Cutaneous aging is a complex biological phenomenon affecting the different constituents of the skin. To compare the effects of intrinsic and extrinsic aging processes, a total of 83 biopsies were collected from sun-exposed and protected skin of healthy volunteers representing decades from the 1st to the 9th (6-84 years of age). Routine histopathology coupled with computer-assisted image analysis was used to assess epidermal changes. Immunoperoxidase techniques with antibodies against type I and type III collagens and elastin were used to quantitatively evaluate changes in collagen and elastic fibers and their ultrastructure was examined by transmission electron microscopy. Epidermal thickness was found to be constant in different decades in both sun-exposed and protected skin; however, it was significantly greater in sun-exposed skin (P = 0.0001). In protected skin, type I and III collagen staining was altered only after the 8th decade, while in sun-exposed skin the relative staining intensity significantly decreased from 82.5% and 80.4% in the 1st decade to 53.2% and 44.1% in the 9th decade, respectively (P = 0.0004 and 0.0008). In facial skin the collagen fiber architecture appeared disorganized after the 4th decade. The staining intensity of elastin in protected skin significantly decreased from 49.2% in the 1st decade to 30.4% in the 9th decade (P = 0.05), whereas in sun-exposed skin the intensity gradually increased from 56.5% in the 1st decade to 75.2% in the 9th decade (P = 0.001). The accumulated elastin in facial skin was morphologically abnormal and appeared to occupy the areas of lost collagen. Collectively, the aging processes, whether intrinsic or extrinsic, have both quantitative and qualitative effects on collagen and elastic fibers in the skin.

Follicular microinflammation plays an integral role in the pathogenesis of AGA in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases.

The results of this study suggest that beneficial effects of such modalities on facial skin were accomplished primarily by increasing the amounts of collagen I and collagen III and improving the morphologic appearance of collagen and elastic fibers.

The checkpoint protein p53, which is activated by DNA damage, is involved in the decision whether the cells should stop replication and proceed to repair their DNA or die by apoptosis. We evaluate the expression of p53 and the number of apoptotic cells in normal sun-exposed (face) and protected (abdomen) skin in Egyptians between 6 and 77 years of age. The degree of p53 expression in facial skin significantly increases from a score of 1.5 +/- 1.5 (mean +/- SEM) in the 1st decade to 4.8 +/- 0.3 in the 8th decade (p = 0.02), while no significant changes are detected in the protected skin (p = 0.1). Overall, the level of expression is significantly higher in sun-exposed facial skin than in abdominal skin (p = 0.007). However, p53 expression versus age is significantly higher in the facial skin of older age groups in both males (p = 0.003) and females (p = 0.02). The pattern of staining was found to be dispersed (wild-type) in the majority (97.3%) of biopsies from sun-exposed skin and in all biopsies from non-exposed skin. The expression of wild-type p53 in type IV-V skin therefore correlates with both site and age of the individual. In contrast, the number of apoptotic cells significantly decreases with advancing age in sun-exposed skin (p = 0.005). Increased age-associated expression of p53 in sun-exposed skin, but not in protected areas of skin, is found to reflect an accumulation of the wild-type protein, as judged by the staining pattern. The decrease in apoptotic cells with age may suggest the accumulation of senescent cells in the skin and their relative resistance to apoptosis. Such alteration in the proliferation/apoptosis balance could play a role in tumorigenesis.

Vitiligo affects both melanocytes and keratinocytes causing degenerative changes. These changes were present in both the leucodermic and the apparently normal perilesional skin. PUVA increases the number of active epidermal melanocytes in the three tested areas and recovers the melanocyte and keratinocyte degeneration.