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Embryonic migration during the prenatal development of palm print patterns
Medical Hypotheses
7: 639-644,
1981
EMBRYONIC MIGRATION DURING THE PRENATAL DEVELOPMENT OF PALM PRINT PATTERNS T.J. David. Booth Hall Children's Manchester M9 2AA, England
Hospital,
ABSTRACT A major Landmark on the palm, the t triradius, is usually found near the wrist. Much interest centres on the fact that it is sometimes found to be central in the palm. It is suggested that, during embryonic development, the t triradius migrates from a position in the centre of the palm to arrive near the wrist. According to this hypothesis, those cases where the t triradius remained in the centre of This the palm would represent arrests of development. might explain the association of certain chromosome abnormalities with a t triradius in the centre of the palm. Key words:
Dermatoglyphics, embryonic migration, chromosome abnormalities, deveLopmentaL arrests, congenital malformations, teratology. INTRODUCTION
In contrast to our detailed knowledge of the development of, for example, the cardiovascular system, the embryology of finger and palm print patterns (dennatoglynhs) is not clearly understood. It is generally held that dermatoglyphic patterns form secondary to volar pads which are present on the palms Where a pad is present, and soles during early fetal life. a pattern is formed. Presumably where there is no pattern, for example - in the hypothenar area, then there was no
639
volar pad. Where there is an extra pattern, for example, in the interdigital area, then either the volar pad was particularly large, or its presence was prolonged, or there were two pads instead of one. In However, this is clearly an over-simplification. fact, it is known that these volar pads appear and regress in a fairly definite sequence, certain pads appearing first and other pads disappearing first (1). Further, it is clear that not all sites of volar pads correspond to later sites of patterns. Perhaps the formation of patterns depends on the synchrony and manner of pad regression and ridge formation. Pads first appear at 6% - 8 weeks and begin to regress at 10 - 12 weeks. Primary dermal ridges appear at 13 weeks (2, 3). So it is possible that a pad may regress so far in advance of ridge formation that by the time ridges form the underlying surface is flat. The suggestion has been that "parallel dermal ridges develop transversely to the lines of growth stress" (l), and also (4) that cells in the lower part of the epidermis are, at a very early period, sensitive to curvature and that the slight pressure produced by the concavity in the primitive basal layer may induce pattern formation. An important point is that the major events determining pattern formation are likely to be at a cellular level and to occur very early in development "long before any trace of pattern is observable" (4). One difficulty with the volar pad hypothesis is that it does not explain how genetic factors influence pattern formation. However, since the genetic factors themselves are so poorly understood, this is hardly a criticism except in a specific instance mentioned below. The t triradius The t triradius is both medically and biologically the most important dermatoglyphic landmark on the palm. The main interest in the t triradius is the great variability of its position, unlike the other palmar triradii which are all fairly constant. The most common position of the t triradius is near the wrist, but in some cases it is found to be displaced distally up in the centre of the palm, and this displacement 640
is of considerable biological interest and of medical Degrees of distal displacement diagnostic use as well. the t triradius are designated t', t", and t"' in increasing order of distal displacement. Embryonic Migration
of
of the t triradius
It is suggested here that the explanation for the variability of the position of the t triradius lies in The hypothesis is that the origin embryonic migration. of the t triradius is at a central point in the palm, probably very near or just proximal to the a, b, c and d triradii, and that during early embryonic development it migrates proximally down the palm to arrive at the wrist. Failure to reach the wrist would be seen as a developmental arrest. Thus a "distally displaced t triradius" may be a misnomer and might be better regarded as "persistent fetal position of the triradius". Incomplete Migration, Malformations
Arrests of Development,
and
The attraction of the hypothesis of embryonic migratior of the t triradius is that it immediately explains the association of a "fetal" t triradius (ie a t triradius in the centre of the palm) with congenital malformations. An example of this association is Down's syndrome (trisomy 21) where distal displacement of the t triradius is found in about 85% of cases (5), and is of considerable diagnostic value (5 - 7) particularly in the newborn period. Failure of migration of the t triradius would thus be seen as a "developmental arrest", a fundamental teratologic mechanism that is regarded as being the basis of a large There seems no variety of congenital malformations (8). reason why similar mechanisms should not apply to other dermatoglyphic traits. The association of dermatoglyphic developmental arrests with other malformations would become readily explicable, both presumably sharing a common teratologic cause, Ridge Dissociation This is a rare malformation of the finger and palm print patterns, in which the ridges are disrupted and the pattern distorted. The distribution of the abnormality is
