The first visible sign of pattern baldness is characterized by a slight, often spot-like hair loss located in the temple or crown on men’s head. In terms of the histology of the hair follicle, a slight degeneration over a small peri-vascular area on the lower third layer of the covering connective tissue of the affected hair follicles – which are usually in the growth phase – can be noted during the initial phase of pattern baldness. In the affected follicles, the pink collagen fibers indicate normal tissue sheath is replaced by basophilic smudging and stains in the elastic tissue found in the foci.

Thick pigmented hairs called “terminal hairs” are commonly located on the scalp, beard, armpits and pubic area, and are influenced by hormones. On the other hand, hormones do not influence the vellus hairs, the hairs that are tiny and colorless. A common and usually major feature seen on biopsied hair samples taken from patients with pattern baldness is the significant loss of the anagen hair. Anagen hairs penetrate in to the subcutis through the dermis in the scalp. Instead of finding the anagen hairs, these hairs are replaced by secondary pseudo-vellus hairs characterized by remnants of angiofibrotic tracts called follicular streamers or stellae. The decline in the number of hair follicles is apparent in the biopsied hair sample, although miniature follicles are identifiable on the horizontal sections of the scalp biopsies.

The horizontal sections of the scalp biopsies are useful in the diagnosis of pattern baldness since they possess numerous hair follicles to be studied. The samples of scalp biopsies under study leads to the identification of many pseudovellus hair follicles found in the papillary dermis. These findings eventually lead to the development of the theory that insists in the miniaturization or transformation of large affected hair follicles of terminal hairs into fine vellus-like hairs rather than the total destruction of the terminal hairs.

When the hair starts to thin down, it goes upward to the papillary dermis from the reticular dermis, leaving a trail of long streamers behind it. In doing so, it cycles up and down through the anagen and the telogen found in the papillary dermis in the form of a small vellus-like hair. If treatment is applied on these hairs to turn them into terminal hairs, the hair simply travels downward the long streamer or tract it left to transform and generate into terminal hair. The presence of arrector pili muscle and angiofibrotic streamers helps in differentiating miniaturized hairs of androgenic alopecia from the true vellus hairs. However, fibrosis is noted in a small number of scalp biopsies and in only 10% of the cases is follicular fibrosis noted.

Histological data analysis shows a significant drop in the ratio of terminal to vellus hairs from more than 6:1 to less than 4:1 and the anagen to telogen ratio changed from 12:1 to 5:1. Supporting studies show that balding scalp experiences moderate inflammation of the hair follicles and is more common in the scalp of men with androgenic alopecia compared to that of the normal controls. This inflammation in pattern baldness is seen as a mild to moderate case of peri-infundibular lymphohistiocytic inflammatory infiltrate. This inflammation or fibrosis may be an indicator of the prognostic value in the re-growth pattern in alopecia as revealed in the results of the study. It documents 55% of the hair follicles in the scalp that exhibited inflammation or fibrosis demonstrated certain response to topical minoxidil therapy as opposed to the 77% to the hair follicles with no inflammation. Although this feature is present in the two thirds of the biopsied samples with alopecia cases, it is also evident in the one third of the biopsied normal scalp.

In the later stage of pattern baldness, the connective tissue streamer seen in all telogen follicles has the probability to become broader and has more cellular in male pattern hair loss compared to the sheath seen with normal follicles. In the advanced stages of the condition, the stele is more probable to become a fibrotic column. An observation not necessarily indicating alopecia could be seen in the pattern of hair loss in male includes the restriction of the mild lymphohistocytic infiltrate in the upper follicle. This was also observed in the cases without hair loss.

The results of the work of Hori and colleagues highlighted the apparent decrease in the epidermal, dermal, and subcutaneous thicknesses in males experiencing advanced alopecia compared to the normal control. This decrease in the thickness of the skin could be a major factor in the loss of substance of the normal hair follicle and the degradation of the connective tissue itself.

Conclusion

The pattern baldness is characterized by the miniaturization of hairs as observed in the clinically affected scalp areas. This pattern was suggested the histologic findings of representative scalp biopsies. Those patterns of pattern baldness that become apparent in affected hairs (including hairs with varying diameters) are increases in number of vellus hairs, increases in telogen count, and a substantial decrease in terminal hairs. The overall scalp hair density appears to be preserved until the last stage of the alopecia development is reached. An increased number of mast cells (cells that play an important role in the body's allergic response) is also a noted pattern of hair loss. The histopathologic findings in female pattern hair loss are indistinguishable from those of male pattern hair loss, and differ only in matters of degree.