Skin diseases affecting friction ridge skin

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Introduction

Embryological development of friction ridge skin is a key element in the uniqueness of the features observed in the impressions used for friction ridge comparative science. Understanding how the skin develops along with its morphology aids latent print examiners in explaining the two fundamentals of the comparative science of friction ridge analysis: uniqueness and permanence.

Required Reading:

Maceo, A. (2011). “Chapter 2: Anatomy and Physiology of Adult Friction Ridge Skin.” The Fingerprint Sourcebook. Available: https://www.ncjrs.gov/pdffiles1/nij/225322.pdf

Wertheim, K. (2011). “Chapter 3: Embryology and Morphology Friction Ridge Skin.” The Fingerprint Sourcebook. Available: https://www.ncjrs.gov/pdffiles1/nij/225323.pdf

Objectives

Understand the stages of fetal growth and friction ridge development throughout these stages

Understand how volar pad development and shape affects the resulting fingerprint patterns

Understand the difference between primary and secondary friction ridges

Understand the development of friction ridge minutiae features

Be able to identify the different layers of skin and their function

Explain how genetics affects friction ridge features

Comprehend the functions of skin

Assignment

You must answer both questions for full credit.

Give an example of and explain how skin diseases affect friction ridge skin.

In no less than 500 words: explain how genetics and the in-utero environment affect friction ridge skin development.

Submit your answer in Blackboard.

Embryological Development of Friction Ridge Skin

Friction ridge skin possesses unique features that develop before birth and are persistent throughout life until decomposition after death. Over one hundred years of empirical data consisting of observation and statistical studies lays the foundation for the uniqueness and persistence of friction ridge skin. Biological uniqueness, which states that no two living organisms are alike, aids in the foundation that friction ridges are unique. Embryological development accounts for the uniqueness of the friction ridge features, which posses their adult morphological features between 10.5 and 16 weeks estimated gestational age.

0-2 weeks Estimated Gestational Age

During this time period, the primary development involves fertilization of the female ovum and the rapid division of cells called cleavage.

3-8 weeks Estimated Gestational Age

As cleavage ends, different genes are activated moving certain cells inward in a process called gastrulation. In this process, the primary tissue distinctions form between the ectoderm, mesoderm, and endoderm. The ectoderm later forms the epidermis; the mesoderm forms the muscle, components of the vascular system and the connective tissue seen in the dermis. The endoderm cells eventually form the organs.

Having been specialized in their function, the cells begin to differentiate beginning with the formation of the spinal cord and brain in a process termed neurulation. Differentiation continues in a block-like fashion forming muscles, connective tissue and vertebrae.

During this gestational period, the developing embryo also undergoes the process of morphogenesis wherein the limbs develop rapidly at about four weeks estimated gestational age. Originally paddle-like in its structure, the hands change to the adult morphology with the formation of the fingers and the rotation of the thumb. The initial step in friction ridge formation also occurs with the development of the volar pads on the palms of the hands and soles of the feet.

9-12 weeks Estimated Gestational Age

Embryological development, the development of the nervous system and organs continues. Friction ridges begin to develop at around 10.5 weeks estimated gestational age and continuing onto the second trimester.

Second Trimester

During the second trimester, bone growth is active. On the hands and feet, the volar pads begin to regress and the friction ridges continue growing until 16 weeks estimated gestational age. Sweat glands mature during this period along with the friction ridge size growth and maturation.

A: Paddle-like hand formation

B: Separation of the fingers

C: Appearance of volar pads

D: Infant-like appearance of hand morphology by 8 weeks

Photo courtesy of: Wertheim, K. (2011). “Chapter 3: Embryology and Morphology of Friction Ridge Skin.” Fingerprint Sourcebook National Institute of Justice. Available: https://www.ncjrs.gov/pdffiles1/nij/225323.pdf.

Hand Development

The development of the hand occurs in several phases. During the estimated gestational age period of 5-6 weeks, the hand is initially paddle-like in shape. While shaped like a paddle, the hand also possesses finger-like projections that develop muscle and cartilage during the 6-7 estimated gestational age. Also, at approximately six weeks, the volar pads, which are swellings of the mesenchymal tissue located under the dermis of the palmar and plantar surfaces. Fingers begin to separate from the paddle like hand between 7-8 weeks estimated gestational age. At this point, the hand begins to develop flexion creases such as the crease located in the thenar region of the hand (radial longitudinal crease). External morphology exhibits that of an infant at 8 weeks estimated gestational age. Flexion creases of the fingers begin to form at about 9 weeks estimated gestational age.