64-l
always quite characteristic, being most marked on the thumb and becoming progressively less evident through the digits to the little finger (9). The palms are often not involved, but if they are it is always the region of the t triradius that is first affected. If the t triradius is subject to migration then this might explain the propensity of ridge dissociation to be located around the The fact that ridge dissociation is not t triradius. usually associated with a t" or t"' does not matter indeed it possibly supports the migration hypothesis since it may be that the migration itself predisposes to this particular ridge disturbance. Dermatoglyphics
and the Sex Chromosome
Complement
Dermatoglyphs are known to be affected by the sex chromosome complement. One feature, the total finger ridge count (the summed ridge counts of all ten fingers, an estimate of pattern size), has a linear relationship with the sex chromosome complement (10). The most likely explanation for this relationship is that the sex chromosome complement affects cell division and thereby growth (ll), and the very low total ridge count found in the poly-X syndromes could be seen as a developmental arrest due to poor growth. Similar mechanisms may well operate in autosomal chromosomal abnormalities such as trisomy 21. Fingerprints
and Ridge Migration
The concept of migration of triradii has wider implications. It may be that formation of fingerprint patterns depends on a small degree of migration of ridges on the fingerpad. An arrest of this migration would lead to a relatively short or flat pattern, ie an arch. Nearly all arches have a small central hump suggesting a little axial centrifugal migration. This would be consistent with the very low pattern intensity found in distal phalangeal hypbplasia (12). Difficulties One problem is been observed. If determining pattern before any trace of is unlikely ever to
that dermatoglyphic migration has never it is true that the major events formation occur at a cellular level long pattern is visible (4), then migration be observed.
642
The other problem is the single gene disorder "ridgesThis is inherited as an off-the-end syndrome" (13). The fingerprints are completely autosomal dominant trait. different from normal in that the ridges, instead of running horizontally across the fingertip, run vertically off the end of the fingertip. This bizarre syndrome features some curious palmar dermatoglyphic abnormalities which include gross distal displacement of the t triradius. The "ridges-off-the-end" phenomenon is harder to explain on a migration basis as it would represent unimpeded centrifugal migration of the fingerpad tissue immediately adjacent to the triradius. For this to be an arrest of development one would have to postulate the failure of a normal developmental process which impedes migration. The issue is germane to the hypothesis because in the "ridges-off-the-end" syndrome the t triradius is always in a t" or t"' position. CONCLUSION Much difficulty has arisen in the field of dermatoglyphics because of our failure to study the subject in its developmental context. The hypothesis set out here suggests that at least one variable dermatoglyphic trait (and possibly others) are the result of embryonic migration. Proof can only come by experimental interference with the development of the limbs, and this clearly cannot be done in man. Indirect evidence might be sought by examining a variety of cases of proven developmental arrest. Direct experimental interference might be possible in primates who are also well endowed with dermatoglyphic patterns. REFERENCES 1.
Mulvihill JJ, Smith DW. The genesis of dermatoJ Pediat 75: 579, 1969. glyphics.
2.
Okajima M. Development of dermal ridges in the fetus. J Med Genet 12: 243, 1975.
3.
Quantitative differences in morphoBabler WJ. genesis of human epidermal ridges. P. 199 in Wertelecki W, Plato CC. Dermatoglyphics - Fifty
643
Birth Defects: Years Later. Original Article Series, Vol 15, No 6, Alan R Liss, 1979. New York. 4.
Penrose LS, Ohara PT. The development of the epidermal ridges. J Med Genet 10: 201, 1973.
5.
Walker NF. The use of dennal configurations in the diagnosis of mongolism. Pediat Clin N A 5: 531, 1958.
6.
Deckers JFM, Oorthuys AMA, Doesburg WH. Dermatoglyphics in Down's syndrome, 1 Evaluation of discriminating ability of pattern areas. Clin Genet 4: 311, 1973,
7.
Preus M. A diagnostic index for Down's syndrome. Clin Genet 12: 47, 1977.
8.
Smith DW. Dysmorphology 69: 1150, 1966.
9.
Congenital malformations of human dermatoDavid TJ. Arch Dis Child 48: 191, 1973. glyphs.
10.
Penrose LS. chromosomes.
11.
Barlow P. The influence of inactive chromosomes Humangenetik 17: 105, 1973. human development.
12.
Schaumann B, Alter M. Dermatoglyphics Disorders (New York: Springer-Verlag),
13.
David TJ. syndrome.
(teratology).
J Pediat
Finger-print pattern and the sex Lancet 1: 298, 1967. on
in Medical 1976.
"Ridges-off-the-end" - a dermatoglyphic Human Heredity 21: 39, 1971.
