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Loss of Ridged Skin Before Birth (This article is reprinted from the February 1965 issue of Finger Print and Identification Magazine.)
by HAROLD CUMMINS, Ph.D. Dr. Henry W. Baird III, of Philadelphia, recently published an account of a family in which some members, representing three successive generations, lack skin ridges of fingers, palms, toes, and soles.1 Their ridgeless condition is entirely dissimilar to the types of defect that have come to attention heretofore, hence it seems desirable to acquaint identification workers with this strange family. Dr. Baird, while preparing his article, had submitted photographs and other materials on these cases for my comment; generously he has permitted me to make the present use of the article, which quoted the essentials of my interpretation, now expanded. For orientation, it is well to characterize the two basic situations in which skin ridges may be defective or absent: (1) initially imperfect differentiation of ridges, dating from the fetal period during which ridges form; (2) secondary destruction of ridges. Faulty Ridge Development This type of defect has become familiar to readers of FINGER PRINT AND IDENTIFICATION MAGAZINE through a series of articles, several of which are cited in the references following this text.2--5 An extreme example is illustrated in Fig. 1, the palm of a child with Down's syndrome.6 In the hands and feet of this child almost the entire expanse that should bear ridges presents only pebblings; the “pebbles” in limited areas are aligned as if they were potential ridges and occasional patches of actual ridges occur. Individuals who possess a defect of this nature commonly exhibit it over much less extensive areas, but in all cases the abnormality has the same fundamental character. The “pebbles” of the affected regions are actually units of ridges, units that failed to consolidate because of a fault in embryonic development. (The beading of normal ridges that is sometimes evident reflects their composition of such joined units.) In a strict sense the condition is not to be described as absence of ridges. To be sure, ridges are not literally present as ridges but their elements exist, separately rather than joined. The condition may be likened to the normally pebbled state of skin on the snouts of some animals, for example the dog (Figure 2). Here the units occur both singly and in groups, often in rosette form. Destruction of Ridges Various agencies, both natural and artificial, may lead to destruction of ridged epidermis in the living person: certain diseases such as leprosy and syphilis, deep burns, abrasions, etc. Among them, abrasion is of immediate interest because of its close relation to the cases about to be described. Abrasion may be best introduced by reference to the instances that received much publicity in 1957--58, when a New Orleans dermatologist (Dr. James W. Burks) held that the future of finger print identification was threatened by the fact that patterns can be completely removed by this process. In clinical dermabrasion, or skin planning, designed for example to remove facial blemishes, an area of skin is first frozen and then planed by a rapidly revolving circular wire brush. After Dr. Burks applied this method to finger patterns he found the new epidermis that grew over the abraded surface to be smooth and utterly devoid of ridges. This is the anatomical character of Dr. Bairds cases also, but there are important historical differences: the epidermis had been destroyed by a natural process rather than by an artificial one, and destroyed before birth instead of in postnatal life. We are now prepared to consider the singular family reported by Dr. Baird, who had personally examined the twenty--four members [a chart was referred to and used in the original article]. Thirteen of them lack ridges over fingers, palms, toes, and soles, except that in both hands of two persons the little fingers and ulnar portions of the palms do not have the defect. Of these thirteen: bilateral webbing of toes (2--3 or 2--3--4--5) also occurs in five; bilateral flexion contractures of one or more fingers are present in seven members, and similar contractures of toes (usually 3, 4, and 5) occur in nine. It is important to note the presence of these digital anomalies, webbing and contractures, because they are probable a developmental by--product of the process that led to ridgelessness of the skin, as explained below. The ridgeless skin appeared as in Figure 4. Prints (Figure 5), even those made by one as experienced as Mr. Edwin A. Hoffman III, were only smudges. In the young infant the skin was thin and red, but in older children and adults it had become thick, hard, and callused. A piece of skin from one of the children, cut away during surgery for correction of digital contractures, was studied microscopically in serial sections. It showed, among other features: thickening of the cornified superficial layers; sweat glands, though none of the ducts reached the surface; characteristics of scar tissue in the dermis. To understand the nature of the ridgeless state in these cases, it is necessary to construct the probable developmental events. This reconstruction can only be deduced form the observed characteristics of the affected individuals, combined with knowledge of an unusual pathological involvement of skin that occurs prenatally. This condition is one of the forms of epidermolysis (death and dissolution of epidermis). Only an isolated patch of skin may be involved, for example on the scalp or leg, or there may be multiple and more extensive areas. Regardless of extent, the disintegrated epidermis sloughs and the denuded surface is then gradually covered by a growth of cells arising form the persistent skin appendages (hair follicles and gland ducts--sweat gland ducts only in the cases here considered) and from the adjoining margins of intact epidermis. Ridges are here absent because their formation is dependent upon embryonic capacities of epidermis and dermis that do not persist as late as the period of sloughing. Inherited Epidermolysis In Dr. Baird's family it is clear that epidermolysis is inherited (as a Mendelian dominant) and that under genetic control it is confined to ridge areas. It is postulated that sloughing was not initiated earlier than the fourth month of intrauterine life inasmuch as sweat glands originate as downgrowths form the epidermis at that time; sweat glands are present, as noted above, notwithstanding that at least most of their ducts had been disjoined from the surface. Ridges would have been formed by that time, hence their loss is descriptively equivalent to postnatal destruction by other means such as skin planning. Sloughing was followed by natural tissue repair. In the most severely affected cases the repair induced scarring and contractures of digits. Since none of the unaffected family members has webbing of toes, it is suggested that the webbing present in five ridgeless members is not of the ordinary from, which is heritable. It seems probable that the denuded surfaces of toes became joined in the healing process, in the manner that digits may thus join after severe burns unless their surfaces are kept apart by proper dressings. In brief, this is a family carrying a heritable trait that leads to dissolution and sloughing of ridged skin before birth. The trait was transmitted from the grandfather to all three of his children and through them to nine of the sixteen grandchildren. The association of another type of epidermal pathology, milium, is of possible significance genetically. Milium, which was present in all the ridgeless members but in none of the unaffected ones, is the occurrence of whitish papules; each papule is a nest of cornified epidermal cells. In this family such papules were invariably present on the face at birth, but they gradually disappeared in the early months. Milium may be passed over with this bare mention, in view of the focus of interest on ridgelessness. References 1 Baird, Henry W. III, “Kindred Showing Congenital Absence of the Dermal Ridges (Fingerprints) and Associated Anomalies,” Journal of Pediatrics, Vol. 64, No. 5 (1964). 2 Anon., “Hands of Mystery,” Finger Print and Identification Magazine, Vol. 31, No. 7 (1950). 3 Anon., “Printless Japanese Police Officer Still Mystery to Experts,” Finger Print and Identification Magazine, Vol. 31, No. 9 (1950). 4 Cummins, Harold “Why Takeshita Lacks Patterned Friction Skin,” Finger Print and Identification Magazine, Vol. 31, No. 11 (1950). 5 Okamoto, Kazuo, “The Extraordinary Finger Prints of the Boy of Nagoya,” Finger Print and Identification Magazine, Vol. 39, No. 12 (1958). 6 Wolf, U., H. Brehme, H. Baitsch, W. Kunzer, and H. Reinwein, “Aplasia of the Dermal Ridge Patterns in Mongolism (G--Trisomy),” The Lancet, Vol. 2 (1963), No. 7313.
This article was reprinted in “THE PRINT” |