Knowledge of the way in which acne lesions evolve is a prerequisite of any adequate interpretation of histological and  immunological  studies.  Similarly,  the  development of animal or human models of inflammation requires this type of background information.

 

  The  morphogenesis of acne lesions is  a  dynamic process. Most  lesions exhibit  a polymorphic  appearance, rather than resolve directly.' The inflamed lesions represent a compromise between  the production of active  mediators,  and  the  response  to  them. This involves a  whole  range of  reactions  that  determines whether a lesion progresses or  resolves.

 

  Development of lesions can be accurately recorded by tracing over  them onto transparent sheets uniquely positioned on the skin. This is called mapping-out,  and the delineated sheets, maps . If lesions are mapped-out once, and then again after several hours, 'new' lesions can be identified, and reinspected over a period of time, to observe their changing morphology.

 

The mean lifespan of less active papules is five days and active papules, nine days; less active pustules, five days and active pustules, six days. Nodules can exist for over four weeks. We have no data on cysts; clinical observation indicates that they are very slow to resolve and may remain for  some months. Not surprisingly, the most active lesions  survive the longest.

However, it is not possible to  predict precisely how long an individual lesion will last when it first appears. This depends upon several integrated factors initially, depending on the original lesion type, and the extent of inflammation, but this may be modified by the nature of any intermediate phases produced  during its subsequent development or resolution. There is no set pattern of behaviour characteristic  for each morphogenic type, but there is a tendency to follow one or two routes.

Less active  papules predominantly resolve via a macule; for them the popular routes are either to become more or less inflamed or pustular. Less active pustules mostly resolve via a macule or become papular.  Active  papules,  active pustules and  nodules mainly resolve via a less active lesion and subsequently through a macular phase. The following fundamental trends are observed: Most acne lesions:

1 Do not resolve directly but usually via other interme  diate stages which can represent either development or regression, before finally disappearing. All active lesions tend to  produce intermediates, but  some lesions can disappear very  quickly - within twenty  four hours.

2 Only exhibit one other stage, some display two, but few  have three or four.  Lesions  may produce their original form again as a secondary or tertiary change.

3 Disappear as a resolving macule (the most predomi  nant intermediate). Macules can  be very persistent, lasting, in some instances, 2-3 weeks. They contri  bute markedly to the  inflamed appearance of acne, presenting a serious  cosmetic  problem  during the recovery  stage. The  more active lesions  tend to persist for longer as macules. The only other published data on the morphogenesis of acne lesions was by Orentreich and  Durr2 who investigated,  by serial photography over  four months,  one male  patient  with  moderate  acne.  It  is  difficult to generalize from one patient since there may be patientto-patient variation, but these authors' data showed that inflamed lesions commonly lasted an average of thirteen days and arose from blackheads or whiteheads. Orentreich and Durr found that some blackheads could remain unchanged for as long as three months before becoming inflamed. This author's department has not investigated blackheads.

However,  it was found  that some whiteheads may undergo resolution without involving  an obvious  inflamed  lesion; 67 per  cent of whiteheads resolve within  four days while 33 per cent develop into inflamed lesions. Inflamed lesions  that arose from a clinically obvious whitehead had a longer lifespan than those that did not. This data supports the long-held suggestion that  inflamed  lesions often arise from noninflamed lesions.  Early inflamed papules have been observed to arise in similar proportions,  directly or via a  mature comedone, both whiteheads and blackheads to an equivalent degree; 51 per cent of inflamed lesions arose without clinical evidence of a comedone.

 

  Investigations  into the morphogenesis of acne lesions are not easy to conduct since they demand regular visits by patients. It is  not known what physiological factions influence the lifespan of inflamed lesions. For example, site, sex, menses, duration of acne and its severity could modulate  their progress. Our technique of mapping lesions could provide the basis for a human model to investigate the  effect  of physiological features  and various therapies on the morphogenesis of acne lesions.

 

  Several  investigations have been performed to study the effect of biological materials injected intradermally into the skin. Strauss and Kligman found that injection of sebum produces an intensive lymphocytic infiltrate.

3 The biopsies were taken one  week after injection so early changes were not investigated. Central necrosis was common and ulceration of the epidermis was also seen. Intradermal comedonal material produced a greater  inflammatory response but no comment was made as to the predominent cell type except that giant cells were common. Removal of free fatty acids reduced the inflammatory response.

 

  Injections of similar quantities of sebum, comedone and bacteria  showed that comedonal  material evoked the greatest inflammatory reaction.

4 The inflammatory response was also polymorphonuclear.

 

  Dalziel  and Marks have developed a model of acne inflammation by injecting cornefied (callus) material into guinea-pigs and humans. 5 An intensive polymorphonucleocyte response occurs and giant cells are also a universal feature. Although this system may be a model of late-stage acne inflammation, it does not reflect the more subtle changes or early acne inflammation.