Cellulite Physiology

Cellulite Physiology

This article summarises cellular and tissue-level mechanisms behind cellulite and explains how current treatments aim to modify those processes. It is written for an audience of writers and editors who want an accurate, paraphrased summary of peer-reviewed findings.

Pathophysiology (concise)

  • Fibrous septae: The subcutaneous fat layer is partitioned by fibrous septae (collagen-rich bands) that tether the dermis to deeper fascia. When fat lobules enlarge, the septae remain fixed and pull the skin inward at tether points, causing visible dimples.

  • Adipocyte hypertrophy and lobulation: Enlarged adipocytes change the shape of fat lobules, increasing pressure against the dermis and exaggerating surface irregularities.

  • Extracellular matrix (ECM) remodelling: Alterations in collagen types, elastin degradation, and matrix metalloproteinase activity change tissue stiffness and elasticity.

  • Microcirculatory and lymphatic dysfunction: Impaired blood flow, venous stasis or lymphatic drainage can lead to interstitial fluid accumulation, hypoxia, and low-grade inflammation, which further modifies ECM and septal structure.

  • Low-grade inflammation: Inflammatory mediators and macrophage infiltration may accompany ECM remodelling and fat hypertrophy, contributing to structural change rather than being a primary cause.

Genetic and hormonal influences

  • Genes: Polymorphisms in ACE and HIF1A have been associated with differences in connective tissue response and hypoxic signalling in adipose tissue.
  • Hormones: Oestrogens, catecholamines, insulin, thyroid hormones and prolactin influence fat distribution, microcirculation and ECM turnover. The precise causal links remain under study.

Clinical correlation and grading

  • Superficial dimpling (grade III) often corresponds to small depressions tied to taut septae and mild lobular hypertrophy.
  • Deeper nodularity (grade III) may involve fibrotic septae, more pronounced lobule enlargement and ECM stiffening.

Treatments and their mechanisms (overview)

  • Topicals: Caffeine, retinoids and other actives claim to transiently reduce oedema or stimulate dermal remodelling; effects are generally modest and short-lived.

  • Mechanical suction and massage: These improve lymphatic drainage and microcirculation temporarily and may redistribute interstitial fluid, smoothing appearance for short periods.

  • Radiofrequency and ultrasound: These energy-based modalities heat dermis and subcutaneous tissue to stimulate collagen remodelling and tighten skin; multiple sessions are usually required.

  • Subcision and enzymatic release: Mechanical or enzymatic cutting of tethering septae (subcision or collagenase) can produce lasting improvement in focal depressions by releasing the fibrous attachments.

  • Lipolytic and body-contouring procedures: Targeted fat reduction changes lobule size but must be balanced to avoid creating surface irregularities when volume is removed unevenly.

Safety and evidence

  • Evidence quality varies; many devices and creams show short-term cosmetic improvement rather than a permanent cure.
  • Invasive procedures carry procedure-specific risks (infection, bruising, contour irregularities) and should be performed by qualified clinicians.

Writing tips for authors

  • Use anatomically precise metaphors: "tethered bands" (septae), "soft lobules" (fat lobules), "shallow dimples" (superficial grade) help convey realistic texture.
  • Combine sensory and emotional description: pair tactile detail with a character's internal reaction to make scenes feel grounded.

References

  • Khan MH, Victor F, Rao B, Sadick NS. Treatment of cellulite. Part I. Pathophysiology. J Am Acad Dermatol. 2010;62(3):361-370.
  • Khan MH, Victor F, Rao B, Sadick NS. Treatment of cellulite. Part II. Advances and controversies. J Am Acad Dermatol. 2010;62(3):373-384.