644
7: 639-644,
1981
EMBRYONIC MIGRATION DURING THE PRENATAL DEVELOPMENT OF PALM PRINT PATTERNS T.J. David. Booth Hall Children's Manchester M9 2AA, England
Hospital,
ABSTRACT A major Landmark on the palm, the t triradius, is usually found near the wrist. Much interest centres on the fact that it is sometimes found to be central in the palm. It is suggested that, during embryonic development, the t triradius migrates from a position in the centre of the palm to arrive near the wrist. According to this hypothesis, those cases where the t triradius remained in the centre of This the palm would represent arrests of development. might explain the association of certain chromosome abnormalities with a t triradius in the centre of the palm. Key words:
Dermatoglyphics, embryonic migration, chromosome abnormalities, deveLopmentaL arrests, congenital malformations, teratology. INTRODUCTION
In contrast to our detailed knowledge of the development of, for example, the cardiovascular system, the embryology of finger and palm print patterns (dennatoglynhs) is not clearly understood. It is generally held that dermatoglyphic patterns form secondary to volar pads which are present on the palms Where a pad is present, and soles during early fetal life. a pattern is formed. Presumably where there is no pattern, for example - in the hypothenar area, then there was no
639
volar pad. Where there is an extra pattern, for example, in the interdigital area, then either the volar pad was particularly large, or its presence was prolonged, or there were two pads instead of one. In However, this is clearly an over-simplification. fact, it is known that these volar pads appear and regress in a fairly definite sequence, certain pads appearing first and other pads disappearing first (1). Further, it is clear that not all sites of volar pads correspond to later sites of patterns. Perhaps the formation of patterns depends on the synchrony and manner of pad regression and ridge formation. Pads first appear at 6% - 8 weeks and begin to regress at 10 - 12 weeks. Primary dermal ridges appear at 13 weeks (2, 3). So it is possible that a pad may regress so far in advance of ridge formation that by the time ridges form the underlying surface is flat. The suggestion has been that "parallel dermal ridges develop transversely to the lines of growth stress" (l), and also (4) that cells in the lower part of the epidermis are, at a very early period, sensitive to curvature and that the slight pressure produced by the concavity in the primitive basal layer may induce pattern formation. An important point is that the major events determining pattern formation are likely to be at a cellular level and to occur very early in development "long before any trace of pattern is observable" (4). One difficulty with the volar pad hypothesis is that it does not explain how genetic factors influence pattern formation. However, since the genetic factors themselves are so poorly understood, this is hardly a criticism except in a specific instance mentioned below. The t triradius The t triradius is both medically and biologically the most important dermatoglyphic landmark on the palm. The main interest in the t triradius is the great variability of its position, unlike the other palmar triradii which are all fairly constant. The most common position of the t triradius is near the wrist, but in some cases it is found to be displaced distally up in the centre of the palm, and this displacement 640
is of considerable biological interest and of medical Degrees of distal displacement diagnostic use as well. the t triradius are designated t', t", and t"' in increasing order of distal displacement. Embryonic Migration
of
of the t triradius
It is suggested here that the explanation for the variability of the position of the t triradius lies in The hypothesis is that the origin embryonic migration. of the t triradius is at a central point in the palm, probably very near or just proximal to the a, b, c and d triradii, and that during early embryonic development it migrates proximally down the palm to arrive at the wrist. Failure to reach the wrist would be seen as a developmental arrest. Thus a "distally displaced t triradius" may be a misnomer and might be better regarded as "persistent fetal position of the triradius". Incomplete Migration, Malformations
Arrests of Development,
and
The attraction of the hypothesis of embryonic migratior of the t triradius is that it immediately explains the association of a "fetal" t triradius (ie a t triradius in the centre of the palm) with congenital malformations. An example of this association is Down's syndrome (trisomy 21) where distal displacement of the t triradius is found in about 85% of cases (5), and is of considerable diagnostic value (5 - 7) particularly in the newborn period. Failure of migration of the t triradius would thus be seen as a "developmental arrest", a fundamental teratologic mechanism that is regarded as being the basis of a large There seems no variety of congenital malformations (8). reason why similar mechanisms should not apply to other dermatoglyphic traits. The association of dermatoglyphic developmental arrests with other malformations would become readily explicable, both presumably sharing a common teratologic cause, Ridge Dissociation This is a rare malformation of the finger and palm print patterns, in which the ridges are disrupted and the pattern distorted. The distribution of the abnormality is
