Research into psoriasis--the last decade.

Abstract

Psoriasis is an infuriating disease. It is an arrogantly trivial disorder placqued on to a systemically unimportant organ. Yet it affects 1-2% of the population,62 some of whom are so badly afflicted that life is reduced to a biological chore. This is the frustration: the psoriatic without his spots is totally fit. So that, in terms of personal happiness and social usefulness, research into psoriasis has more to achieve than many of the spectacular endeavours of contemporary medical science. All of us Increased Metabolic Activity As would be expected from the histological and histochemical findings there is much biochemical evidence of increased metabolic activity with increased oxygen consumption in the plaques." K. M. Halprin and A. Okawia studied carbohydrate metabolism in the lesions and in normal looking skin between the lesions.74 They found no enzyme deletions or gross reduction, and therefore rejected the idea of a specific enzyme defect in an important metabolic pathway. What they did find led them to the important general conclusion that "the reorganization of cellular metabolism necessary to sustain the increased rate of proliferation in the psoriatic plaque, occurs not by increasing the concentration of one or few key enzymatic steps but by increasing each of the enzymes responsible for a whole series of reactions . . ." Almost all the biochemical, and many of the histochemical studies point in the same direction; a general increase in metabolism within the plaques and no specific biochemical defect.The histological suspicion of increased mitotic activity in the epidermis has now been confirmed in a number of ways.S. Rothberg and his colleagues showed the rapid passage of 14-C glycine through the epidermis,75 but the most satisfying of the earlier analyses was that of E. J. van Scott and T. M. Eckel,76 who showed the speed-up of epidermal turnover by histiometric methods. The advances which followed owe themselves to the method of local injection of isotopes intradermally and subsequent analysis either by autoradiography77 78 or by scintillation counting.79 These and other studies show that in the psoriatic plaques epidermal turnover is about 10 times faster than in the skin of normal people. This rapid turnover occurs in both germinative cell layer and the granular layers.77 9 It is well known from conventional histology that there are many more suprabasal mitotic cells in psoriatic than in normal skin. I find it an intriguing paradox that the increase shown autoradiographically80 is not as great as the increa'e shown by conventional histology. Could this mean that the duration of mitosis is less in suprabasal than in basal cells in psoriasis?Abnormal Keratinization There have been a good many studies, particularly histochemical, of the abnormal keratinization in psoriasis67 71 72 and its relationship to the depleted granular cell layer. One early study showed a change in the x-ray diffraction pattern of the keratin, suggesting an abnormal aggregation of the keratin fibrils.81 The crystalline ...

Immobilization‐induced and crowded environment‐induced stress delay barrier recovery in murine skin

“…8 Moreover, a number of epidermal dermatoses, ranging from occupational dermatitis to psoriasis, may be triggered by extended injury to the epidermis. 17,18 Furthermore, we previously reported that prolonged barrier disruption, produced by repeated topical acetone treatment or tape stripping, induced epidermal hyperplasia, cytokine secretion and inflammation. 12 As certain clinical disorders, in which barrier function is abnormal, are also characterized by epidermal hyperproliferation and cutaneous inflammation, the decline in barrier homeostasis might induce these skin disorders.…”

Pathological crosstalk in vitro between T lymphocytes and lesional keratinocytes in psoriasis: necessity of direct cell-to-cell contact

“…1 In the past, the disease was thought to originate from a primary disorder in epidermal keratinocytes that led to their hyperproliferation and incomplete maturation. [2][3][4] Leukocyte infiltration was only viewed as a secondary event. However, the implication of the immune system as an initiator of the symptoms in psoriasis was slowly recognized in the 1980s when new evidences, such as successful treatment with cyclosporin A, a T-cell immunosuppressant, demonstrated the necessity of immune cells in the development of lesions.…”

Psoriasis as a Chess Board — An Update of Psoriasis Pathophysiology

“…Further investigations in the 1970s revealed the role of immunologic factors in psoriasis. However, the dominant thought was that psoriasis was a disease of faulty epidermopoiesis due to impaired autocontrol mechanisms [12]. Hunter et al wrote "More work on cell turnover and its regulation will give the clue to psoriasis" [13].…”