre–Racouchot syndrome occurs in sun-damaged skin and includes open and closed comedones.

Nevus comedonicus or comedo nevus is a benign hamartoma (birthmark) of the pilosebaceous unit around the oil-producing gland in the skin. It has widened open hair follicles with dark keratin plugs that resemble comedones, but they are not actually comedones.

Dowling-Degos disease is a genetic pigment disorder that includes comedo-like lesions and scars.

Familial dyskeratotic comedones is a rare autosomal dominant genetic condition, with keratotic (tough) papules and comedo-like lesions.

CCCA tends to present itself in the 20s and progresses over 20–30 years. One should consider this diagnosis in African Americans with what appears to be a female-pattern hair loss.

There is currently researching being done to find more treatments dependent on the different pre-existing conditions.

Studies are being conducted in which madarosis can be related to malignancy. A study by Groehler and Rose found that there was a statistical significance between these two. They concluded that patients malignancy lesions on the eyelid have a higher chance of having madarosis than a patient with a benign lesion. They stated that despite the fact that it is significant, the absence of madarosis does not mean the lesion cannot be malignant.

In many leprosy cases, madarosis is a symptom or a quality after diagnosis. However, in India, leprosy is common and researchers report a case of madarosis before diagnosis of leprosy with no skin lesions, only madarosis. This allowed for quicker treatment.

A main reason many people have madarosis is due to the chemotherapy drugs. There was a clinical trial in 2011 that tested an eyelash gel called bimatoprost. This gel enhanced the eyelashes in quantity and thickness. They tested this on 20 breast cancer patients who were undergoing chemotherapy. Results seemed positive, in that the group of people who used the gel had growth of eyelashes after the chemotherapy drugs.

The cat must have a supply of niacin, as cats cannot convert tryptophan into niacin like dogs. However, diets high in corn and low in protein can result in skin lesions and scaly, dry, greasy skin, with hair loss. Another B vitamin, biotin, if deficient causes hair loss around the eyes and face. A lack of B vitamins can be corrected by supplementing with a vitamin B complex, and brewers yeast.

Loose anagen syndrome (also known as "Loose anagen hair syndrome") is primarily described in fair-haired children who have easily dislodgable hair.

There are various causes of madarosis.

- Ophthalmological conditions: blepharitis is an infection of the eyelid. Anterior blepharitis is either "staphylococcal blepharitis,"or "seborrhoeic blepharitis" and posterior blepharitis is due to the meibomian gland.

- Dermatologic conditions: there are multiple types of dermatological conditions that can result in madarosis. These include Atopic dermatitis, Seborrhoeic dermatitis atopic dermatitis, and Psoriasis on the eyelids can result in madarosis. Others include: frontal fibrosing alopecia, ulerythema ophryogenes, acne rosacea, telogen effluvium, follicular mucinosis, and cutaneous sarcoidosis.

- Nutritional defects: Severe malnutrition can cause chronic hair loss. Hypoproteinemia causes hair loss by early onset of telogen. Zinc deficiencies like acrodermatitis enteropathica, can lead to the loss of eyebrow/eyelash hair. Other deficiencies like biotin and iron make it possible for loss of hair as well.

- Infections: There are many bodily infections that can cause the loss of eyelashes/eyebrows. The most common infection may be leprosy, such as lepromatous leprosy. Syphilis or other viral infections like herpes or HIV can cause the loss of eye hair as well. Fungal infections, like paracoccidioidomycosis, trichophyton, or microsporum, are also possible infection causes.

- Trauma: Most trauma injuries cause madarosis from the psychological standpoint, known as trichotillomania

- Drugs/Medications: Crack cocaine or chemotherapy drugs. Other drugs include:propranolol, valproic acid, barbiturates, MMR vaccine, botulinum toxin, epinephrine, antithyroid drugs, anticoagulants, and lipid-lowering drugs

- Genetics

- Autoimmune disorders: alopecia areata, discoid lupus erythematosus, chronic cutaneous lupus erythmatosus, Graham-Little syndrome, and Parry Romberg syndrome

- Other diseases: hypothyroidism, hyperthyroidism, hypoparathyroidism, hypopituitarism, and amyloidosis

There only prevention method is determining the underlying condition before treatment options are too late.

