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Role of Inflammation in Acne Pathology

Role of Inflammation in Acne Pathology

 

Acne vulgaris is a condition of the skin that results when the hair follicles are clogged with oil and dead cells of the skin. It usually appears in areas of the skin that has a large number of the oil glands such as the face, neck, back, upper part of the chest and shoulders. It is also called acne, and it is most common in teenagers, and it has a prevalence of 70-80%. Depending on the severity of the condition, it might result in emotional distress and scaring of the skin. Pathology is the study of causes and the effects of disease while inflammation is the response that is triggered by damage of the body tissues. The purpose of this paper is to review the current understanding of the acne pathology while focusing on the role that inflammation has.

Inflammation has been considered to be involved significantly in the development of acne. Evidence from the clinical platform, histological and immunological areas have supported the involvement of inflammation (Tanghetti, 2013). Most of the studies that have been done provide evidence for inflammatory involvement. For example, in a study that involved histological examination of early acne lesion, the biopsied lesions showed morphological characteristics of small papules with little erythematous flare. More than half of them were considered as microcomedones.

In the study, lymphoid perivascular infiltrate was found to be among the earliest histological changes that occurred. In the later stages, there was an accumulation of the polymorphonuclear leukocytes which results in distension and formation of pustules. The distension is followed by distention which then causes rupture of the lesion (Tanghetti, 2013). This shows that inflammatory foci develop early and thus giving evidence of early inflammation involvement.

              Besides, there is evidence that indicates the involvement of inflammation in all the developmental stages of the acne vulgaris lesions. In the early stages, there is the presence of the microcomedones and comedones while in the late stages, there are inflammatory pustules, papules, and nodules (Tanghetti, 2013). The inflammation in both stages has been implicated to the presence of proinflammatory mediators. There is evidence of inflammation during the early stages of acne development, and they include, the up-regulation of the proinflammatory mediators, proinflammatory role of the sebaceous lipids, the early involvement of the TLRs and PPARs, and the likelihood of neurogenic component facilitated by the up-regulation of the neuropeptide.

            Furthermore, emerging data have therefore considered acne vulgaris as a primary inflammatory condition (Tanghetti, 2013). This has been supported by the available immunological, histological and clinical evidence because they suggest the involvement of inflammation in all the stages. The immunochemical pathways which show the establishment and the development of the inflammatory process are complex, and it has not been fully clarified. However, there may be an involvement of the P. acnes.

             However, the inflammatory response was found to occur even when P. acnes was not present, but in both early and late acne development stages, the must be an existence of other pathways of inflammation for the activations and progress of the condition (Dreno et al., 2015). It is therefore clear that inflammation plays a vital role in the development of all acne vulgaris lesions. Sufficient evidence is available to prove that, and consequently, it will be wrong to consider the early stages of acne vulgaris as non-inflammatory.

 

 

 

References

Dreno, B., Gollnick, H. P. M., Kang, S., Thiboutot, D., Bettoli, V., Torres, V., ... & Global Alliance to Improve Outcomes in Acne. (2015). Understanding innate immunity and inflammation in acne: implications for management. Journal of the European Academy of Dermatology and Venereology, 29, 3-11.

Tanghetti, E. A. (2013). The role of inflammation in the pathology of acne. The Journal of clinical and aesthetic dermatology, 6(9), 27.

624 Words  2 Pages
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