4th Cause of Acne (out of 4 main causes)

The exact mechanism of inflammation in acne is not clear. A comedone is present in about 88% of inflamed papules and duct rupture is seen in one third of papular in 36 hours after the onset of inflammation. But two third of ducts are ruptured by 72 hours. Inflammatory mediators (interleukins, tumor necrosis factor TNF & prostaglandins) move through the duct into the dermis. The inflammation in dermis is not produced by bacteria but it is most likely due to inflammatory mediators that diffuse from follicles which are produced by the microorganism P. acnes.

As the lesion (inflammation) progress, prior to duct rupture the inflammation is of type IV immunological reaction. Later on in moderate and severe inflammation, duct rupture and a macrophage giant cell foreign body reaction takes place. There is also activation of classical and alternative complement pathways.

P. acnes are the source of antigenic stimulus. P. acnes produces three proteases (enzyme which break protein), lipase and phosphates enzymes in vitro, all of these may be responsible for inflammation .

The cell wall of P. acnes if broken down is a potent chemo attractor of polymorphonuclear and mononuclear cells. P. acnes also produce a prostaglandin like substance, that is why non-steroidal anti inflammatory drugs (NSAIDS) have an anti acne effect.

Cytokines also play a role in the inflammation in acne. Ductal cells produce interleukin (IL-1-? & IL-?) and TNF which are inflammatory mediators. Leukotrienes B4 (LTB4) is an inflammatory mediator which is synthesized from arachidonic acid, a free fatty acid. Synthesis of LTB4 is catalyzed by 5-lipoxygenase enzyme and increased by inflammatory mediators. Leukotriene precursors (from which a drug is formed) are produced in sebaceous glands. Almost all the above events are independent of bacteria.

In an study with anti inflammatory drug, it was seen that in three months there was 70% reduction of inflammatory lesions which suggest that bacteria are not always involved in inflammation in acne. Some authors suggest that there is systemic involvement in the pathogeneses of acne. This is supported by the fact that antibodies against P. acnes a type of polypeptides are found in patients with acne, but not in normal subjects. But this may be due to some lipids entering circulation when duct ruptures and causing immunologic reactions.

Finally in summery acne patients are not immunological misfit, but some immunological reaction though take place.

Related Posts

Leave a Comment

Loading...