As dermatologists, acne is the bread and butter of our practice, yet the disease harbors many mysteries as to the sequence of events leading to the development of its lesions. Acne is a disease that leaves lasting physiological and physical scars. Many of our patients feel exceptionally self-conscious about their skin with even a mild breakout. Teenagers will plead to stay home from school, and our adult patients may choose to work from home. Are our patients paranoid, or is society judging them negatively purely because of the fact that they have acne? A study was conducted asking both adults and teenagers to assign attributes to a young woman shown in a photograph. The same woman was depicted in one photograph with a clear complexion and in another with a mild acne eruption. Both adults and teenagers were more likely to assign positive attributes (intelligent, happy, healthy, trustworthy) to the clear-skinned woman,1 whereas the young woman depicted with mild acne was perceived as shy, stressed, and boring. This study highlighted the importance of proper and aggressive treatment for our acne patients.
As we attempt to develop a better understanding of this complicated disease, basic tenets of the pathophysiology of acne have been reexamined. The traditional view of acne lesion progression is that the microcomedone is the initiating event in the development of all acne lesions. This subclinical lesion forms from abnormal keratin desquamation and excess sebum production, along with proliferation of Propionibacterium acnes. Both noninflammatory and inflammatory lesions develop from this primary lesion. If P acnes proliferates and generates inflammatory mediators, inflamed papules and pustules develop. In addition, inflammatory lesions may develop from noninflammatory lesions.2,3
Recent studies suggest that subclinical inflammation may precede the development of the microcomedone. Jeremy et al conducted an immunohistochemical study to determine whether inflammatory events occur pre- or posthyperproliferation of the follicular epithelium.4 They examined biopsies from patients with acne in both involved (n=12) and uninvolved (n=20) areas of the back. As a control, they looked at back-skin in patients without acne (n=10). Inflammatory markers such as T cells, neutrophils, macrophages, α6-integrin, and interleukin (IL)-1 were examined and compared. Significant inflammatory factors were identified around clinically normal follicles of uninvolved skin from acne patients before epithelial hyperkeratinization. These findings included large numbers of CD4+ T cells over and above the constitutive level of surveillance T cells in normal skin, accompanied by a large macrophage presence equivalent to that seen in clinically apparent early (<6 hours) inflamed lesions. In addition, levels of IL-1 were upregulated around hair follicles in uninvolved skin, and aberrant integrin expression was observed in the epidermis around these uninvolved follicles as well as inflamed lesions. Thus, this study provides evidence for the involvement of inflammatory events in the very earliest stages of acne lesion development.
Recent evidence suggests not only that inflammation may be a primary event in acne, but that it may persist throughout the lesion life cycle. Seventy-seven percent of biopsy specimens of atrophic scars demonstrate inflammatory cell infiltrates.5 In addition, the residual dyschromias reveal inflammation in persistent inflammatory erythema and persistent inflammatory hyperpigmentation.6 Moreover, P acnes promotes inflammation not only as a viable microorganism, but also because even its nonviable state is proinflammatory and is slowly degraded.7
Propionibacterium acnes plays a central role in the pathogenesis of acne. It is controversial as to whether P acnes colonization is a primary event or a secondary event in lesion initiation.8