Peeling skin syndrome (also known as "Acral peeling skin syndrome," "Continual peeling skin syndrome," "Familial continual skin peeling," "Idiopathic deciduous skin," and "Keratolysis exfoliativa congenita") is an autosomal recessive disorder characterized by lifelong peeling of the stratum corneum, and may be associated with pruritus, short stature, and easily removed anagen hair.

The acral form can be associated with "TGM5".

HED2 is suspected after infancy on the basis of physical features in most affected individuals. GJB6 is the only gene known to be associated with HED2. Targeted mutation analysis for the four most common GJB6 mutations is available on a clinical basis and detects mutations in approximately 100% of affected individuals. Sequence analysis is also available on a clinical basis for those in whom none of the four known mutations is identified.

Cats cannot synthesize vitamin A from plant beta-carotene, and therefore must be supplemented with retinol from meat. A deficiency in vitamin A will result in a poor coat, with hair loss, with scaly and thickened skin. However an excess of vitamin A, called hypervitaminosis A, can result from over feeding cod liver oil, and large amounts of liver. Signs of hypervitaminosis A are overly sensitive skin, and neck pain causing the cat to be unwilling to groom its self, resulting in a poor coat. Supplementing vitamin A with retinol to a deficient cat, and feeding a balanced diet to a cat with hypervitaminosis A will treat the underlying nutritional disorder.

The hair is normal in quantity and is usually silvery-blond or straw-colored. It is disorderly, it stands out from the scalp, and cannot be combed flat. The underlying structural anomaly is longitudinal grooving of the hair shaft, which appears triangular in cross section. This is caused by mutations in one of three possible genes; "PADI3", "TGM" or "TCHH3." The characteristic hair shaft anomaly can be demonstrated in asymptomatic family members by scanning electron microscopy. To be noticeable, 50% of hairs must be affected by the structural abnormality. Improvement often occurs in later childhood. An autosomal dominant mode of inheritance has been suggested though an autosomal recessive pattern with varying degrees of penetrance has also been noted. The stiffness of the uncombable hair has been reasoned to be due to the triangular form of the hair shaft in cross section. It has been suggested that the condition may result from premature keratinization of the inner root sheath.

Sabinas brittle hair syndrome is inherited as an autosomal recessive genetic trait.

In a study by Howell et al. patients were located and studied by means of complete histories and physical examinations, analyses of serum trace metals, ceruloplasmin concentration, urine and serum amino acids, and routine metabolic urine screens. In addition, serum and urine luteinizing hormone (LH) and follicle-stimulating hormone (FSH) values were determined, and were interpreted in conjunction with total plasma estrogen, estradiol, and testosterone levels. Close examination demonstrated the scalp hairs were very brittle, coarse, wiry in texture, and broke off quite easily with mechanical trauma such as combing and brushing. Some hairs could be visualized in their follicles, which were broken off at the skin line. Most patients had accompanying hyperkeratosis (thickening of the skin) of moderate degree on exposed surfaces. Maxillary hypoplasia (midfacial retrusion) was significant in many patients. The brittle, short hair, reduced eyelashes, crowded teeth, and dull appearance created a characteristic facial appearance. Post-pubertal patients had development of secondary sexual characteristics consistent with their age, except for sparse pubic escutcheons. All cases studied demonstrated some degree of mental deficiency; I.Q.'s ranged between 50–60. A deficiency in eye–hand coordination was also noted.

Individuals affected by certain ED syndromes cannot perspire. Their sweat glands may function abnormally or may not have developed at all because of inactive proteins in the sweat glands. Without normal sweat production, the body cannot regulate temperature properly. Therefore, overheating is a common problem, especially during hot weather. Access to cool environments is important.

Rapunzel syndrome, an extreme form of trichobezoar in which the "tail" of the hair ball extends into the intestines, can be fatal if misdiagnosed. In some cases, surgery may be required to remove the mass; a trichobezoar weighing was removed from the stomach of an 18-year-old woman with trichophagia.

Several studies have examined salivary flow rate in individuals and found parotid and submandibular salivary flow ranging from 5 to 15 times lower than average. This is consistent with the salivary glands being of ectodermal origin, although some findings have suggested that there is also mesodermal input.