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Specific Gravity

15 May

Speciﬁc  Gravity

The specific gravity of sebum given  by Butcher  and  Coonin  (19) from the forehead sebum of normal individuals was  0.911 + 0.01 g/cm3  for all samples. Burton  (16) confirmed this for three  normal subjects  when  scalp  sebum was  used.

Surface Tension

The surface tension (Table 4) at temperatures varying from 26.58C to 318C was found to be an average of 24.89 dynes/cm for forehead sebum of normal subjects.  A very close  value  (22.9 + 0.9 – 24.2 + 1.1) was  also  obtained for scalp  sebum of normal and  acne patients.


The viscosity  increased from 0.55 to 0.98 poise, as temperature decreased from 388C to 28.58C.  The sebum separated into  various components when the  temperature was  lowered from  298C  to 308C  and  ceased  to flow  at 158C  to 178C  (19). Burton (16) reported a viscosity  of 0.32 + 0.03 poise  at  358C,  0.82 + 0.22 poise  at  258C, and   1.71 + 0.70  poise  at  208C.  In  addition, it  was  found that  the  viscosity   of scalp  sebum and  forehead sebum was  similar in normal individuals. Burton  also reported that  the mean  viscosity  of the sebum from  10 acne patients taking  tetra- cycline  was  higher than  with  seven  patients not taking  tetracycline at 358C.


The role of sebum in acnegenesis is poorly understood. Acne vulgaris, a multifac- torial disease of the skin, is found in areas rich in sebaceous follicles. It is character- ized  by seborrhea, disturbed keratinization in the  follicles  with  comedones, and subsequent  inflammatory papules,  pustules  and   nodular  abscesses, and   scars (15). The  pathology of acne  is described in  various other  chapters in  this  book but a brief review  here sets the stage for relevance of the studies of sebum described later in this chapter. There are three essential factors as a group that may cause acne.

1.    There is an increase in androgen production in puberty, which  induces enlarge- ment  of sebaceous follicles and  increased sebum production (21).

2.    Follicular hyperkeratinization leads to retention hyperkeratosis, that is, obstruc- tion of the pilosebaceous duct by accumulation of an excessive amount of keratin as an important factor in the pathogenesis of acne (22).

3.    P. acnes proliferate in the follicle, producing a variety of extracellular inflamma- tory  products, which  excite an inflammatory response (23).

The  primary event  in acne  is faulty  keratinization and  the  production of come- dones. In  the  secondary stage,  inflammation can  occur  in  the  comedones. Two pathways define  the subsequent development of the lesions  of acne. In the nonin- flammatory pathway, the  microcomedo proceeds to mature into  closed  and  open comedones through distention of the follicle wall and  lumen. In the inflammatory pathway,  the   extracellular  products  of  P.  acnes  incite   inflammation.  P.  acnes

colonization occurs relatively early in acne, and the production of extracellular pro- ducts  by this  organism provides multiple potential mechanisms for the  develop- ment  of inflammation. Among the earliest  findings, drugs that  reduce fatty  acids (FFA), such  as  tetracycline, are  beneficial  in  inflammatory acne  (24). It must  be noted that  skin surface-derived lipids  produce an inflammatory papule or nodule when they  are injected  into the human skin (25). Furthermore, certain  fractions of the  sebaceous  secretion,  especially  fatty  acids   and   squalene, when  applied  to rabbits’  ears promoted follicular  hyperkeratosis and  comedone formation (26 – 28).

In the absence  of comedones, the large infundibulum channels are filled with the white  pasty  sebaceous material. It is the normal content of a sebaceous follicle, not of an acne lesion. Sometimes, the follicles are filled with a cocoon-type skeleton of  corneocytes, having  20  to  40 cells  surrounding the  central   fine  hair,  with   a channel left free in the  sebum of which  P. acnes and  staphylococci may  be found (15). This is called  a follicular  filament or follicular  cast. A comedo can arise  from a follicular filament. It is believed that  the lipid  composition of the follicular  casts may  play  a role in acne genesis.  It was  demonstrated by Nordstrom et al. (7) that about  29% of the net weight of follicular  casts was lipid. In addition, the hydrolysis of the triglycerides in the follicular casts was much  higher than  on the skin surface.

