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Acne Vulgaris(AV) Pathogenesis:

Abstract

It is the most common skin disorder(D/O), regardless of gender, skin color or ethnicity. For a long time it was thought it is due to abnormal desquamation of the keratinocytes and hyperkeratinization of the sebaceous glands which causes acne lesions. However the pathogenesis of acne believed to be due to an inflammatory skin D/O which is present before the acne lesions manifestation.

Introduction

AV is a chronic inflammatory skin D/O which involves pilosebaceous unit. It is a a most pervasive skin D/O regardless of gender, skin color and ethnicity.

For many years it is thought acne lesions develop due to hyperkeratinization and abnormal desquamation which facilitated by increase in circulating androgen during puberty.

It is thought the above development provides a medium which Propionibacterium Acne colonizes. This will result in inflammatory and chemotactic elements and inflammation.

However recent studies shows subclinical inflammatory cells before and during hyperkeratinization and manifestations of microcomedone.

Further investigations like biopsies, showed inflammatory cells like CD3, CD4, Interleukin (IL1),

And macrophages are present even in normal appearing skin of AV patients as well as in acne lesions.

The paradigm of pathogenesis of AV has shifted from a simple hyperproliferation of sebaceous glands to an inflammatory skin D/O.

The role of Propionibacterium Acne (P.acnes)in pathogenesis of AV

The exact mechanism of P.acnes in AV still under study, however considerable evidence delineates its involvement in AV.

Studies have shown P.acne activates cytokine and other inflammatory responses via its receptors.

In addition P.acnes has several genotypes 1, 2 and 3 also subtype A and B. type 1A has an extremely high association with acne.

Gene Array profiling

In lieu of evidences of chronic subclinical inflammatory process in the pathogenesis of AV and discovering numerous biomarkers in the process AV, gene expression profiling in AV been studied which revealed 211 genes been upregulated in the biopsies of the AV lesions.

 

AV and scarring

AV patients has different responses to scarring base on their initial cell mediated immune response type. Patients with less prone to AV scarring shows more CD4, T-cell and macrophage and more HLA DR. Also shows more angiogenesis in early stage of AV legions developments.

Conclusions:

Recent discoveries has changed the pathogenesis of AV from a primarily a hyperproliferative D/O of pilosebaceous unit to chronic inflammatory skin D/O.

Furthermore it also been discovered that not all type P.acne are involved in AV lesions which further supports the AV not primarily an infectious disease as it is rather an inflammatory D/O.

Furthermore the inflammation continues even after the resolution of papules and pustules.