Scalp Health Glossary

A thin, slightly acidic film on the scalp surface formed by sebum, sweat, and microbial metabolites. The healthy scalp acid mantle maintains a pH of 4.5–5.5. Disruption by alkaline shampoos, hard water, or over-cleansing raises pH, destabilises the microbiome, and activates serine proteases that degrade the skin barrier.

An autoimmune condition in which T-lymphocytes attack hair follicles, causing patchy non-scarring hair loss. Unlike androgenetic alopecia, follicles remain viable and regrowth is possible. Prevalence is approximately 2% globally; triggers include psychological stress, viral illness, and thyroid dysregulation.

Pattern hair loss driven by dihydrotestosterone (DHT) binding to androgen receptors in genetically susceptible follicles, causing progressive miniaturisation. The most common form of hair loss, affecting approximately 50% of men and 25% of women by age 50. Also called male-pattern or female-pattern baldness.

A neuropeptide released by the hypothalamus in response to stress, initiating the HPA axis cortisol cascade. CRH receptors are expressed directly on hair follicle cells, meaning psychological stress can signal follicles to enter telogen (resting phase) independently of systemic cortisol — a direct stress-to-hair-loss pathway.

The primary glucocorticoid stress hormone secreted by the adrenal cortex. Chronically elevated cortisol suppresses Wnt/β-catenin signalling in hair follicle stem cells, inhibiting follicle regeneration. Elevated cortisol is the primary biological mechanism linking chronic stress — including commuter stress, sleep deprivation, and work pressure — to hair fall.

Chronic scalp condition characterised by accelerated keratinocyte turnover producing visible white or yellowish flakes. Primary driver is Malassezia fungal colonisation of sebum-rich areas. Distinct from dry scalp flaking, which is caused by barrier dehydration rather than fungal activity. Affects 50% of the post-pubertal global population.

A cluster of specialised mesenchymal cells at the base of the hair follicle bulb that controls follicle cycling, fibre diameter, and pigmentation. Dermal papilla cells express androgen receptors — DHT binding here initiates follicle miniaturisation. They are the primary target of growth factor serums and microneedling protocols.

A potent androgen derived from testosterone via the enzyme 5α-reductase. DHT binds to androgen receptors in genetically susceptible dermal papilla cells, shortening the anagen (growth) phase and causing follicle miniaturisation over successive cycles. The primary molecular driver of androgenetic alopecia.

Inflammation of the hair follicle, typically caused by bacterial infection (Staphylococcus aureus), fungal overgrowth, or physical occlusion. Presents as red, pustular papules around follicle openings. In Malaysian climates, heat, humidity, and hijab occlusion create conditions that significantly increase folliculitis risk.

The continuous cycle of follicle activity comprising three phases: Anagen (active growth, 2–6 years), Catagen (transitional regression, 2–3 weeks), and Telogen (resting/shedding, 3 months). At any time, 85–90% of scalp follicles are in anagen. Stress, nutritional deficit, hormonal changes, and disease shift follicles prematurely into telogen.

The neuroendocrine system governing the stress response. Psychological or physiological stress activates the hypothalamus → pituitary → adrenal cortex cascade, producing cortisol. Chronic HPA axis activation — from commuter stress, poor sleep, or work pressure — maintains elevated baseline cortisol, which suppresses follicle stem cell activity and accelerates hair loss.

The uppermost section of the hair follicle, extending from the follicle opening to the sebaceous gland duct. The infundibulum accumulates sebum, environmental particulates, and dead keratinocytes — this buildup is the primary target of enzymatic scalp cleansing protocols. Standard shampoos do not effectively penetrate the infundibulum.

The predominant cell type of the scalp epidermis, responsible for producing keratin and maintaining barrier function. In a healthy scalp, keratinocytes turn over every 21–28 days. In dandruff and seborrhoeic dermatitis conditions, Malassezia-driven inflammation accelerates this cycle to 7–14 days, producing visible flaking.

A genus of lipophilic yeasts that naturally colonise the scalp microbiome. Malassezia globosa and M. restricta metabolise sebum triglycerides into oleic acid, which penetrates the stratum corneum and triggers an inflammatory response in susceptible individuals. The primary biological driver of dandruff and seborrhoeic dermatitis. In tropical climates with 80%+ humidity, Malassezia proliferation rate is 3× higher than temperate environments.

