Alopecia (hair loss)
Physiology of the hair cycle
The human hair follicle is an autonomous epithelial and mesenchymal structure with a lifelong capacity for cyclic regeneration. It houses a niche of epithelial stem cells located in the follicular bulge, which ensure follicle regeneration with each new cycle. The dermal papilla, a condensation of specialized fibroblasts at the base of the follicle, orchestrates the transition between cycle phases via paracrine signals involving the Wnt, BMP, Hedgehog and FGF pathways. Keratinization of the hair shaft is ensured by matrix keratinocytes, which differentiate into several concentric layers (cortex, cuticle, medulla) in contact with melanin synthesized by follicular melanocytes.
The duration of the anagen phase is the main determinant of maximum hair length: a short anagen phase (2 years) produces short hair that doesn't exceed 20 to 25 centimetres, while a 7-year anagen phase allows potential growth of 100 centimetres. The duration of the anagen phase is under hormonal control (androgens shorten the anagen phase of androgen-sensitive scalp follicles in androgenetic alopecia, while prolonging the anagen phase of follicles on the face and trunk), nutritional (iron, zinc, biotin and protein deficiencies reduce anagen duration) and environmental (intense acute stress, severe systemic diseases).
Classification of alopecia
| Category | Key features | Possible regrowth | Main examples |
|---|---|---|---|
| Diffuse non-scarring alopecia | Homogeneous thinning of the hair over the entire scalp; anatomically intact hair follicle; absence of fibrosis or destructive inflammation of the follicle; frequent systemic or hormonal cause | Yes, if the cause is identified and treated | Acute and chronic telogen effluvium; diffuse female androgenetic alopecia; thyroid alopecia; nutritional alopecia; diffuse drug-induced alopecia |
| Localized non-scarring alopecia | Delineated bald patches with smooth, supple skin without atrophy; hair follicles present but in a prolonged telogen phase or reversibly damaged; clear demarcation between affected and healthy areas. | Yes in most cases | Peeling (alopecia areata); male androgenetic alopecia (vertex and temporal gulfs); ringworm (tinea capitis); traction alopecia; trichotillomania |
| Primary cicatricial alopecia | Definitive destruction of the hair follicle by a primitive inflammatory process centered on the follicle; atrophic, shiny scalp skin with no visible follicular orifices; often associated with local inflammatory symptoms (pruritus, burning, pain). | No (irreversible) | Lichen planus pilaris (LPP); Brocq's pseudopelade; discoid lupus erythematosus of the scalp; dissecting cellulitis; decalvitating folliculitis; Graham-Little syndrome |
| Secondary scarring | Follicular destruction by a non-primary pathological process: severe infection, neoplasia, trauma, irradiation, thermal or chemical burns, post-surgical scarring, etc. | No (irreversible) | Kerion (severe inflammatory ringworm); scalp skin metastases; thermal burns; chronic radiodermatitis; congenital skin aplasia |
Non-scarring alopecia: detailed descriptions
Androgenetic alopecia (AAG)
Androgenetic alopecia is the most common form of alopecia in both sexes. It results from the progressive miniaturization of the scalp's androgen-sensitive hair follicles under the effect of dihydrotestosterone (DHT), the active metabolite of testosterone produced locally in the follicle by type II 5-alpha-reductase. DHT binds to the follicular androgen receptor and leads to a progressive reduction in the duration of the anagen phase (from 7 years to sometimes less than 1 year in very miniaturized follicles), a shortening and thinning of the hair shaft and, ultimately, a transformation of the terminal follicle into an unpigmented vellous follicle. The process is genetically determined (polygenic transmission with a strong maternal component), progressive and irreversible in the absence of treatment.
