Evolving perspectives on the etiology and pathogenesis of acne vulgaris.
As the pathophysiology of acne is complex and multifactorial, the continued influx of new basic science and clinical information requires careful analysis before drawing conclusions about what truly contributes to the development and progression of this chronic disease. Our objective is to review the latest evidence and highlight a number of important perspectives on the pathophysiology of acne. An improved understanding of acne pathogenesis should lead to more rational therapy and a better understanding of the role of P acnes opens new perspectives for the development of new treatments and management. Further research may be directed at targeting receptors, adhesion molecules, cytokines, chemokines or other pro-inflammatory targets implicated in the activation of immune detection and response (i.e., toll-like receptors [TLRs], protease-activated receptors [PARs]) that appear to contribute to the pathophysiology of acne. Therapeutic options that reduce the need for topical and/or oral antibiotic therapy for acne are welcome as bacterial resistance to antibiotics is a clinically relevant concern both in the United States and globally.
Lawrence F
LF
Eichenfield
James Q
JQ
Del Rosso
Anthony J
AJ
Mancini
Fran
F
Cook-Bolden
Linda
L
Stein Gold
Seemal
S
Desai
Jonathan
J
Weiss
David
D
Pariser
Joshua
J
Zeichner
Neal
N
Bhatia
Leon
L
Kircik
D000152:Acne Vulgaris / Q000175:diagnosis* / Q000209:etiology* / Q000628:therapy; D000900:Anti-Bacterial Agents / Q000008:administration & dosage; D003879:Dermatologic Agents / Q000008:administration & dosage; D006801:Humans; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011425:Propionibacterium acnes / Q000187:drug effects / Q000302:isolation & purification; D012629:Sebum / Q000378:metabolism
D000900:Anti-Bacterial Agents; D003879:Dermatologic Agents