Cryotherapy in acne revisited

Traditionally, freezing-related direct cellular injury is thought to be responsible for the efficacy of cryotherapy in treating acne. Acute inflammation with predominant neutrophils develops 3 to 6 h after liquid nitrogen spraying; 12 to 24 h after, the lymphocytes and macrophages are recruited. Although not fully founded in evidence, it is generally regarded that freezing causes inflammatory lesions to disappear faster than without treatment. This effect may explain cryosurgery’s superior efficacy in treating more severe subtypes of acne lesions, i.e., cysts and keloids. As shown in histological observations, cryotherapy produces cold damage to the fibrotic cyst wall, resulting in the chemotaxis of neutrophils, whose proteases will subsequently destroy the cyst wall and allow healing. Histological studies also found that cryotherapy eventually causes a reduction in myofibroblasts and mast cells in keloidal lesions, in addition to the normalization of collagen structure and organization.

Another histologic finding of cryo-treated acne lesions is vascular disruption. Histologic studies of the refrigerant sprayed on the pig skin showed vascular engorgement with extravasated red blood cells at 15 and 30 s on day zero and normal healing at a subsequent biopsy on day seven. Cryotherapy exhibited significantly better results than intralesional triamcinolone in a randomized study with 11 patients with multiple acne keloids, especially in early vascular lesions. Cryotherapy is effective in treating cystic acne, another subtype characterized by a distinct vascular component. In some patients, pyogenic granuloma-like vascular proliferations form in areas of cystic activity, suggesting that factors unique to cystic acne may play a role in this vascular proliferation. Interestingly, pyogenic granuloma itself responds well to local cryotherapy, which aligns with findings that vascular-mediated injury is responsible for the therapeutic efficacy of cryotherapy in microvascular-perfused tissue.

Possible Mechanisms of Action

Important factors that play a role in the genesis of acne formation include hormones, inflammatory mediators, Cutibacterium acnes, and genetics. Testosterone and androgens cause activation and proliferation of keratinocytes, sebaceous cells, and ductal lining cells of the hair follicle, which accumulate in the pilosebaceous unit and result in the formation of pore obstruction and more sebum production. Oxygen availability within the cells can be compromised by the pressure exerted inside the pilosebaceous unit, providing ideal environmental conditions for the growth of C. acnes, which further promotes acne formation.

Several suggested mechanisms of acne cryotherapy include restoration of microflora, improvement of skin microcirculation, normalization of follicular hyperkeratosis, improvement of sebum evacuation, and immunomodulation. Reversal of follicular hyperkeratosis initially has been suggested, based on the findings that cryotherapy induces molecular changes resulting in a decreased expression of Ki-67, an epidermal proliferation marker that is an indicator of ductal hyperproliferation during acne development.

A second suggested mechanism is the immunomodulatory action of cryotherapy, which has been also studied in a variety of disorders. Cold has an initial inflammatory effect, but an anti-inflammatory effect becomes evident 24–48 h after freezing the lesion, and faster reabsorption of the lesion occurs. Several reports showed the clinical efficacy of local cooling in the relief of inflammatory acne, producing better results in papulopustular acne than in nodular lesions. It has been noted that cold exposure induces the release of fewer proinflammatory cytokines (IL-2, IL-6, IL-8, IL-9, and TNF-α, among many others) and more anti-inflammatory cytokines (mainly IL-10). In addition, it improves humoral and cellular immunity, stimulating B lymphocytes and natural killer lymphocytes (NK cells). Local cryotherapy has been shown to decrease the level of interleukin-1β, prostaglandin-E2, and nuclear factor-κB, which are known to be elevated in inflammatory acne lesions in vivo. In keloidal lesions treated with cryotherapy, CD163+ M2 macrophages and matrix metalloproteinase-9 were significantly increased, indicating that cryotherapy-recruited macrophages supply matrix metalloproteinase-9, which function in fibrotic resolution during treatment.

Ref:

Revisiting the Role of Local Cryotherapy for Acne Treatment: A Review and Update

Nark-Kyoung Rho

J Clin Med. 2022 Dec 20;12(1):26. doi: 10.3390/jcm12010026

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