Orville J. Stone

Chronic Paronychia in Children

Thumb-sucking is the most frequent predisposing factor of chronic paronychia in children. There are two basic components in chronic paronychia. One is a pocket which holds moisture and allows the sur vival of many different organisms. The other is an anatomic deformity of round ing out and retraction of the posterior nail fold because of foreign material in the dermis. The dermal change with the subsequent rounding out and retraction assures the continuing presence of the pocket. Chronic monilial disease usually local izes at sites of pre-existing defects. Mo nilia contribute to the disease process by irritation on the surface and by penetra tion of debris into the dermis. This debris stimulates chronic inflammation which in turn often aggravates the original defect.

PSORIASIS—A DEFECT IN INFLAMMATION*

In 1924, Civattei suggested that the primary histologic lesion in psoriasis and in seborrheic dermatitis is the intraepidermal pustule. He suggested that the pustule occurs in seborrhea as the result of external organisms and in psoriasis because of an internal defect. Recently, Pinkus and Mehregan^ reviewed the ideas of Civatte on the development of Munros abscess. They agreed that the pustule was the primary histologic lesion, but they could not rule out a preceding biochemical event in the epidermis. Their theory, based on the histologic examination of clinical disease, essentially states that the papilla becomes edematous and its capillary becomes engorged. The capillary squirts a load of serum and leukocytes into the suprapapillary epidermis, thereby damaging the keratinocytes in this region. The leukocytes then move upward with the epidermal cells. In their discussion, they niade it clear that they felt that this is a broad mechanism involving skin diseases.

The effect of stannous fluoride and stannous chloride on inflammation

Abstract Scratches were made to the depth of the upper dermis on the abdomen of rabbits. The scratches were covered by patch tests for 18 hours with solutions of stannous fluoride or stannous chloride. Both these substances produced a destructive reaction with intraepidermal polymorphonuclear leukocyte pustules occurring on each side of the scratch. Stannous fluoride was destructive at lower concentrations than stannous chloride. When these substances were patch tested over nontraumatized tissue, no tissue damage occurred. It is suggested that stannous fluoride and stannous chloride may interfere with the enzymes of inflammation. Salts of fluoride, iodide, nickel, arsenic, and mercury are known occasionally to produce a pustular reaction when used to patch test humans.

The Effect of Arsenic on Inflammation

There is clinical and experimental evidence that an amount of arsenicals which will not produce lesions on normal skin will markedly increase the severity of a quantitated, induced, bacterial infection. It is also known that suppression of early inflammation increases the severity of bacterial infections. Art experimental model is presented in which arsenic is shown to prevent one type of early inflammation. It is proposed that arsenic damages enzymes of inflammation which are active before the cellular phase occurs.

The Effect of Tar on Wound Healing

In experimental animals, 5% crude coal tar produced a 45.9% delay in wound healing. This may have resulted from the direct effect of tar on the wound or from the known fact that tar increases the severity of infections. Efforts were made to control infection, and no clinical evidence of infection occurred. This data might be clinically significant, at least for areas such as the skin and lungs where organisms are present.

The effect of tar on infection

Abstract Sites on the backs of adult white rabbits were covered with 5% crude coal tar ointment for 24 hours, and control sites were covered with the ointment base. The tar and control sites were each injected with a similar number of micrococci. The sites were then covered again with tar and control ointments. After an additional 24 hours, the size of the induration was measured. The average diameter of induration at the tar sites was 12.7 mm and at control sites 4.3 mm. Killed organisms produced only 1- to 2-mm papules at both tar and control sites.

THE ISOMORPHIC PUSTULAR RESPONSE IN SUBCORNEAL PUSTULAR DERMATOSIS

Intraepidermalpolymorphonuclearpustules appear in a number of dermatologic disorders, including? psoriasis, seborrheic dermatitis, subcorneal pustular dermatosis, acrodermatitis enteropathica, pustular bacteroid of Andrews, keratosis blenorrhagica, impetigo herpetiformis, dermatitis repens, acrodermatitis continua, pustulosis palmaris et plantaris, pseudocarcinomatous hyperplasia, and keratoacanthoma.

SEBORRHEIC DERMATITIS—HYPERREACTIVE INFLAMMATION TO SAPROPHYTES*

In 1924, Civatte* suggested that the primary histologic event in seborrheic dermatitis and psoriasis is the intraepidermal pustule. He suggested that it occurs in seborrheic dermatitis as a result of external organisms and in psoriasis because of an internal defect. Recently, Pinkus and Mehregan^ reviewed the ideas of Civatte on the development of Munros abscess. Their theory based on histologic examination of clinical disease, essentially states that the papilla becomes edematous and its capillary becomes engorged. The capillary squirts a load of serum and leukocytes into the suprapapillary epidermis, thereby damaging the keratinocytes in this region. The leukocytes then move upvŝ ard with the epidermal cells.