| Parameter | Male (male AAG) | Female (Female AAG) |
|---|---|---|
| Prevalence | 30 % of men at age 30; 50 % at age 50; 70 % at age 70 | 6 % before age 50; 30 to 40 % after age 70; sharp increase in the postmenopausal period due to a drop in estrogen levels |
| Characteristic topography | Bitemporal recession (temporal gulfs) and vertex thinning; progressive confluence according to Hamilton-Norwood classification (stages I to VII); preservation of occipital crown hair (donor area for transplantation) | Diffuse, predominantly central thinning of the scalp (widening hairline); classification by Ludwig (stages I to III) or Sinclair (stages 1 to 5); preservation of the frontal implant line in 90 % of cases (differentiating sign of telogen effluvium); rarely male pattern. |
| Diagnosis | Clinical in the vast majority of cases; dermoscopy: miniaturization of rods (diameter heterogeneity greater than 20 %, specific sign), peripilosebacitis, yellow spot signs; no systematic biological work-up in men unless secondary cause is suspected. | Systematic biological workup to rule out a secondary cause: CBC, ferritin, TSH, androgen workup (total testosterone, SDHEA, 17-OH-progesterone if clinical hyperandrogenism), zinc, vitamins B12 and D; scalp biopsy in case of diagnostic doubt (anagen/telogen ratio, follicular miniaturization). |
| First-line treatment | Topical minoxidil 5 % solution or foam once or twice a day (accelerates the anagen phase, increases follicular blood flow, partial inhibition of keratinocyte apoptosis); finasteride 1 mg/day per os (type II 5-alpha-reductase inhibitor, reduces intracranial DHT by 70 %); the two treatments are complementary and their combination is more effective than each alone | Topical minoxidil 2 % or 5 % (solution or foam) once or twice a day; low-dose oral minoxidil (0.25 to 1 mg/day) increasingly used as second-line treatment with superior efficacy to topical forms; finasteride not recommended as first-line treatment for women of childbearing age (teratogenic for the male foetus); possible for post-menopausal women; spironolactone 100 to 200 mg/day antiandrogenic alternative for women with biological hyperandrogenism |
Telogen effluvium
Telogen effluvium is a diffuse, reversible alopecia resulting from the premature, synchronized resting of a large number of anagen follicles, which abruptly enter the telogen phase under the effect of a systemic trigger. Two to four months after the causal event (corresponding to the duration of the telogen phase), these follicles simultaneously expel their hair shafts, producing an often impressive diffuse hair loss of 300 to 500 hairs per day, or more. Most patients consult us alarmed by the amount of hair lost, with no apparent link to an identified causal factor (delay of 2 to 4 months between shock and hair loss).
| Type | Duration | Common causes | Prognosis |
|---|---|---|---|
| Acute telogen effluvium | Less than 6 months; massive loss then spontaneous cessation with complete regrowth | Childbirth (postpartum effluvium, 2 to 4 months postpartum, physiological and auto-resolving within 6 to 12 months); prolonged high fever (severe influenza, COVID-19 documented as a frequent cause since 2020); major surgery under general anesthesia; severe acute hemorrhage; very restrictive hypocaloric diet (less than 1,000 kcal/day); intense acute psychological stress; abrupt start or discontinuation of hormonal contraception | Excellent; complete regrowth expected in 6 to 12 months after treatment of the cause; reassuring to explain to the patient at the first consultation, since anxiety often aggravates causal stress. |
| Chronic telogen effluvium | Over 6 months; persistent diffuse fall with fluctuations; differential diagnosis of female GAA | Chronic martial deficiency (ferritin below 30 to 40 µg/L; most frequent cause of chronic telogen effluvium in women of childbearing age in Quebec); subclinical or proven hypothyroidism; deficiency of zinc, vitamins B12, D or biotin; chronic anemia; chronic inflammatory diseases (lupus, IBD, RA); short bowel syndrome; chronic liver disease; protein deficiency (poorly managed vegan diets, malnutrition); long-term medication | Good if the cause is identified and corrected; regrowth takes 6 to 18 months after normalization of biological parameters; some cases remain idiopathic with fluctuating evolution over several years. |
Peeling (alopecia areata)
Pelade is a non-scarring autoimmune alopecia characterized by a loss of tolerance of cytotoxic CD8+ T lymphocytes to follicular melanocytes in the peribulbar zone, leading to an abrupt cessation of the anagen phase. The peribulbar lymphocytic infiltrate destroys the follicular immune privilege, a microenvironmental structure that is normally immunotolerant. Lifetime prevalence is around 1.7 % in the general population of Quebec, with onset possible at any age, peaking between 20 and 50, and evenly distributed between the sexes. The association with other autoimmune diseases (Hashimoto's thyroiditis, vitiligo, rheumatoid arthritis, lupus, celiac disease) has been documented and justifies targeted biological screening.
