Occlusive hydrocolloid dressings decrease keratinocyte population growth fraction and clinical scale and skin thickness in active psoriatic plaques

doi:10.1016/0923-1811(90)90221-X

Journal of Dermatological Science

Volume 1, Issue 2, March 1990, Pages 93-96

https://doi.org/10.1016/0923-1811(90)90221-X Get rights and content

Abstract

Clinical studies suggest a therapeutic role for occlusion in the treatment of psoriasis. Previous studies, using multiparameter $RNA DNA$ flow cytometric analysis of epidermal suspensions obtained from active plaques, demonstrated increased keratinocyte growth fraction which reversed with successful medical treatment. Because keratinocyte growth fraction reflected disease activity, it was used in this study in addition to clinical evaluations in order to determine the efficacy of occlusion in the treatment of psoriatic plaques.

In each of 9 patients, scale, skin thickness and erythema were compared in one occluded and one control plaque using an analog scale. Both scale and skin thickness, but not erythema, were decreased after 2 weeks of occlusion. However after 10 weeks, no additional differences were seen when compared with assessments made after 2 weeks, suggesting that the benefits of occlusive therapy occurred early. After 10 weeks of occlusion, the keratinocyte growth fraction was significantly decreased in occluded plaques. This study demonstrates that occlusion plays a synergistic role with other therapeutic modalities in ameliorating psoriatic plaques.

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Cited by (32)

