A significant breakthrough in understanding the causes of hypersensitivity in sensitive skin was presented at the 50th Convention of the Japanese Cosmetic Science Society. Researchers from the Kao Company highlighted the role of epidermal tight junctions in skin discomfort and offered promising solutions for the 71% of adults with sensitive skin. Their research earned the Convention President’s Award at the society’s annual event, underscoring its potential for advancing dermatological science.
Identifying the Issue
Kao’s Skin Care Research Laboratory, led by Kenji Kabashima, MD, PhD, chair and professor of dermatology at Kyoto University’s Graduate School of Medicine, discovered that sensitive skin contains a higher number of nerve fibers closer to the skin surface — reaching just below the stratum corneum at the granular layer of the epidermis — compared with healthy skin.
This layer contains structures known as tight junctions that keep cells in close contact to prevent the entry of foreign substances and the evaporation of moisture. They also help maintain nerve fiber positioning deeper within the epidermis.
In atopic dermatitis, however, it is believed that the weakening of the tight junctions allows nerve fibers to extend to just below the stratum corneum where they can cause discomfort. This suggests that tight junction dysfunction may play a role in skin sensitivity, which can include barrier compromise, vasomotor instability, and heightened neurosensory awareness.
Examining claudin-3, a structural component of tight junctions, researchers found a reduction in its expression in sensitive skin that could potentially contribute to tight junction dysfunction. This impairment could allow nerve fibers to extend closer to the skin’s surface, triggering sensations like tingling and burning.
In order to further investigate this mechanism, researchers conducted comprehensive gene expression analysis of skin tissue. They then assessed the transepithelial electrical resistance (TEER) value — a known indicator of barrier integrity — in normal human epidermal keratinocytes with selectively reduced claudin-3 activity. Results showed that TEER values decreased significantly, demonstrating claudin-3’s contribution to tight junction function.
These findings suggest that discomfort in sensitive skin may be triggered by increased nerve fiber invasion deep into the stratum corneum, likely due to decreased epidermal tight junction integrity with suppressed claudin-3 expression.
A Promising Solution
Dr. Kabashima’s team also explored potential remedies designed to improve epidermal tight junction function and reduce discomfort. They found that γ-amino-β-hydroxybutyric acid, an amino acid derivative, enhanced the performance of tight junctions.
A subsequent eight-week clinical trial involving 40 women with sensitive skin tested a prototype formulation containing this ingredient.
Results demonstrated that:
- The formulation significantly reduced discomfort
- Participants reported decreased tingling and burning sensations
These outcomes indicate that enhancing tight junction function using γ-amino-β-hydroxybutyric acid may offer a meaningful approach to alleviating symptoms in sensitive skin.
Conclusion
The research reveals that altered nerve fiber distribution within the epidermis may be a key contributor to sensitive skin, with decreased claudin-3 expression implicated in tight junction dysfunction. By enhancing the function of tight junctions through continuous use of a formulation containing γ-amino-β-hydroxybutyric acid, characteristic tingling and burning sensations in sensitive skin decreased.
Kao Laboratory plans to continue its research into the structure and function of the skin. Their goal is to deepen the fundamental understanding of sensitive skin and develop technologies that will improve the quality of life for affected individuals.