With the separation of the fingers, the development of the friction ridge skin continues. Between 9 and 10 weeks, the volar pads on the hands remain well rounded after which time they begin to differentiate in their shape and size. Regression of the palmar volar pads begin at about 11 weeks estimated gestational period followed by those on the fingers. By 16 weeks estimated gestational age, the volar pad has merged with the epidermis of the palmar and plantar surfaces of the feet. The programmed development of volar pads and flexion creases results in the general crease and ridge configuration being consistent among humans.

Appearance and development of volar pads is represented in the image to the left. The illustration does not account for the growth of the finger.

Volar pads are important factors in determining overall pattern types of the fingers. It is understood that the topology of the surface of the volar pad creates stresses, which are potentiated during friction ridge development and aid in the overall development of the configuration of friction ridge features. Overall, the curvature in the surface of the volar pad helps determine what ridge flow pattern will develop. Generally, a high volar pad will produce whorl flow patters while a low/flat volar pad will produce that of an arch. A medium height volar pad will produce a loop slanting flowing outward depending on the slant of the volar pad.

The figure above depicts the normal starting locations of friction ridge development on the finger and their progression to covering the palmar surface of the finger. This image also depicts the resulting pattern formation on a finger possessing a high volar pad (more typically a whorl pattern).

The image above depicts the theorized ridge and minutiae formation of a finger possessing a low volar pad (more typically an arch pattern).

Primary Friction Ridge Formation

Depending upon the reference, friction ridge formation begins between 10 and 12 weeks estimated gestational age when the cells of the epidermis quickly divide, thus leaving bands of thickening tissue on the bottom side of the epidermis. Imprinting into the basal layer, these thickening bands on the bottom of the epidermis will determine the overall patterns that ultimately form on the surface of the volar pad.

The prevailing theory in the development of friction ridge skin involves that of a unit that consists of a pore. Each ridge unit also consists of rapidly dividing cells, which increase the diameter of the ridge unit until such time as they collide into each other linearly. At this point, the ridge units fuse together to form the linear ridges of friction ridge skin. Between approximately 10.5 weeks when the primary ridges form on the volar pad to approximately 16 weeks estimated gestational age, the primary ridges extend into the epidermis, mature and expand further toward the dermis.

The figure to the left depicts the ridge unit theory of primary ridge formation. Each ridge unit emerges on the surface of the friction ridge skin, linearly, until they merge together forming friction ridges at approximately 10.5 estimated gestational age.

While the mechanistic foundation for the formation of minutiae remains unclear, several researchers have examined fetal tissue in order to understand minutiae morphogenesis. Many factors occur during primary friction ridge growth such as: rapid growth of the hand/fingers, formation of new primary ridges and expansion of the existing primary ridges. As the existing primary ridges expand, there is a need to fill the space with which they occupied. Bifurcations are formed when new ridges pull away from the migrating primary ridge into the empty space with which it occupied. When a new developing ridge becomes “sandwiched” between two existing primary ridges, an ending ridge is formed.

The figure to the left depicts the primary theory for minutiae development.

Secondary Ridge Formation

During the estimated gestational age of 15 weeks, the primary friction ridges experience bidirectional growth: both the downward penetration of the sweat glands of the friction ridge unit and the upward projection of new cell growth. The secondary ridges (furrows) appear between 15 and 17 weeks when they form between primary ridges and result in the down-fold of the basal layer of the epidermis. It is at this point that the minutiae formation occurring in the primary friction ridges ends and the formations contained within the palmar and plantar surfaces become set.

General Anatomical Features of the Skin

While the foundation for friction ridge Comprised of three anatomical layers, epidermis, dermis, and hypodermis, the morphology of friction ridge skin is a direct result of its function: grasping and flexing. In addition to grasping and flexing function, the three anatomical layers of skin also act as a protective barrier to the body and act to regulate body temperature.

The external most surface of the skin is called the epidermis, which functions to prevent water loss by means of evaporation from the body. Being the outermost surface of the skin, the epidermis also plays a part as a receptor organ and a protective barrier that is comprised of melanocytes that protect the primary skin cells (keratinocytes) from DNA damage from harmful UV rays of the sun.

A layer of connective tissue named the dermis supports the epidermis. The connective tissue of the dermis is comprised of gelatinous material, cells, fibers and blood vessels. This layer’s primary function is to serve as a barrier to regulate temperature, acts as a blood reservoir and acts in sensory reception.

The innermost layer of skin is known as the hypodermis, and is comprised primarily of fat cells. The fat cells of this layer of skin serve as an energy reserve. All three layers of skin are connected by fibers.

The sole appendages of the three layers of friction ridge skin are that of the eccrine sweat gland. While these glands are also distributed throughout the skin on the entire body, they exist in the highest concentration (2500-3000/2.5 cm2) and they are the largest eccrine sweat pores on the body.

General structure of friction ridge skin

Photo courtesy of: Maceo, A. (2011). “Chapter 2: Anatomy and Physiology of Adult Friction Ridge Skin.” Fingerprint Sourcebook National Institute of Justice. Available: https://www.ncjrs.gov/pdffiles1/nij/225322.pdf.