Abnormal epidermal barrier recovery in uninvolved skin supports the notion of an epidermal pathogenesis of psoriasis
2014, Journal of Investigative Dermatology
Citation Excerpt :
Psoriasis is generally considered to be an immunologically initiated disorder, which shares certain common susceptibility loci with autoimmune diseases (Zhang, 2012). Yet, both clinical experience (Gottlieb et al.,1990; Griffiths et al., 1995; Volden et al., 2001) and recent molecular studies (Mischke et al., 1996; Kim et al., 2011; Vermeij et al., 2011; Bergboer et al., 2012) support an emerging concept that psoriasis could be “driven” by a primary defect in epidermal permeability barrier function. Clinicians know well that psoriasis predictably flares during winter months (Park and Youn, 1998; Kwon et al., 2012) when the barrier is under additional stress owing to low stratum corneum (SC) hydration, which accelerates transepidermal water loss (TEWL) rates (Lin, 2009; Muizzuddin et al., 2013).
Genetics of psoriasis: Evidence for epistatic interaction between skin barrier abnormalities and immune deviation
2012, Journal of Investigative Dermatology
Citation Excerpt :
Various other successful antipsoriatic therapies such as corticosteroids, dithranol, and methotrexate may act on many points in the vicious circle, as they are found to be immunosuppressive but can also affect keratinocyte proliferation and differentiation (Gottlieb et al., 1992; Schwartz et al., 1992). Even the observed moderately beneficial effects of skin occlusion as a monotherapy could be explained by decreasing the exposure to exogenous stimuli using an artificial skin barrier (Gottlieb et al., 1990). In summary, there are now more than 25 psoriasis risk genes known, and two of them (HLA-C*06 and LCE3C_LCE3B-del) contribute a significant proportion of the population attributable risk.
Psoriasis was until recently regarded as a T-cell-driven disease with presumed (auto)immune mechanisms as its primary cause. This view was supported by clinical data and genetic studies that identified risk factors functioning in adaptive and innate immunity, such as HLA-C*06, ERAP1, the IL-23 pathway, and NF-κB signaling. Candidate gene approaches and genome-wide association studies, however, have identified copy number polymorphisms of the β-defensin cluster and deletion of late cornified envelope (LCE) 3B and 3C genes (LCE3C_LCE3B-del) as psoriasis risk factors. As these genes are expressed in epithelial cells and not by the immune system, these findings may cause a change of paradigm for psoriasis, not unlike the reported filaggrin association that has profoundly changed the views on atopic dermatitis. In addition to genetic polymorphisms of the immune system, genetic variations affecting the skin barrier are likely to contribute to psoriasis. Recent studies have shown epistatic interactions involving HLA-C*06, ERAP1, and LCE3C_LCE3B-del, which makes psoriasis a unique model to investigate genetic and biological interactions of associated genes in a complex disease. We present a model for disease initiation and perpetuation, which integrates the available genetic, immunobiological, and clinical data.
Epidermal vascular endothelial growth factor production is required for permeability barrier homeostasis, dermal angiogenesis, and the development of epidermal hyperplasia: Implications for the pathogenesis of psoriasis
2008, American Journal of Pathology
Citation Excerpt :
Although immunological models have long dominated views on the pathogenesis of inflammatory skin disease, primary inherited abnormalities in epidermal barrier function are now strongly linked to atopic dermatitis.62–65 Evidence in support of an epidermal barrier-driven (outside-inside) pathomechanism of psoriasis is also gaining traction, based on well-established clinical observations that: i) new psoriatic lesions develop at sites of external trauma (isomorphic or Koebner phenomenon)53–55; ii) severity of the psoriatic phenotype correlates with the extent of the permeability barrier abnormality66; iii) barrier restoration by occlusion alone can clear psoriatic lesions67–70; as well as iv) studies in transgenic mice with deletions/overexpression of several different epidermal proteins that develop a psoriasiform skin phenotype.71,72 Pertinently, overexpression of vegf in the epidermis of transgenic mice provokes a psoriasiform dermatosis, including prominent angiogenesis, inflammation, and epidermal hyperplasia,73 whereas conversely, pharmacological inhibition of either VEGF expression (eg, with retinoids or cyclosporin A),74,75 or angiogenesis76 can improve psoriasis.
Primary abnormalities in permeability barrier function appear to underlie atopic dermatitis and epidermal trauma; a concomitant barrier dysfunction could also drive other inflammatory dermatoses, including psoriasis. Central to this outside-inside view of disease pathogenesis is the epidermal generation of cytokines/growth factors, which in turn signal downstream epidermal repair mechanisms. Yet, this cascade, if sustained, signals downstream epidermal hyperplasia and inflammation. We found here that acute barrier disruption rapidly stimulates mRNA and protein expression of epidermal vascular endothelial growth factor-A (VEGF-A) in normal hairless mice, a specific response to permeability barrier requirements because up-regulation is blocked by application of a vapor-impermeable membrane. Moreover, epidermal vegf^−/− mice display abnormal permeability barrier homeostasis, attributable to decreased VEGF signaling of epidermal lamellar body production; a paucity of dermal capillaries with reduced vascular permeability; and neither angiogenesis nor epidermal hyperplasia in response to repeated tape stripping (a model of psoriasiform hyperplasia). These results support a central role for epidermal VEGF in the maintenance of epidermal permeability barrier homeostasis and a link between epidermal VEGF production and both dermal angiogenesis and the development of epidermal hyperplasia. Because psoriasis is commonly induced by external trauma [isomorphic (Koebner) phenomenon] and is associated with a prominent permeability barrier abnormality, excess VEGF production, prominent angiogenesis, and epidermal hyperplasia, these results could provide a potential outside-inside mechanistic basis for the development of psoriasis.
A hyperosmotic stimulus elevates intracellular calcium and inhibits proliferation of a human keratinocyte cell line
2000, Journal of Investigative Dermatology
Occlusion has previously been used to treat psoriatic plaques and was shown to improve the condition. We investigated the consequences of applying a mechanical stress, in vitro, on the HaCaT keratinocyte cell line. A mechanical load applied to cells can be mimicked by a hyperosmotic stimulus. Exposure of HaCaT keratinocytes to different hyperosmotic solutions (final osmolarity in the range 350–600 mOsm, produced by sucrose addition) resulted in an inhibition of cell proliferation after 96 h of treatment. As keratinocyte maturation is regulated by calcium levels, we measured hyperosmotic-stimulus-induced changes of intracellular calcium ([Ca²⁺]_i) by single-cell image analysis employing FURA-2/AM. The hyperosmotic stimulus produced a rapid transient 2.6-fold elevation of [Ca²⁺]_i followed by a gradual decay to the basal level. The transients originated from extracellular as well as from intracellular calcium pools and did not respond to voltage-sensitive calcium channel blockers. The hyperosmotic stimulus was shown to increase the cellular expression of involucrin, a differentiation marker, following 72 h of incubation, as measured by flow cytometry. Treatment of cells with the [Ca²⁺]_i chelator BAPTA/AM almost completely blocked the [Ca²⁺]_i elevation, but did not alter cellular growth or the induction of differentiation observed after hyperosmotic stimulus. It is suggested that treatment of keratinocytes with hyperosmotic stimulus can induce short-time effects (calcium transients) as well as long-term cellular maturation.
Signal transduction pathways in epidermal proliferation and cutaneous inflammation
1995, Clinics in Dermatology
Prolonged occlusion in the treatment of psoriasis: A clinical and immunohistologic study
1995, Journal of the American Academy of Dermatology
An occlusive dressing that is both cosmetically acceptable and long term is needed for psoriasis treatment. The mechanisms that underlie the efficacy of occlusion in psoriasis are unknown.
We performed a clinical and immunohistologic study in patients with psoriasis of the effects of occlusion, topical corticosteroid alone, and occlusion plus corticosteroid, with a new prolonged dressing as the occlusive therapy.
Nineteen patients completed a 3-week study of efficacy of prolonged occlusion dressing, fluocinonide ointment, or a combination of the two. An immunohistologic study was performed in 10 patients with psoriasis treated for 1 week with prolonged occlusion.
The combination of fluocinonide ointment and occlusion produced significantly more improvement than either treatment alone (p < 0.01). There was no significant difference between the efficacy of prolonged occlusion or fluocinonide ointment. On 4-week follow-up plaques treated with occlusion alone or combined fluocinonide and occlusion were still significantly improved (p = 0.05 and p < 0.001, respectively). None of the immunohistologic and proliferation markers assessed in psoriatic plaques was significantly affected by occlusion as compared with untreated plaques.
Prolonged occlusion is an effective therapy for psoriasis either as monotherapy or in combination with a high-potency topical corticosteroid. However, the mechanism of action of prolonged occlusion alone in the improvement of psoriasis is unknown.

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Regular paperOcclusive hydrocolloid dressings decrease keratinocyte population growth fraction and clinical scale and skin thickness in active psoriatic plaques

Abstract

J Invest Dermatol

J Invest Dermatol

J Am Acad Dermatol

Effect of plastic occlusive dressings on psoriatic epidermis

Br J Dermatol

Regular paper
Occlusive hydrocolloid dressings decrease keratinocyte population growth fraction and clinical scale and skin thickness in active psoriatic plaques