- Patchy peeling (localized alopecia areata) : one or more rounded or oval, well-defined alopecic patches, smooth healthy skin with no visible atrophy or inflammation; variable size from a few millimeters to several centimeters; exclamation sign (exclamation-point hairs, base reduced in diameter, characteristic of expanding active areas); associated onychopathy in 10 to 20 % of cases (cracked nails, leukonychia, trachyonychia); variable prognosis, spontaneous regrowth in 60 to 80 % of limited forms within 1 year.
- Ophiastic alopecia: involvement of the occipitotemporal marginal zone in a crown-shaped band; more resistant to treatment and with a poorer prognosis than the classic patchy forms.
- Alopecia totalis: complete loss of scalp hair; affects 5 to 10 % of patients; prognosis for complete regrowth less than 10 %; psychological impact often severe.
- Pelade universelle (alopecia universalis): complete loss of all body hair (eyelashes, eyebrows, armpits, pubic area, limbs); most severe form; prognosis for complete regrowth less than 5 % without active treatment; JAK inhibitors (jakinibs) approved by Health Canada represent a major therapeutic advance in these severe forms.
Medicated causes of alopecia
Many drugs commonly prescribed in Quebec can induce alopecia, most often by a telogen effluvium mechanism (premature cessation of the anagen phase), more rarely by anagen effluvium (abrupt cessation of matrix mitosis, as in chemotherapy).
| Drug class | Drugs most frequently involved | Type of alopecia |
|---|---|---|
| Cytotoxic chemotherapies | Cyclophosphamide, doxorubicin, paclitaxel, docetaxel, etoposide, irinotecan; alopecia occurs 2-4 weeks after the start of treatment, is severe and diffuse | Anagen effluvium (cessation of matrix mitosis); regrowth after cessation of treatment in almost all cases; persistent alopecia possible with certain taxanes (mainly docetaxel) |
| Anticoagulants | Unfractionated heparin and low-molecular-weight heparins; warfarin; direct oral anticoagulants (rivaroxaban, apixaban, dabigatran) less frequently | Moderate telogen effluvium, 2 to 3 months after initiation; reversible on discontinuation or dose reduction in most cases |
| Systemic retinoids | Isotretinoin (Accutane); acitretin; alitretinoin; dose-dependent, frequent, often treatment-limiting | Mixed telogen and anagen effluvium; regression in 2 to 6 months after discontinuation or dose reduction; rarely permanent |
| Thymoregulators and antiepileptics | Sodium valproate (Depakene, frequent and dose-dependent, 12 to 28 % of patients); lithium; carbamazepine less frequently | Chronic telogen effluvium during treatment; molecule change or dose reduction is sometimes necessary; zinc and selenium supplementation may alleviate valproate-induced alopecia |
| Hormones and hormone treatments | Androgenic progestin-only oral contraceptives (levonorgestrel, norgestrel); progestin implants and IUDs; anabolic androgens; long-term corticoids | Telogen effluvium or unmasking of a genetically predetermined AAG; change of contraception to an estrogen-progestin pill with a non-androgenic progestogen (drospirenone, cyproterone acetate) often sufficient |
| Immune checkpoint inhibitors | Pembrolizumab, nivolumab, ipilimumab, atezolizumab; pelade-like alopecia reported in 1-2 % of patients, sometimes interpreted as a favorable sign of antitumor response | Induced peeling (alopecia areata), often multifocal; may improve with local or systemic immunosuppressive therapy without necessarily discontinuing immunotherapy |
| Other common medications | Methotrexate; ACE inhibitors (captopril, enalapril); beta blockers (propranolol, metoprolol, atenolol); alpha and beta interferons; levodopa; cimetidine; systemic azole antifungals; allopurinol | Diffuse telogen effluvium, generally moderate and reversible on discontinuation; always consider a recently started medication in the case of unexplained telogen effluvium |
Scarring alopecia: key clinical points
Scarring alopecias account for around 7 % of all alopecias. They represent a relative dermatological emergency, as irreversible follicular destruction progresses in the absence of treatment. Diagnosis is based on scalp biopsy (two 4 mm punch biopsies, one in healthy skin at the periphery of the active patch and one in the center of the active patch, for histology and direct immunofluorescence) and dermoscopy (absence of follicular pores, perifollicular fibrosis, periorificial erythema and desquamation, depending on the entity).