64-l
always quite characteristic, being most marked on the thumb and becoming progressively less evident through the digits to the little finger (9). The palms are often not involved, but if they are it is always the region of the t triradius that is first affected. If the t triradius is subject to migration then this might explain the propensity of ridge dissociation to be located around the The fact that ridge dissociation is not t triradius. usually associated with a t" or t"' does not matter indeed it possibly supports the migration hypothesis since it may be that the migration itself predisposes to this particular ridge disturbance. Dermatoglyphics
and the Sex Chromosome
Complement
Dermatoglyphs are known to be affected by the sex chromosome complement. One feature, the total finger ridge count (the summed ridge counts of all ten fingers, an estimate of pattern size), has a linear relationship with the sex chromosome complement (10). The most likely explanation for this relationship is that the sex chromosome complement affects cell division and thereby growth (ll), and the very low total ridge count found in the poly-X syndromes could be seen as a developmental arrest due to poor growth. Similar mechanisms may well operate in autosomal chromosomal abnormalities such as trisomy 21. Fingerprints
and Ridge Migration
The concept of migration of triradii has wider implications. It may be that formation of fingerprint patterns depends on a small degree of migration of ridges on the fingerpad. An arrest of this migration would lead to a relatively short or flat pattern, ie an arch. Nearly all arches have a small central hump suggesting a little axial centrifugal migration. This would be consistent with the very low pattern intensity found in distal phalangeal hypbplasia (12). Difficulties One problem is been observed. If determining pattern before any trace of is unlikely ever to
that dermatoglyphic migration has never it is true that the major events formation occur at a cellular level long pattern is visible (4), then migration be observed.
642
The other problem is the single gene disorder "ridgesThis is inherited as an off-the-end syndrome" (13). The fingerprints are completely autosomal dominant trait. different from normal in that the ridges, instead of running horizontally across the fingertip, run vertically off the end of the fingertip. This bizarre syndrome features some curious palmar dermatoglyphic abnormalities which include gross distal displacement of the t triradius. The "ridges-off-the-end" phenomenon is harder to explain on a migration basis as it would represent unimpeded centrifugal migration of the fingerpad tissue immediately adjacent to the triradius. For this to be an arrest of development one would have to postulate the failure of a normal developmental process which impedes migration. The issue is germane to the hypothesis because in the "ridges-off-the-end" syndrome the t triradius is always in a t" or t"' position. CONCLUSION Much difficulty has arisen in the field of dermatoglyphics because of our failure to study the subject in its developmental context. The hypothesis set out here suggests that at least one variable dermatoglyphic trait (and possibly others) are the result of embryonic migration. Proof can only come by experimental interference with the development of the limbs, and this clearly cannot be done in man. Indirect evidence might be sought by examining a variety of cases of proven developmental arrest. Direct experimental interference might be possible in primates who are also well endowed with dermatoglyphic patterns. REFERENCES 1.
Mulvihill JJ, Smith DW. The genesis of dermatoJ Pediat 75: 579, 1969. glyphics.
2.
Okajima M. Development of dermal ridges in the fetus. J Med Genet 12: 243, 1975.
3.
Quantitative differences in morphoBabler WJ. genesis of human epidermal ridges. P. 199 in Wertelecki W, Plato CC. Dermatoglyphics - Fifty
643
Birth Defects: Years Later. Original Article Series, Vol 15, No 6, Alan R Liss, 1979. New York. 4.
Penrose LS, Ohara PT. The development of the epidermal ridges. J Med Genet 10: 201, 1973.
5.
Walker NF. The use of dennal configurations in the diagnosis of mongolism. Pediat Clin N A 5: 531, 1958.
6.
Deckers JFM, Oorthuys AMA, Doesburg WH. Dermatoglyphics in Down's syndrome, 1 Evaluation of discriminating ability of pattern areas. Clin Genet 4: 311, 1973,
7.
Preus M. A diagnostic index for Down's syndrome. Clin Genet 12: 47, 1977.
8.
Smith DW. Dysmorphology 69: 1150, 1966.
9.
Congenital malformations of human dermatoDavid TJ. Arch Dis Child 48: 191, 1973. glyphs.
10.
Penrose LS. chromosomes.
11.
Barlow P. The influence of inactive chromosomes Humangenetik 17: 105, 1973. human development.
12.
Schaumann B, Alter M. Dermatoglyphics Disorders (New York: Springer-Verlag),
13.
David TJ. syndrome.
(teratology).
J Pediat
Finger-print pattern and the sex Lancet 1: 298, 1967. on
in Medical 1976.
"Ridges-off-the-end" - a dermatoglyphic Human Heredity 21: 39, 1971.
644