Pathogenesis of acne vulgaris

      Pathogenesis of acne vulgaris is complex, influenced by many factors and sometimes controversial. There are four important things that is associated with acne, which is an increase in sebum secretion, keratinization of the follicle, bacteria, and inflammation (inflammation).

1. Increased secretion of sebum
          The first factor that plays a role in the pathogenesis of acne is the increased production of sebum by the sebaceous glands.  Patients with acne will produce more sebum than those not exposed to the quality of sebum on acne though both groups were similar. One component of the sebum triglycerides may play a role in the pathogenesis of acne. Triglycerides are broken down into free fatty acids by Propionibacterium acnes , the normal flora found on pilosebacea unit. Free fatty acids are then led to the colonization of Propionibacterium acnes , provoking inflammation and can be comedogenic
         Androgen hormones also affect the production of sebum. Similar to the activity on keratinocytes infundibuler follicular, androgens bind to and affect the activity sebosit. People with acne have elevated androgen serum is higher than with people who are not affected by acne. 5a-reductase, an enzyme responsible for converting testosterone into DHT potent in its activity is increased in the body of a predilection for the onset of acne on the face, chest and back.
      The role of estrogen in the production of sebum is not known with certainty. Estrogen dose required to reduce sebum production is much greater when compared with the doses required to inhibit ovulation. Mechanism by which estrogen may play a role is to directly counteract the effects of androgens in sebaceous glands, inhibiting production of androgens in gonadal tissue through negative feedback of gonadotropin releasing hormone, and regulate gene that suppresses the growth of sebaceous glands or lipid production.

2. follicular keratinization  
        Follicular epidermal hyperproliferation results in the formation of the primary lesion of acne is the microcomedo. The top of the hair follicle epithelium, the infundibulum into hyperkeratosis with increased cohesion of the keratinocytes. Excess cells and cohesion forces cause the formation of the ostium follicular plug. Plug is then led to the concentration of keratin, sebum, and bacteria accumulate in the follicle. This then leads to widening of the upper hair follicle, which then form the micro-comedo. Stimulus for keratinocyte proliferation and increased adhesion is still unknown. But there are several factors that allegedly led to hyperproliferation of keratinocytes that androgen stimulation, decrease in linoleic acid, and increased activity of interleukin (IL)-1a. Androgen hormones may play a role in keratinocyte follicular to cause hyperproliferation. Dihydrotestosterone (DHT) is a potent androgen which plays a role against the onset of acne. 17ß hydroxysteroid dehydrogenase and 5a-reductase is an enzyme that acts to convert dehydroepiandrosterone sulfate (DHEAS) into DHT.
         When compared with epidermal keratinocytes, follicular keratinocytes showed increased activity of 17ß-hydroxysteroid dehydrogenase and 5a-reductase, which in turn increases the production of DHT. DHT can stimulate the proliferation of follicular keratinocytes. Another thing that supports the role of androgen in the pathogenesis of acne is that in people with complete androgen insensitivity are not affected by acne.
       Follicular keratinocyte proliferation is also regulated by the presence of linoleic acid. Linoleic acid are essential fatty acids in the skin that will decline in people affected by acne. Quantity of linolic acid will be back to normal after treatment with isotretinoin. Linoleic acid levels can lead to abnormal follicular keratinocyte hyperproliferation and the production of proinflammatory cytokines. There is the assumption that linoleic acid is produced by a fixed quantity but will experience dilution due to increased production of sebum. IL-1 also has a role in the hyperproliferation of keratinocytes. In human follicular keratinocytes showed hyperproliferation and formation of micro-comedones when given IL-1. IL-1 receptor antagonists may inhibit the formation of microcomedone.

3. Bacterium
     The third factor that is bacteria. Propionibacterium acnes also has an active role in the inflammatory process that occurs. Propionibacterium acnes  is a gram-positive bacteria, anaerobic, and microaerobic found in sebaceous follicles. Teens with acne have a higher concentration of Propionibacterium acnes  than normal people. However there is no correlation between the number of Propionibacterium acnes  found on the sebaceous gland and severity of disease.

4. inflammatory
      At first, it has been suggested that the inflammatory process following the formation of blackheads, but there is new evidence that dermal inflammation actually precedes the formation of blackheads. Skin biopsies taken at that do not have blackheads and acne tends to show an increase in dermal inflammation compared with normal skin. A skin biopsy of the newly formed blackheads inflammatory activity showed a much more powerful. Microcomedones will expand into keratin, sebum, and bacteria are more concentrated. Although this expansion will cause distension resulting in follicular wall rupture. Extrusion of keratin, sebum, and bacteria into the dermis resulting in a rapid inflammatory response. The dominant cell type in the first 24 hours of rupture of comedones are lymphocytes. CD4 + lymphocytes were found around pilosebacea unit, where CD8 + cells found in the perivasculer. One to two days after the rupture of comedones, neutrophils become the predominant cells that surround microcomedones.
     The fourth element of the pathogenesis of acne are hyperproliferation follicular keratinocytes, seborrheic, inflammation, and Propionibacterium acnes are the steps that are interrelated in the formation of acne.

Do you wanna know more informations about acne?
check here!
1. About Acne Vulgaris
2. What are causes of Acne Vulgaris?
3. Clinical Manifestasions and Classification of Acne
4. How to diagnose Acne Vulgaris?

5. What are skin diseases which similar with acne vulgaris?
6. How to treat Acne Vulgaris?

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