Creative Touch Permanent Makeup and Aesthetics

Pyrrolidone carboxylic acid (PCA) is an organic acid produced in the stratum corneum through the spontaneous cyclisation of glutamine – one of the amino acids released when filaggrin undergoes proteolytic degradation in the outer layers of the epidermis. It is not sourced from diet directly, nor synthesised through an enzymatic pathway in the conventional sense; it forms as a natural consequence of filaggrin breakdown during the terminal stages of keratinocyte differentiation. PCA is one of the most abundant components of natural moisturising factor (NMF) by weight and is considered a primary driver of the corneocyte’s internal water-binding capacity. PCA is also referred to as pyroglutamic acid or pyroglutamate in biochemistry literature

How PCA Works

PCA is intensely hygroscopic – it attracts and holds water molecules through hydrogen bonding, maintaining hydration within the corneocyte against the osmotic gradient that would otherwise draw water toward the drier skin surface. This intracellular water-retention function is distinct from the role of the extracellular lipid matrix ( ceramides, cholesterol, and free fatty acids), which limits water loss by restricting permeability between cells. PCA operates inside the cell; the lipid matrix operates around it. Both are required for full stratum corneum hydration, and their failure modes are different – lipid barrier disruption and NMF depletion produce overlapping but mechanistically distinct presentations of dry skin.

PCA and the Acid Mantle

Beyond its humectant role, PCA is one of the primary proton donors responsible for the stratum corneum’s acidic surface pH of approximately 4.5–5.5. Research directly comparing PCA and trans-urocanic acid (UCA) at equivalent concentrations found that 10mM PCA reduces medium pH to 4.50, demonstrating stronger proton donation than UCA at the same concentration. This acid mantle contribution matters beyond surface antimicrobial defence: the pH 4.5–5.5 environment that PCA helps generate is the same environment required for optimal activity of acidic sphingomyelinase and beta-glucocerebrosidase – the enzymes that convert ceramide precursors to functional barrier lipids. PCA depletion therefore has downstream consequences for ceramide production that extend well beyond the hydration deficit it directly creates. ^[2]

What Reduces PCA Levels

Because PCA is water-soluble, it is vulnerable to leaching from the stratum corneum through surfactant exposure and repeated water contact. Controlled patch studies with sodium lauryl sulphate ( SLS) demonstrate measurable PCA reduction following surfactant exposure, with filaggrin-derived NMF components – including PCA – taking longer to recover than sweat-derived components such as urea and lactate. ^[1] Any condition that reduces filaggrin expression – FLG gene mutation, or inflammatory suppression by IL-4 and IL-13 – simultaneously reduces the glutamine supply from which PCA forms, meaning PCA levels directly reflect filaggrin status. PCA concentration in tape-stripped stratum corneum has been proposed as a practical biomarker for filaggrin deficiency and barrier compromise.