The differences in the rate of sebum production in acne patients and  normal controls have  so far been  the only consistent finding that  links  sebum secretion to acnegenesis (4,7). It has  long  been  thought that  acne is a result  of an abnormality of sebum or sebaceous gland function. Yet, the current concept of follicular  kerati- nization in the pathogenesis of the disease makes this relationship difficult to justify. However, four major reasons based  on circumstantial but compelling evidence that link sebum to acne include:

1.    Acne develops at puberty, when sebaceous glands become  very active  (29).

2.    The rate of sebum secretion is generally higher in acne subjects  than  in normal individuals, though not  all persons having high  sebum secretion suffer  from acne (30).

3.    Some components of sebum are irritants and can be comedogenic in inflamma- tory  acne.

4.    Acne is improved by any modality that  reduces sebaceous gland activity  (31).

This  indicates that  sebum is probably an  essential factor  in the  pathogenesis  of acne, but not necessarily the only one.

It is possible that  the  changes in the  horny layer  could  be the  result  of an alteration of the  nature of the  sebum, so that  it causes  keratinization of the  duct and  leads  to  comedone formation. The  macromolecular structure of the  sebum could  change to  a more  crystalline state  that  forms  a blockage  and  impedes its own flow through the sebaceous duct  and infundibulum or alternatively cause irri- tation  to the follicular  epidermal lining.  Gonzalez-Serva (32) and  Abramovits and Gonzalez-Serva (33) have  speculated that  acne  involves the  build  up  of an intra- ductal  calculus termed  sebolith, which   results  from   crystallization  of  sebum. They   proposed  that   the   sebolith  punctures  and   erodes  the   follicular  lining, leading to  rupture and  inflammation. The  proliferation of bacteria could  be  the result  of a change  in sebum composition or structure, so that  either  it provides a richer,  more  bioavailable medium  for  bacterial growth or  it  no  longer  contains inhibitory factors.  In such  a manner, sebum can be involved. The authors believe that  the characterization of the lipids  of the sebaceous follicles  and  their  physical

behavior may  provide more  detailed information on the possible role of sebum in acne vulgaris.

Electron  microscopy studies on comedones showed the  presence of yeasts, bacteria,  keratinized cells, sebum, and hairs. In these comedones, sebum was a ubi- quitous component and   appeared as  an  osmiophilic granular  material, which varied in  amount from  scanty  to  abundant  between the  keratinized cells  (34). Depressions between the microridges of the keratinized cells had  the greatest pro- pensity for sebum. Many  yeast  and  bacteria  occupied these  sebum-rich areas  and their  surfaces were  covered with  fatty material.

The composition of the lipid components of comedones was also examined by Nicolaides et al. (13) and  compared with  the skin  surface  lipids.  Chapter 3 by Dr. Wertz  covers  this  in  more  detail,   but  findings relative   to  the  purposes of  this chapter are summarized here.  The lipids  in comedones contain all the same  lipid classes  as  sebum, but  some  are  in  different proportions. Triglycerides represent only  a small  portion of the  comedonal lipids  (7%) and  fatty  acids  represent 55% of the lipids.  Wax esters  are only 14% of the lipids  compared with  24% in surface sebum. Free cholesterol is also much  higher in comedonal lipids.  Another notable difference is a larger  amount of saturated fatty  acids  in comedonal lipids—about

70% of the  comedonal FFA are saturated compared with  only  65% of the  surface sebum. The  differences between comedonal and  surface  lipid  reflect  the  contri- bution of epidermal lipids  to the  mix.  Epidermal lipids  do  not  contain any  wax esters,   and   cholesterol is  derived from  epidermal lipid.   Epidermal  lipids   also provide saturated fatty  acids  to  the  mix.  The  reduced amounts of triglycerides are due  to nearly  complete bacterial hydrolysis of this class to FFA.

Since sebum is a mixture of the different lipid components discussed earlier, it is important to understand how each component affects the macromolecular struc- ture  and  the physical – chemical  behavior of sebum, and  how  this is altered in dis- eases  of the pilosebaceous unit,  for example, acne. It is, therefore, useful  to know how variations in the components, for example, concentration and ratio of different components, their carbon  chain length, and the ratios of unsaturation to saturation, affect the macromolecular structure of sebum and  how  this  relates  to the compo- sition  of sebum in acne  lesions  in particular comedones. The  ultimate goal  is to determine how  this  composition can  be  altered in  the  skin  of acne  patients to correct  the  defects  in the  infundibulum and  the  sebaceous duct,  and  to facilitate penetration of anti-acne drugs into the pilosebaceous unit.

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