Acne vulgaris (AV) is the most common skin disorder seen in ambulatory dermatology practices in the US. As a result, advances in pathophysiology that can lead to new therapies are always of high interest. 
Our understanding of the pathophysiology of AV is evolving as new technologies have shown the presence of inflammatory pathways throughout all stages of acne lesion formation. As our understanding of the pathophysiology of AV increases, researchers can focus on targeting specific points in cascades of inflammation as they develop new therapies to treat AV. 
Conventional View of Pathophysiology. The conventional pathophysiologic model of AV states an acne lesion is initiated subclinically as follicular hyperkeratosis, which leads to formation of a microcomedone. AV then becomes apparent as closed and/or open comedones emerge, both associated with a lack of visible inflammation.1-3 Some AV lesions may progress to become visibly inflamed, appearing as papules, pustules, and/or nodules. Ultimately, AV evolves with some lesions remaining as comedones, while others progress to superficial or deep inflammatory lesions, eventually resolving with normal appearing skin, discoloration, or scarring. As each follicle goes through its own independent pathophysiologic “life cycle,” most patients present at any given point in time with a mixture of AV lesions in various stages.3
Inflammation in Acne Pathophysiology. Advances in immunohistochemistry and other research techniques have brought forth new information on AV pathophysiology. Studies have included detailed analyses of cellular infiltrates, gene expressions, and chemical messengers (e.g., cytokines, chemokines) present at different stages of AV lesion formation, including before the emergence of visible lesions. It is now known that both follicular hyperkeratosis and perifollicular inflammation occur early during subclinical development of an AV lesion.1-3 This subclinical inflammation is primarily a lymphocytic process at the outset and changes qualitatively and quantitatively as the life of the AV lesion progresses. An early inflammatory papule is associated with a greater density of lymphocytic infiltrate. Perifollicular inflammation may also be augmented with a greater infiltrate density that is more rich in neutrophils, presenting as a deeper papule, pustule, or a nodule. The latter occurs more often in association with follicular wall rupture. Although the cellular content and density of inflammation may be different among different AV lesion types, and the cellular mix and cytokines that present may change as lesions progress, inflammation is a constant and central part of an AV lesion throughout its entire life cycle.1,3
Targets of Acne Treatment. It is well recognized that pathophysiologic targets for acne treatment include comedogenesis, sebum production, androgenic mechanisms, and inflammatory pathways. Important information has been gleaned over the past decade on AV pathophysiology that may translate to development of newer therapeutic approaches. An example includes the role IL-1β in AV lesion initiation and development. IL-1β is believed to play an important role in the initiaton of AV lesions, including comedogenesis, and in the propagation of inflammation in AV.4
There is also newer information on the complex interrelationship between Propionibacterium acnes, a bacterium of the normal flora which inhabits and inflammation in AV. Different subtypes of P acnes exist, with only some strains more commonly associated with the presence of AV.5 Proinflammatory strains of Pacnes are known to induce major inflammatory cytokines IL-1, IL-8 and IL-12 in human monocytes and IL-6 in human keratinocytes, findings that support reduction in colony counts of as one of the approaches used to treat AV.6 Reduction in P acnes has been directly correlated with clinical improvement in AV.7
 
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