Acne and Rosacea
Acne and Rosacea
Understand the pathophysiology of acne vulgaris with regard to the interplay of different factors, Foot Pad
including the local milieu of the pilosebaceous unit, hormones, bacteria, and systemic factors.
Understand the individual steps required for comedogenesis at the level of the pilosebaceous unit.
Recognize the clinical types of acne and its common variants, as well as correlate the basic histologic
features of each.
Understand the basic proposed pathophysiology of rosacea with regard to the possible roles of the
vasculature, nervous system, environment, and skin flora.
Recognize the clinical subtypes of rosacea as well as appreciate the basic histopathologic features of
The pilosebaceous unit and sebum
Acne is centered on the pilosabecous unit.
At age 7 sebum production increases called adrenarche, and peaks in the 20’s
Sebaceous glands are made of sebocytes which accumulate lipid as they grow. Sebocytes
are secreted by holocrine secretion into the lumen of the gland then into the
Sebum composition is unique made of squalene, cholesterol, wax esters.
Regulation of sebaceous glands
Androgens are required for sebum production esp T and DHT, but don’t explain it all b/c
sebum production does not parallel androgen levels. And is not proportionately
more in men that women.
DHEAS is a weak androgen and via 5areductase is the driving force for sebum แผ่นแปะเท้า
Normal keratin is loosely organized in granules in the follicle.
Increased keratin density and decreased keratinocyte apoptosis.
Lower levels of fatty acids to dilute the keratin
IL-1 may play a role as well as there is more of this in an acne prone follicle.
Proprionibacterium acnes is a G+, non-motile, anaerobic bacterium, and may play an
important role in acne. May break down ffa’s leading to inflammation. May also
produce chemotactic factors to attract PMN’s and T cells.
Clinical manifestations of acne
Closed comedone- Inflammatory infiltrate by the lymphocyte. This grows to become the
Open comedone- or blackhead is similar in formation to closed comedone, black color is
due to melanocytes.
As the inflammation proceeds the papulopustule forms that is red and tender, and filled
with PMN rich pus blocking the follicle. daddy
Acne fulminans is severe acne known as acute febrile ulcerative acne, and is systemic,
this can be a hospitalizeable emergency.
Neonatal acne can be caused by malassezia furfur yeast
Infantile acne caused by premature DHEAS production
People working with oils and tars as well as chlorinated hydrocarbons (chloracne
Yuschenko with dioxin poison)
Drug Induced acne can be caused by steroids
Endocrine acne classical case is a woman with cystic acne, hirsutism, irregular
menstruation, fertility problems, and obesity. These all point to the hyperadrenogenic state usually caused by polycystic ovary syndrome (PCOS).
Insulin has been related to PCOS the insulin growth factor can stimulate the ovary
increasing androgen production and at the same time inhibit of a sex hormone binding globulin amplifying the problem.
Glycemic foods may contribute by increasing insulin levels.
Highest risk in fair skin northern Europeans
Defect may lie in the vascular system (patients are more likely to get migraines, and
blood flow is higher in patients, also see telangiectasia)
the organism demodex, a follicle mite, has been implicated
Stage 1: pre-rosacea, vascular flushing
Stage 2: vascular rosacea, lasting redness
Stage 3: persistent inflammed rosacea, inflamed papules and pustules, but no comedones.
Stage 4: end stage rosacea, fibrosis, sebaceous overgrowth, can get rhynophyma.
Must also keep an eye on ocular rosacea as it may cause irritation and blindness.
Steroid rosacea too can make the face “angry” looking.