Previous chapters have reviewed  the evidence  that patients with acne have an increased sebum excretion rate, but since this seborrhoea persists  after spontaneous resolution of acne there must be other factors necessary for the development of the condition. There is no doubt that acne is associated histologically and clinically with  evidence of ductal  hypercornification. The prime significance of this is doubted  by Shuster1 but receives support from Kligman, Strauss, Plewig and Cunliffe.  Needless to  say  this author strongly disagrees with  Shuster - patients who have had acne, still have a seborrhoea but have no comedones and no acne.

 

  The fact that there is sebum outflow resistance can be demonstrated simply by cleansing the skin with an organic solvent,  placing a sheet  of absorbent paper against the skin for a few minutes and then treating the paper with a fat stain such as osmium tetroxide.  In a subject with acne some  unstained gaps are  seen corresponding to functionally obstructed ducts, daily examination of which reveals that  at these sites inflamed lesions frequently develop.

The more recently discovered 'Sebotape' is another useful way of demonstrating these functionally occluded ducts.

Also recently it has  been  demonstrated by measuring sebum excretion overlying blackheads that there is a  functional obstruction  to the outflow of sebum.

It may appear to be a paradox that a patient with acne can have obstruction of pilosebaceous ducts and yet have  an increased  sebum excretion. This, however,  is easily explained.  An individual  has thousands of sebaceous follicles producing sebum. If only thirty or forty become functionally blocked, representing only a small percentage of the total glands,  then that individual will nevertheless have obvious  acne. This small number of blocked ducts will not significantly reduce the seborrhoea.

 

  How may the pilosebaceous  ducts  become obstructed? This chapter will discuss the varied anatomical changes associated  with ductal hypercornification. Little is known about the cellular dynamics of the duct. More however is known about factors which have been claimed to be a trigger to ductal cornification. Some of the factors claimed to  be important have been derived from animal experiments, especially from the rabbit ear model for comedogenesis. This model will be critically discussed. Also covered are the physiological interrelationships between cornification and sebum excretion.

 

  It is necessary to remind the reader that sebum does not  flow  simply  through a cylindrical pilosebaceous tube; the flow of sebum is complex, occurring through the  central parts of the  duct and between the desquamating corneocyte lamellae  .  It is assumed that comedone  formation  is a retention of hyperproliferating keratinocytes - but much more research is  required to explain the  precise events involved.