Epidermis

The external most layer of skin, the epidermis, consists of layered tissue that is constantly renewing itself. This layer of skin is comprised of several different types of cells, the primary of which is known as a keratinocyte. Keratinocytes encompass over ninety percent of the epidermal cell population and are constantly pushed up from the base of the epidermis and sloughed off when they reach the surface. Interestingly, the chemical composition of the keratinocyte changes as it migrates toward the surface of the epidermal layer, only being identified by its maintenance of keratin filaments.

Much like the skin is divided into different layers, the epidermis also consists of several layers. The inner most surface of the epidermis, next to the dermis, is that of the stratum basale. This layer is only one cell thick and primarily consists of keratinocyte cells; however, melanocytes and Merkel cells can be intermittently placed throughout the layer. The cells inhabiting the stratum basale are also associated with the dermis in the basement membrane zone, which exists to provide support and acts as to filter nutrients and blood to the epidermal basal layer cells.

At the basal layer, the keratinocytes are constantly dividing through the process of mitosis. The mitotic division occurs in a manner wherein the original cell remains at the basal level with the new cell sitting right on top of it. As the original cell divides again, each new cell sits atop the original cell at the basal layer thereby pushing up each cell as the mitotic division is repeated.

Depiction of epidermal keratinocyte mitosis

As the basal layer keratinocytes continue to divide, the divided cells are consistently pushed, one cell at a time, up toward the surface of the epidermis. After generating upward from the basal layer, the newly divided cells sit in the suprabasal layer wherein they are termed transient amplifying cells. These cells are eventually pushed upward into the next layer of the epidermis termed the stratum spinosum where they begin to differentiate in shape and composition. Keratinocytes are pushed further outward into the stratum granulosum and continue in their structural and chemical compositional differentiation. Cells in this stage begin to fill with keratin and are abruptly pushed further out to the stratum lucidum where they are considered to be keratinized wherein they have completed apoptosis, programmed cell death. The outermost layer of the epidermis is known as the stratum corneum. In this layer, the keratinocytes are arranged in a “brick and mortar” arrangement where the cells are surrounded by lipids. Despite the cells are dead, having completed the apoptosis process in the stratum lucidum, they continue their structural differentiation as they are pushed toward the outermost surface of this layer. Initially, these cells are thicker with more densely packed keratin; however, as the cells are pushed outward, the cell is allowed to be shed due to the fact that structures called desmosomes are degraded and the cell becomes more ridged.

Epidermal layers

Dermis

The dermal layer of skin exists immediately below the basal layer of the epidermis. This stratum of skin consists of connective tissue that exists in two layers: the outermost papillary layer and the inner reticular layer.

The outermost papillary layer of the dermis is that of loose connective tissue as well as anchoring fibrils that aid in securing the dermal layer of skin to the epidermis. Another component of this layer are the dermal papillae, which are peg-like projects of the dermis that exist between the primary (ridges) and secondary (furrows) ridges of the friction ridge skin. These features are important in providing adhesion between the dermis and epidermis as well as serving to increase the surface area for nourishment to the epidermal layer. An important feature of the dermal papillae is that these features are malleable in nature, allowing them to respond to the change seen with the epidermal-dermal junction in repose to sheering stress placed on the skin and aging.

The innermost layer of the dermis, the reticular dermis, is comprised of compact connective tissue that contains large quantities of collagen and elastic fibers. This layer serves the function of providing strength to the dermis. Fibrous material connects the dermal layer to the hypodermis.

Sweat Glands

The sole appendage of the friction ridge skin is that of the eccrine sweat gland, which function simultaneously as a group performs the function of increasing friction between the surface of an object and the friction ridge skin.

Hypodermis

There is an abrupt transition from the reticular dermis to the adipose (fat) tissue of the hypodermis, which serves as an energy reserve, cushion for the underlying bone and allows for the movement on the skin laying above it. The sweat produced by eccrine glands is primarily water (99 – 99.5%) with the remaining components consisting of salts, inorganic and organic materials.

Friction Ridge Skin Persistence

Persistence of friction ridge skin lays in its physical attachments as well as the regulation and differentiation of the main cell type, keratinocytes. Due to the cell proliferation occurring at the basal layer of the epidermis, the three-dimensional morphology of the friction ridge skin on the stratum corneum layer is maintained. Due to the constant sloughing off of skin cells at the surface of the epidermis, the affect of aging and the potential to damage the friction ridge skin resulting in scars, the friction ridge skin is said to be persistent.

