How does hormone fluctuation contribute to acne pathophysiology?
Hormone fluctuations, particularly increases in androgens, stimulate sebaceous glands to produce more sebum, leading to clogged pores. This environment fosters the growth of Propionibacterium acnes bacteria and inflammation, contributing to acne development. Hormonal changes during puberty, menstrual cycles, and stress can exacerbate this process.
What role do bacteria play in acne pathophysiology?
Bacteria, particularly Cutibacterium acnes, contribute to acne pathophysiology by colonizing hair follicles, breaking down sebum, and provoking an inflammatory response. Their proliferation can lead to follicular rupture and further inflammation, exacerbating acne lesions.
What is the role of inflammation in acne pathophysiology?
Inflammation is a crucial component of acne pathophysiology, as it occurs in response to the proliferation of Cutibacterium acnes within the clogged pilosebaceous unit. This immune response leads to the formation of inflamed lesions like papules, pustules, and cysts, exacerbating the severity and persistence of acne.
How does diet impact acne pathophysiology?
Diet impacts acne pathophysiology by influencing hormonal levels and insulin signaling. High glycemic index foods can increase insulin and insulin-like growth factor-1 (IGF-1), promoting sebum production and acne. Dairy products may also elevate IGF-1 and androgens, exacerbating acne. Reducing these foods may help alleviate acne symptoms.
How does excess sebum production contribute to acne pathophysiology?
Excess sebum production leads to acne by clogging hair follicles, creating an environment conducive to the proliferation of Cutibacterium acnes bacteria. This accumulation of sebum, along with dead skin cells, triggers inflammation and the formation of comedones, papules, and pustules characteristic of acne lesions.