The Cervicogenic Pathogenesis Hypothesis of Melasma: A Mechanical Model Based on the "Investing Fascia–Six-System Coupling"

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Authors

Publication Details

Journal
Zenodo (CERN European Organization for Nuclear Research)
Published
2026-09-12
DOI
https://doi.org/10.5281/zenodo.22721259
Primary Topic
Dermatologic Treatments and Research
Type
preprint
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preprint

The Cervicogenic Pathogenesis Hypothesis of Melasma: A Mechanical Model Based on the "Investing Fascia–Six-System Coupling"

Xuefeng Huang
Zenodo (CERN European Organization for Nuclear Research)
Dermatologic Treatments and Research
preprint

The Cervicogenic Pathogenesis Hypothesis of Melasma: A Mechanical Model Based on the "Investing Fascia–Six-System Coupling"

Xuefeng Huang
preprint en

Abstract

Melasma is a chronic, recurrent hyperpigmentary skin disorder. The conventional pathological model centers on ultraviolet-induced melanocyte activation, sex hormone–driven melanin synthesis, and skin barrier dysfunction. However, even with adequate photoprotection and standard treatment, a considerable proportion of patients show limited response and frequent relapse, suggesting the existence of pathogenic pathways that have not been fully recognized. In recent years, research on fascial biomechanics, autonomic regulation, and mechanosensitive channels has provided new perspectives for reexamining the pathogenesis of melasma. This article proposes the "cervicogenic investing fascia mechanical constraint" hypothesis. Factors such as prolonged forward head posture, chronic stress, and aging may synergistically drive fibrotic remodeling of the cervical investing fascia. After the loss of elastic buffering, abnormal shear stress generated by daily micro-movements of the head and neck may be transmitted through the three-layer deep cervical fascia network to the carotid sheath, potentially increasing intra-sheath hydrostatic and tissue pressure. This pressure elevation may serve as a common physical signal, affecting the intra-sheath artery, vein, sympathetic trunk, and vagus nerve, and may influence the lymphatic and glymphatic systems through mechanical transmission and venous return coupling. Accordingly, six systems in facial skin may develop functional abnormalities: decreased arterial perfusion and tissue hypoxia; impaired venous return and oxidative stress; lymphatic compression leading to impaired clearance of pigment particles and inflammatory metabolites; reduced glymphatic driving force leading to retention of central stress waste and sustained activation of the hypothalamic–pituitary–adrenal (HPA) axis; sympathetic–sensory nerve interaction leading to neuropeptide release and melanocyte activation; and parasympathetic nerve compression leading to failure of the cholinergic anti-inflammatory pathway. These six system pathways may amplify each other through multiple positive feedback loops, forming a vicious cycle of "mechanical abnormality → increased intra-carotid-sheath pressure → impairment of the six systems → pigmentation → posture worsening → mechanical abnormality aggravation." Based on this, the article proposes a six-system weighted subtyping model and designs testable predictions and a three-stage validation framework based on shear wave elastography (SWE) and multimodal skin imaging. It should be emphasized that this hypothesis remains theoretical, and its core causal chain has not yet been directly validated in patients with melasma.

Zenodo (CERN European Organization for Nuclear Research)
Good health and well-being
Dermatologic Treatments and Research
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