- Lichen planus pilaris (LPP): scarring alopecia most common in women aged 30 to 60; alopecic patches with irregular margins, visible perifollicular hyperkeratosis and purplish erythema around follicular orifices; frequent pruritus and burning; may be associated with cutaneous or mucosal lichen planus; treatment : topical and intralesional corticosteroids (triamcinolone acetonide 5 to 10 mg/mL), hydroxychloroquine 200 to 400 mg/day, pioglitazone 15 mg/day in refractory forms
- Pseudopelade de Brocq: irregular scarring with a «step in the snow» appearance, major skin atrophy without apparent clinical inflammation, pruritus absent; biopsy essential to rule out atrophic LPP or discoid lupus; treatment often disappointing, hydroxychloroquine and cyclosporine in active progressive forms.
- Discoid lupus erythematosus (SLE) of the scalp: hyperkeratotic scaly erythematous plaques with scarring alopecia and characteristic central hypopigmentation; immunological workup (NAA, anti-DNA, complement) to rule out systemic involvement; treatment: strict photoprotection (aggravated by sun exposure), synthetic antimalarials (hydroxychloroquine 200 to 400 mg/day), local corticosteroids, dapsone in refractory forms.
- Folliculitis decalvans: pustular scarring alopecia, predominantly on the vertex and in men; recurrent staphylococcus aureus folliculitis progressing to scarring; prolonged treatment with rifampicin 300 mg twice daily combined with clindamycin 300 mg twice daily for 10 to 12 weeks; isotretinoin in refractory forms.
- Dissecting cellulitis of the scalp (folliculitis and perifolliculitis capitis abscedens and suffodiens): fluctuating nodules and abscesses of the vertex and nape of the neck communicating in subcutaneous tunnels; predominantly in young Afro-descendant men; treatment: isotretinoin 0.5 to 1 mg/kg/day, incisions and drainage, biotherapies (adalimumab) in refractory forms.
Biological assessment of diffuse alopecia
In all cases of telogen effluvium or diffuse alopecia, particularly in women, a biologically oriented workup is essential to identify a treatable systemic cause before concluding that the cause is primary androgenetic alopecia or idiopathic effluvium.