Effects of Aging on Friction Ridge Skin

While the arrangement of the features in friction ridge skin does not change, aging affects the height of the ridges as well as the elasticity of the skin causing wrinkles. As the skin ages, the ridges begin to flatten as the dermal papillae remodel and the epidermis becomes more atrophied. The effect of dermal papillae remodeling is affected by the amount of stress the individual places on the area of friction ridge skin. Since shirring stress causes the existing dermal papillae to branch further in order to the epidermis to increase the adhesion between layers, aging affects the overall number and crowding of papillae.

Aging also results in flattening of the ridges as a result of changes in the epidermis and dermis. While the thickness of the outermost stratum corneum is maintained throughout the lifetime, the proliferation at the basal layer decreases by 30-50% from age 30 to 80. Thinning is then caused by the reduced capacity of the basal layer to produce new cells pushing toward the outer surface of the epidermis. While the arrangement of the friction ridges does not alter as a result of flattening, the distinction between the ridge and the furrow of an impression may be difficult to determine.

Friction ridge skin of a 30-week-old fetus

Older adult friction ridge skin

Wrinkles

Wrinkles occur as a result of dermal thinning. As the dermis thins, elastin fibers lose their elasticity and collagen fibers begin to unravel. As these two fibers compact and subsequently break down, the skin becomes lax and prone to wrinkles.

Scars

Barring injury to the basal, the friction ridge skin remains persistent throughout the lifetime of an individual. When injury occurs that penetrates the basal layer of the skin, the keratinocytes change both structurally and physiologically in order to repair the injury. Injuries are healed in a three-step process of inflammation, proliferation and tissue formation and remodeling.

After an injury occurs, inflammation at the site of injury occurs immediately. Penetration into the dermal layer of skin causes blood loss and spillage into the surrounding tissue. Signals are sent from the site of injury to recruit clot-forming platelets and dermal fibroblast cells are concentrated in the dermal area to repair the wound. In the epidermis, endothelial cells are recruited to repair damaged blood vessels. As the basal keratinocytes adjacent to the wound take over the healing process, phase II of healing begins.

Due to the disruption in the basal layer, basal keratinocytes are exposed to the dermal layer of skin resulting in a dramatic change in their structure and physiology. Ultimately, as a direct result of the structural and physiological changes, the basal keratinocytes adjacent to the site of injury lose their firm attachment at the basal layer. These keratinocytes possess actin filaments, which aid in healing by allowing them to “walk” across the site of injury. As these migrating keratinocytes crawl across the site of injury, the keratinocyte cells behind them begin to divide and fill the space from which they vacated. Since the adjacent keratinocytes divide, cells are provided to aid in covering the wound. As the migrating keratinocyte migrates to cover the wound, the skin in this area contracts causing puckering that is noticeable in friction ridge skin.

As the skin contracts, the leading keratinocytes from either side of the wound eventually meet and form a gap junction that allows for the recreation of the basal membrane over the site of injury. As the basal membrane is established, the keratinocytes begin to divide in the fashion described above to push toward the surface. However, since the injury penetrated the basal layer, disrupted and changed the function of the basal keratinocytes adjacent to the site of the wound, the friction ridges that were previously present in this area are not reconstituted. Since the basal keratinocytes at the injury site have formed a new template, the friction ridge detail that was previously present is unable to be recreated. The skin at the site of the scar is free from both primary and secondary ridges as well as pores leaving it smooth in nature.

Once the dividing keratinocytes have reached the surface at the site of injury, phase III of wound healing begins with the dermal skin remodeling to reinforce the scar tissue seen on the surface. Like friction ridge skin, the resulting scar is unique and three-dimensional in nature. When the friction ridge skin impresses upon a surface, the scar will also leave behind distinctive features in the resulting latent print impression. Comparison of friction ridge skin and latent prints that possess scars follows the same methodology of that which does not contain a scar.

Conclusions

Based upon the embryological development, the role of internal in utero forces along with genetics aids in the understanding that friction ridge skin is unique. The cellular composition aids in understanding the persistence of the friction ridge skin and the structure aids in explaining distortions observed in resulting latent prints.

References:

Ashbaugh, D. (1999). “Ridgeology: Modern Evaluative Friction Ridge Identification.” Royal Canadian Mounted Police. Available: http://onin.com/fp/ridgeology.pdf

Maceo, A. (2011). “Chapter 2: Anatomy and Physiology of Adult Friction Ridge Skin.” Fingerprint Sourcebook National Institute of Justice. Available: https://www.ncjrs.gov/pdffiles1/nij/225322.pdf.

Park, J. et. al. (2010). “Improved Analysis of Palm Creases.” Anatomy & Cell Biology 43(2): 169-177. Available: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998791/.

Wertheim, K. (2011). “Chapter 3: Embryology and Morphology of Friction Ridge Skin.” Fingerprint Sourcebook National Institute of Justice. Available: https://www.ncjrs.gov/pdffiles1/nij/225323.pdf.