The major dermatological textbooks give contradictory statements about the initial events of acne inflammation. Until 1987 the lymphocyte was usually reported to be the initial inflammatory cell.

 

  Strauss and Pochi stressed the importance of the lymphoid series in lesions aged about 2-7 days.4 They describe how the early inflammatory changes are of two types, both of  which  involve  rupture  of  follicular structures. In the  first type of inflammatory lesion, small areas of rupture occur in the follicular wall of normal-appearing  sebaceous follicles.

This  type  of change may actually be seen in the normal individual and, in this instance, presumably heals without further progression. However, in the second type of inflamed lesions, the rupture is generally more extensive and may lead to complete follicular collapse and the formation of an inflammatory pustule. These authors emphasize that the onset of inflammation is often at the site of a closed comedo, where the initial change leading to inflammation is  a  small rupture  in the wall of the  comedo. Adjacent to the area of rupture in both types of lesions is a lymphocytic infiltrate in the dermis. Bacterial stains of histological  sections of the small microscopic breaks did not show any bacteria in this region.

 

  However, the  role of polymorphonucleocytes in the early acne inflammatory phase was emphasized by Kligman who observed that microscopic rupture of the sebaceous follicle is the event that precedes the clinical inflammatory lesion.6 At times he identified invasion of 'intact' follicular epithelium by neutrophils which could also be identified in the lumen  of the follicles at these points,  suggesting increased permeability of the duct epithelium. This implies that  there are chemotactic factor  activators or direct chemotactic  factors which leak out of microscopically intact  follicles and attract neutrophils into  the  site. This author's department would emphasize, from  their own data,  that chemoattraction of polymorphs is an important factor but that in many  early lesions chemoattraction for  lymphoid cells is more relevant.

 

  Subsequent  to Kligman's publication6 the  idea that polymorphonucleocytes are the initiating inflammatory cells, many dermatologists have accepted this as fact. This author's department therefore thought it necessary to reinvestigate the problem7 and ask two questions. What is the initial inflammatory cell and is duct rupture necessary for the development of inflammation? Sixtynine  early inflamed  lesions  have been  investigated.

Periductal focal infiltrate was less frequently seen than a perivascular infiltrate. The polymorphonucleocytes were maximally seen at sixty-seven hours duration, and were more evident  when there was disruption of the duct wall. This dichotomy of distribution is not readily explained. Intraductal polymorphonucleocytes were an almost universal feature of pustules.

 

  In active papules and nodules greater damage of the duct and gland is evident as are macrophages and giant cells.

 

  Dermatologists frequently tell students  and general practitioners that disruption of the follicular wall is an early feature of acne inflammation. However,  in the investigation of this author's department of timed biopsies, disruption of the duct wall was seen in only 14 per cent at six  hours and in  18  per cent at seventy-two hours.

 

  Inflamed  lesions were associated most  often with obvious distension of the pilosebaceous duct but 8 per cent were not obviously distended. In 9 per cent of the lesions there was a definite whitehead, in 27 per cent a definite blackhead, but  in 52 per cent the inflamed lesion arose at the site of a microcomedone.

 

  Table 13.4 shows that in the  early lesions there  is neither spongiosis nor duct rupture in 67 per cent. In only 39 per cent of three-day-old inflamed lesions was there partial or complete destruction of the duct wall. Even at three days 33 per cent of the inflamed lesions show little damage to the duct wall.

 

  Thus, the development of an early inflamed lesion does not depend  on the  presence  of duct rupture (and/or a clinically obvious comedone).  It is also clear that the initial cell in acne inflammation  is the lymphocyte and not the polymorphonucleocyte.  Monoclonal antibody stain showed the lymphocytes to be predominantly T helper  cells. The number of  each subset of lymphocytes was in keeping with a normal response to antigens and not a disturbance of the immune status.

 

  Thus, these data suggest that in the development of early inflamed lesions the inflammation is due  to the diffusion of small molecular weight substances from the duct to produce chemoattraction, initially for lymphocytes and subsequently for polymorphonucleocytes.

 

  Macules  deserve special  reference since  they are rarely mentioned in other texts and yet they are the end result of most inflamed lesions and, at times, contribute considerably to the patient's symptomatology. They can last 2-48 days.  Histology reveals a nonspecific inflammatory reaction  centred around the  blood vessels and follicles. The extent of the inflammation and structural damage to the duct depends upon the initial severity of the  preceding inflammatory lesion. The cellular infiltrate  is predominantly  lymphocytic and  histiocytic: some giant  cells may be  seen.