| Parameter | Clinically relevant threshold | Suspected pathology |
|---|---|---|
| Serum ferritin | Less than 30 µg/L: functional deficiency; less than 70 µg/L: threshold recommended by some experts for optimal regrowth (controversial in the literature); less than 15 µg/L: clear deficiency with depletion of reserves. | Martial deficiency: most frequent cause of chronic telogen effluvium in women of childbearing age; oral iron supplementation (ferrous sulfate 150 to 300 mg/day with vitamin C) until normalization; reassessment at 6 months |
| TSH (thyroid stimulating hormone) | Above 4.5 mIU/L: hypothyroidism; below 0.4 mIU/L: hyperthyroidism; both may cause telogen effluvium | Hypothyroidism (more often) and hyperthyroidism (less often); normalization of thyroid hormones under treatment leads to regrowth in 6 to 12 months. |
| Complete blood count (CBC) | Hypochromic microcytic anemia (martial deficiency); macrocytic anemia (B12 or folate deficiency); leukopenia and thrombocytopenia (lupus, liver disease) | Chronic anemia from any cause; vitamin B12 deficiency (vegans, malabsorption, long-term metformin); folate deficiency; systemic diseases |
| Serum zinc | Less than 10 µmol/L: deficiency | Zinc deficiency: uncommon but correctable cause of telogen effluvium; vegan diets, malabsorption, chronic alcoholism; supplementation with zinc gluconate 30-45 mg/day elemental |
| Androgen balance (women) | Total testosterone, SDHEA (dehydroepiandrosterone sulfate), basal 17-OH-progesterone (morning fasting if late-onset congenital adrenal hyperplasia suspected) | Polycystic ovary syndrome (PCOS): biological and/or clinical hyperandrogenism with anovulation; late-onset congenital adrenal hyperplasia (CAH); virilizing adrenal or ovarian tumor (rare, very high testosterone above 5 nmol/L); indication for antiandrogen therapy. |
| Vitamin D (25-OH-vitamin D) | Less than 50 nmol/L: deficiency; less than 25 nmol/L: clear deficiency | Vitamin D deficiency: prevalent in Quebec (high latitude, prolonged winter); link with alopecia moderate in the literature, but supplementation recommended if documented deficiency for overall bone and immune health |
| Total protein and albumin | Albumin less than 35 g/L | Protein-energy undernutrition; severe malabsorption; chronic liver disease; highly restrictive diets; severe telogen effluvium in mental anorexics corresponds to major protein undernutrition |
Treatment options by type of alopecia
| Type of alopecia | Validated treatments | Expected response time |
|---|---|---|
| Male androgenetic alopecia | Topical minoxidil 5 % (first line, monotherapy or combination); finasteride 1 mg/day per os (first line, superior efficacy to minoxidil alone, synergistic combination); dutasteride 0.5 mg/day (type I and II 5-alpha-reductase inhibitor, more effective than finasteride, not formally indicated but widely used); oral minoxidil 2.5 to 5 mg/day; hair transplantation (FUE or FUT technique) for stabilized advanced stages. | Minoxidil: stabilization at 3 months, visible regrowth at 6 to 12 months, maximum effect at 24 months; finasteride: cessation of progression at 3 to 6 months, regrowth at 12 to 24 months; medical treatments must be maintained indefinitely to avoid relapse. |
| Female androgenetic alopecia | Topical minoxidil 2 to 5 % or oral 0.25 to 1 mg/day (first line); spironolactone 50 to 200 mg/day if hyperandrogenism (second line); non-androgenic estrogen-progestin oral contraceptive (drospirenone, cyproterone acetate) if PCOS; finasteride 2.5 to 5 mg/day in postmenopausal women; hair transplantation for stabilized advanced forms. | Similar to men; response is often less spectacular than in men; primary objective is to stabilize progression; visible regrowth takes 12 to 18 months |
| Limited patchy peeling | Intralesional corticosteroids (triamcinolone acetonide 5 to 10 mg/mL, monthly injections over the alopecic area); potent topical corticosteroids (clobetasol propionate 0.05 %, daily applications); adjuvant topical minoxidil; diphenylcyclopropenone (DPCP) in a specialized center for extensive resistant forms. | Visible regrowth in patches treated with 2 to 3 months of intralesional corticosteroids; complete regrowth rate of 50 to 70 % in limited forms; risk of relapse when treatment is stopped. |
