What Causes Hair Loss: Medical Article
Hair loss can be genetic, hormonal, or triggered by environmental, medical, or lifestyle factors. The most common cause, however, is androgenetic alopecia, also known as male-pattern or female-pattern baldness.Many individuals begin their journey by researching online and experimenting with products like rosemary oil, serums, and dermarollers. These may create temporary improvement by stimulating vellus (baby-fine) hairs, but they cannot reverse long-term genetic loss.
What is Hair Follicle: Histology
The hair follicle is part of the pilosebaceous unit (hair follicle + sebaceous gland + arrector pili muscle) and is best understood as a layered epithelial structure interacting with a mesenchymal compartment. (5)
Anatomic segments: The follicle is commonly divided into the infundibulum (surface → sebaceous duct opening), isthmus (sebaceous duct level → bulge region), and the inferior segment (suprabulbar + bulb), which is most dynamic during cycling. (5,6)
Hair shaft layers: The hair shaft is composed of cuticle, cortex (main structural mass), and sometimes a medulla (variable by hair type). (5)
Root sheaths and perifollicular layers: The follicular epithelium forms an inner root sheath (IRS)—classically Henle layer, Huxley layer, and IRS cuticle—surrounded by the outer root sheath (ORS), which is continuous with epidermis. A distinct companion layer at the IRS/ORS interface has been highlighted in detailed follicle histology. (5,10) Outside the epithelium, supportive connective tissue structures include the glassy membrane and dermal sheath. (5,6)
Bulb, matrix, melanocytes, and dermal papilla: In anagen, the bulb contains a rapidly proliferating matrix that produces the hair shaft and IRS; melanocytes in/near the matrix provide pigment. The dermal papilla serves as a key mesenchymal signaling center that helps regulate follicle growth, size, and cycling. (6,7)
Bulge (stem cell niche): The bulge region within the ORS contains slow-cycling, label-retaining cells and is central to follicle regeneration and cycling biology. (8)
Hair cycle histology: Classic descriptions define anagen (large bulb, active matrix/pigmentation), catagen (apoptosis-driven involution of the lower follicle), and telogen (resting follicle with club hair), forming the basis for interpreting biopsy findings. (7,9) Transverse (horizontal) scalp sectioning is widely used to quantify follicles and cycle stage distribution. (11)
Hair Follicle Physiology
Hair follicles are cycling mini-organs that repeatedly transition through anagen (growth) → catagen (regression) → telogen (rest), with major remodeling of the lower follicle across cycles. (12–14) PubMed+2PubMed+2
Cycle regulation: a regenerative system
The key physiological concept is that the follicle behaves like a self-regenerating system, rebuilding its active growth apparatus in each new anagen. (13) PubMed+1
Dermal papilla–epithelium “command loop”
Hair growth, shaft caliber, and cycling are governed by epithelial–mesenchymal interactions, especially signals between the dermal papilla (DP) and the follicular epithelium. (12,13) PubMed+1
Anagen initiation/maintenance: Wnt/β-catenin signaling
Wnt/β-catenin signaling is fundamental for follicle development and growth-state regulation. (15) PubMed+1 In DP-focused experiments, Wnt/β-catenin activation can help maintain anagen-like (hair-inductive) properties, though it may not fully restore them once lost in culture. (16) PubMed
Catagen induction: TGF-β pathways and programmed regression
Physiologically, catagen involves coordinated involution of the lower follicle. Experimental work supports TGF-β signaling as an endogenous regulator of catagen: TGF-β1 can promote catagen in vivo (mouse). (17) PubMed In humans, TGF-β2 has been implicated as a key mediator during the anagen→catagen transition. (18) PubMed
Immune privilege (anagen-associated protection)
During anagen, the proximal follicle can exhibit relative immune privilege (reduced antigen presentation and local immunosuppressive milieu), which is a recognized physiological feature of the hair cycle. (19) PubMed
Androgen physiology and AGA: paracrine mediators from DP
In androgenetic alopecia (AGA), follicles undergo miniaturization and shortened anagen, largely via androgen-sensitive DP biology and downstream paracrine mediators affecting epithelial growth. (20) PubMed+1 Regional differences in androgen receptor and steroid-converting enzymes (5α-reductase types I/II, aromatase) between frontal vs occipital follicles help explain patterned susceptibility. (21) PubMed Mechanistically, DHT-inducible DKK1 from balding DP cells can contribute to growth inhibition and epithelial apoptosis in experimental systems. (23) PubMed
Lipid mediators: prostaglandin signaling
Prostaglandin pathways also participate in follicle physiology; PGD2 has been reported to be elevated in bald scalp and to inhibit hair growth in experimental models. (22)
Vellus vs. Terminal Hair
Humans have two main types of hair. Check the table below to understand difference between Vellus and Terminal Hair.
| Feature | Vellus Hair (Peach Fuzz) | Terminal Hair |
| Thickness & Structure | Short, thin, fine | Thick, coarse |
| Color & Pigmentation | Light-colored, transparent, non-pigmented | Dark, fully pigmented |
| Length | Very short | Long |
| Common Locations | Face, neck, torso, arms | Scalp, beard, eyebrows, eyelashes, body |
| Growth Rate | Grows ~1–1.5 mm over 6–8 months | Grows continuously, several cm per year |
| Response to Treatments | Number may increase with certain treatments | Target hair type in hair loss treatments |
| Hair Maturity | Never becomes full, dense hair | Fully mature, functional hair |
| Clinical Importance | Cosmetic, minimal protective role | Hair type aimed to be preserved or restored |
Understanding this difference is essential to avoid false expectations from cosmetic products that only act on vellus hairs.