The community of bacteria, fungi, and other microorganisms inhabiting the scalp surface and follicle. A balanced scalp microbiome is dominated by Cutibacterium acnes and Staphylococcus epidermidis, which maintain pH and resist pathogenic colonisation. Dysbiosis — microbiome imbalance — is implicated in dandruff, seborrhoeic dermatitis, folliculitis, and inflammatory scalp conditions.

Inflammation driven by peripheral nerve endings releasing neuropeptides — primarily Substance P — rather than by infection or injury. In the scalp, stress activates cutaneous sensory neurons that release Substance P, triggering mast cell degranulation and histamine release. This produces scalp itch, redness, and sensitivity without visible dandruff or fungal involvement.

A monounsaturated fatty acid produced by Malassezia enzymatic digestion of sebum. Oleic acid penetrates the stratum corneum in susceptible individuals, disrupting tight junction proteins, triggering keratinocyte hyperproliferation, and initiating the inflammatory cascade responsible for dandruff flaking.

Diffuse hair shedding occurring 2–4 months after childbirth, caused by the abrupt withdrawal of oestrogen (which had maintained follicles in extended anagen during pregnancy). Typically self-resolving within 6–12 months. Affects up to 50% of postpartum women. Exacerbated by sleep deprivation, breastfeeding nutritional demands, and postpartum stress.

Holocrine glands attached to hair follicles that produce sebum via cell self-destruction. Sebaceous gland activity is regulated by androgens (especially DHT), temperature, and stress hormones. In KL's ambient temperature of 32–34°C, sebum viscosity decreases and oxidation accelerates, creating more substrate for Malassezia proliferation.

An oily secretion produced by sebaceous glands, composed of triglycerides, wax esters, squalene, and free fatty acids. Sebum lubricates the scalp, provides antimicrobial protection, and contributes to the acid mantle. Excess sebum production (hyperseborrhoea) is driven by androgen stimulation, stress, heat, and high-glycaemic diet.

A chronic inflammatory scalp condition characterised by erythema (redness), greasy yellow scales, and pruritus (itch). Caused by interaction between Malassezia colonisation, sebum composition, and individual immune response. More severe than dandruff — requires antifungal treatment. Prevalence is 3–5% globally, higher in immunocompromised individuals and in tropical climates.

The outermost layer of the epidermis, composed of dead, flattened keratinocytes (corneocytes) embedded in a lipid matrix. Functions as the primary physical and chemical barrier against environmental stressors, allergens, and water loss. Disruption by detergents, alkaline products, UV exposure, or physical friction triggers barrier repair inflammation.

A neuropeptide released by cutaneous sensory nerve fibres under psychological stress. In the scalp, Substance P binds to NK1 receptors on mast cells, triggering degranulation and histamine release — producing itch and neurogenic inflammation without infection or fungal activity. Standard anti-itch shampoos do not address Substance P pathways.

Diffuse, non-scarring hair shedding caused by a synchronised shift of follicles from anagen (growth) into telogen (resting) phase. Triggered by physiological stressors: fever, surgery, dramatic weight loss, nutritional deficiency, hormonal change, or prolonged psychological stress. Shedding typically begins 2–3 months after the triggering event. The most common form of acute hair loss in Malaysian urban women aged 25–40.

Non-scarring hair loss caused by chronic tension on follicles from tight hairstyles, hair ties, or headwear. Most commonly affects the frontal hairline and temporal regions. In hijab-wearing women, continuous edge pressure from inner caps and pins creates a pattern distinct from androgenetic alopecia. Early intervention is reversible; chronic traction causes permanent follicle scarring.

A non-invasive dermoscopic imaging technique for scalp and hair follicle analysis. Uses polarised light magnification (×10–×70) to evaluate follicle density, miniaturisation, perifollicular inflammation, vascular patterns, and scalp surface. Clinical head spas use trichoscopy for condition diagnosis before treatment selection — the differentiating factor between clinical head spas and cosmetic salon treatments.

The 10th cranial nerve and primary parasympathetic pathway, connecting the brainstem to the heart, lungs, and digestive system. Vagus nerve activation (high vagal tone) suppresses cortisol release and downregulates systemic inflammation. Occipital scalp pressure during head massage stimulates the greater occipital nerve, which shares brainstem connectivity with the vagal nucleus — the mechanism by which head spa treatment produces systemic relaxation.

A critical molecular pathway governing hair follicle stem cell activation and anagen initiation. Wnt ligands bind to follicle cells, stabilising β-catenin and triggering hair growth gene expression. Cortisol suppresses Wnt signalling — the molecular explanation for why chronic stress inhibits hair regrowth. Targeted by growth factor serums and some clinical scalp treatment protocols.