| Severe peeling (SALT greater than 50 %) | Baricitinib (Olumiant) 4 mg/day po (approved by Health Canada for severe adult alopecia areata); ritlecitinib (Litfulo) 50 mg/day po (approved for ages 12 and over); short-course systemic corticosteroids for rapidly progressive forms; topical DPCP in a specialized center. | JAK inhibitors: visible improvement at 3 months, maximum response at 36 weeks; continuous treatment required; relapse on discontinuation in most cases; drug insurance coverage varies from plan to plan. |
| Telogen effluvium | Exclusive etiological treatment (iron supplementation if martially deficient, correction of hypothyroidism, discontinuation or substitution of offending medication, nutritional optimization); adjuvant topical or oral minoxidil to accelerate regrowth in prolonged or anxiety-provoking forms; psychological support and therapeutic education on reversibility. | Progressive regrowth after correction of the cause: 3 to 6 months for visible regrowth, 12 to 18 months for normal density recovered; effluvium may worsen temporarily at the start of minoxidil treatment (telogen hair loss displaced by regrowing anagen hair) |
| Scarring alopecia | Entity-specific anti-inflammatory treatment (intralesional corticosteroids and hydroxychloroquine in LPP and SLE; isotretinoin in decalcifying folliculitis and dissecting cellulitis; biotherapies in refractory forms); hair transplantation only if the disease has been stabilized for at least 2 years on a control biopsy; no spontaneous regrowth possible in areas of scarring. | Therapeutic goal: halt progression of scarring alopecia, no regrowth in destroyed areas; anti-inflammatory response assessable at 3 to 6 months; quarterly dermoscopic and clinical follow-up in active phase. |
Hair transplants
Hair transplantation is a surgical reconstructive technique indicated for stabilized androgenetic alopecia (absence of documented progression for at least 12 months), certain scalp scars and alopecia of the eyebrows and beard. It is based on the principle of follicular immunoprivilege: follicles from the occipital donor area, which are insensitive to androgens, retain their permanent character after transplantation into the recipient area.
Two main techniques are used in Quebec. The FUT (Follicular Unit Transplantation or strip) technique involves excising a strip of scalp from the occipital area, dissecting individual follicular units under a microscope and re-implanting them in alopecic areas; it leaves a linear scar but enables large areas to be treated in a single session. The FUE (Follicular Unit Extraction) technique involves the individual extraction of each follicle using a 0.8 to 1.0 mm micropunch, with no visible linear scar, and is preferred by patients with short hair. Final results are visible 12 to 18 months after the procedure, with regrowth of the transplanted hair following a cycle of initial loss (post-transplant shock within 4 to 8 weeks) followed by permanent regrowth. Concomitant medical treatment (finasteride, minoxidil) is strongly recommended to preserve non-transplanted native follicles.
Consult at Clinique Omicron
Clinique Omicron's physicians, at its locations in Quebec, evaluate all forms of alopecia in a dedicated consultation. When faced with telogen effluvium or diffuse alopecia, our practitioners carry out a complete targeted biological workup (ferritin, TSH, CBC, androgen workup in women, zinc, vitamin D, albuminemia) to identify any correctable systemic causes before initiating drug treatment. The prescription of topical and oral minoxidil, finasteride and spironolactone in validated indications is part of our standard practice. In the presence of suspected alopecia, lichen planus pilaris or other scarring alopecia, we coordinate referral to specialized dermatology for histological confirmation and appropriate treatment. Our teams can also prescribe and monitor JAK inhibitor treatments for severe forms of hair loss benefiting from drug coverage, in collaboration with partner dermatologists. The psychological impact of hair loss is systematically addressed during the consultation, and referral to psychological support resources is offered when indicated. Book an appointment at one of our points of service on the South Shore or at one of our branches in Quebec. Teleconsultation is available for interpretation of biological tests and follow-up of ongoing treatments.
The content of this page is provided for informational purposes only and is not intended to replace the advice of a qualified healthcare professional. Consult a physician for any symptoms, questions or decisions you may have regarding your health.
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