A Conundrum: The Science Behind Hyperpigmentation & Sensitive Skin

Hyperpigmentation is a key feature of photoaging, along with the development of wrinkles, loss of skin elasticity and facial volume. Pigmentation isn’t just a cosmetic concern—it can be a sign of underlying inflammation. Post-inflammatory hyperpigmentation for instance arises from conditions such as eczema or other forms of dermatitis, all of which are part of what is widely referred to as sensitive or reactive skin. Acne scars are also a form of hyperpigmentation, beginning with post-inflammatory erythema or redness immediately after acne resolves. This redness is a sign of inflammation, which later becomes pigmentation as the melanocytes begin to produce melanin. Melanin deposited in the superficial and deeper layers become what we know as hyperpigmentation.

Traditionally prescribed tyrosinase inhibitors such as hydroquinone reverse this process by blocking the melanin synthesis pathway. However, hydroquinone is also associated with skin irritation which can occur even with short term use. Sensitive skin for example does not respond well to hydroquinone therapy—it is possible for flare ups to occur necessitating the use of topical steroid therapy. For instance the 3-in-1 hydroquinone-retinoid-steroid formula known by its trade name Triluma was specifically created to counteract these side effects during the treatment of melasma. Such an approach isn’t a solution either—those with sensitive skin are susceptible to side effects of irritation, caused by barrier disruption.

Is it possible to treat hyperpigmentation without the use of prescription topicals? Hyperpigmentation treatment in sensitive skin types deserves a more in depth study— join me as I dive right into the science of this conundrum. I’ll share the latest research on bacterial ferment filtrates as melanogenesis inhibitors, alternative tyrosinase inhibitors and the exciting field of functional dermatology.

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