2014 Group Project 5: Difference between revisions

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<pubmed>19701759</pubmed>
<pubmed>19701759</pubmed> [[Image:Integumentary_histology_02.jpg|frame| 250x250px|Histology of eccrine sweat gland]]
<pubmed>PMC2113922</pubmed>
<pubmed>PMC2113922</pubmed>


===Glands===
===Glands===
[[Image:Integumentary_histology_02.jpg|frame| 250x250px|Histology of eccrine sweat gland]]
[[Image:Integumentary_histology_02.jpg|frame| 250x250px|Histology of eccrine sweat gland]]
*Mammary glands develop from the mammary ridge- a downgrowth of the epidermis (ectoderm) into the underlying dermis (mesoderm). This occurs at about week 6 of development. Prior to puberty, the mammary glands are anatomically indistinguishable.  
*Mammary glands develop from the mammary ridge- a downgrowth of the epidermis (ectoderm) into the underlying dermis (mesoderm). This occurs at about week 6 of development. Prior to puberty, the mammary glands are anatomically indistinguishable.  
*Eccrine and apocrine sweat glands develop from the downgrowths of the epidermis into the underlying dermis. It has been seen and detected in studies from week 21.
*Eccrine and apocrine sweat glands develop from the downgrowths of the epidermis into the underlying dermis. It has been seen and detected in studies from week 21.

Revision as of 01:09, 8 October 2014

2014 Student Projects
2014 Student Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7 | Group 8
The Group assessment for 2014 will be an online project on Fetal Development of a specific System.

This page is an undergraduate science embryology student and may contain inaccuracies in either description or acknowledgements.

Integumentary

--Mark Hill (talk) 15:16, 26 August 2014 (EST) OK you have some headings, how about some content, references, sources for each section. See Lab 3 Assessment.

--Mark Hill (talk) 11:48, 6 September 2014 (EST) This is a start. Less textbook referencing please, more research/reviews from the published literature. Textbooks should not be used as primary sources, I am happy for them to be listed as related literature.

Introduction

Development Overview

Skin

The skin consists of 2 layers: the outer layer (epidermis) and a deeper connective tissue layer (dermis).

  • The epidermis is derived form the ectoderm. Initially it exists as only a single layer of ectodermal cells at 7-8 days of gestation. However, by about 13-14 weeks after gestation, a 3- layered structure of fetal epidermis exists- consisting of the stratum basale, 1 or 2 intermediate layers and the periderm. The peridermal cells eventually become desquamated and form part of the vernix cervix.
    • The 5 definitive layers of the adult skin are evident in the human fetus after 22-24 weeks of gestation. Indirect influences form the dermis help differentiate the epidermis into: stratum basale, stratum spinosium, stratum granulosum, stratum lucidum and stratum corneum.
  • The dermis is derived from the somatic mesoderm and the mesoderm of the dermatones of the body. In the head and neck region, however, the dermis is derived from neural crest cells.
    • The dermis is initially composed of just mesenchymal cells- loosely aggregated mesodermal cells, which later develop into fibroblasts- which secrete increasing amounts of collagen and elastic fibers into the extracellular matrix.


3 other specialised cells of the epidermis also exists- these include melanoblasts, Langherhan cells and Merkel cells.

  • Melanoblasts- are derived from neural crest cells that have migrated into the stratum basale. Mid-pregnancy, melanosomes are observed, differentiating the melanoblasts into melanocytes
  • Langheran cells- are derived from bone marrow (originally form mesoderm) and migrate into the epidermis. They have the function of antigen presentation.
  • Merkel cells- still have an uncertain origin. They have a function related to mechanoreception.


Week Description Phase Diagram
Week Example Example
Week 6-8 Example Weeks 6-8
Week 7-9 Example Weeks 7-9
Week 14 Example Week 14
Week 16 Example Week 16
Week 18 Example Week 18
Week 19 Example Week 19
Week 20 Example Week 20
Week 22 Example Week 22
Adult Example Adult Adult

<pubmed>19701759</pubmed>

Histology of eccrine sweat gland

<pubmed>PMC2113922</pubmed>

Glands

Histology of eccrine sweat gland
  • Mammary glands develop from the mammary ridge- a downgrowth of the epidermis (ectoderm) into the underlying dermis (mesoderm). This occurs at about week 6 of development. Prior to puberty, the mammary glands are anatomically indistinguishable.
  • Eccrine and apocrine sweat glands develop from the downgrowths of the epidermis into the underlying dermis. It has been seen and detected in studies from week 21.
  • Sebaceous glands develop from the epithelial wall of the hair follicle
Cite this page: Hill, M.A. (2014) Embryology Integumentary System - Gland Development. Retrieved October 7, 2014, from https://php.med.unsw.edu.au/embryology/index.php?title=Integumentary_System_-_Gland_Development
Histology of sebaceous gland

Hair

The stages of hair development

Hair originates from the ectoderm. At about 12 weeks, it is believed that specific signals from the dermis begin to induce hair follicle formation. Through reciprocal interactions, cells from the stratum basale grow into the underlying dermis. The epithelial cells influenced by these dermal signals, develop a placode- a thickening of the columnar cells. Signalling from the placode than leads to the development of a dermal condensate, which further induces the downward growth of the placode. The hair follicle, continues to proliferate and enclose the dermal condensate, forming a deep, club-shaped hair bud, with an invaginated dermal papillae. These dermal papillae are rapidly infiltrated by blood vessels and nerve endings. The epithelial cells within the hair bulb, then begin to differentiate into the germinal matrix – which grow, proliferate and keratinise to form the hair shaft and internal root sheet. Other epithelial cells outside of the hair bud, form the external hair sheeth. Mesodermal cells of the dermis that surround the invaginating hair follicle form the dermal root sheeth and the arrecrtor pili muscles.

<pubmed>20590427 </pubmed> <pubmed>11841536 </pubmed> <pubmed>1566372 </pubmed>

Nail

  • Nails also develop from the epidermis.
  • The development and growth of the fingernails occurs earlier in week 10, compared to the toe nails- which only start developing in week 14.
  • Nail development grows first on the tips of the digits, before actually migrating,-with their innervation-onto the dorsal surface. Nails reach the digit fingertips at approximately week 32, while for toenails, it occurs a bit later- at week 36.
  • The nail fold is thickened epidermis, with keratinisation of the proximal end forming the nail plate
Cite this page: Hill, M.A. (2014) Embryology Integumentary System - Nail Development. Retrieved October 7, 2014, from https://php.med.unsw.edu.au/embryology/index.php?title=Integumentary_System_-_Nail_Development


Teeth

Teeth develop from the ectoderm and the underlaying layer of neural crest cells. The dental lamina develops from the oral epithelium (ectoderm) , as a downgrowth into the underlying neural crest layer. The dental lamina gives rise to the tooth buds, which later from enamel organs. These enamel organs give rise to ameloblasts- which produce enamel. The dental papilla, on the other hand is formed by the neural crest cells which underlie the enamel organs. These dental papillae than give rise to the dental pulp and odontoblasts- which produce predentin and dentin, in the adult body.

The stages of embryonic teeth development


Stage Week Description
(A) Lamina Week 6 The oral ectoderm, closely interacts with the neural crest ectomesenchyme. In the Lamina stage, teeth may grow only within the epithelium.
(B) Placode Week 7 The dental lamina and and the dental placodes arise, due to specific signals from adjacent epithelial cells
(C) Bud Week 8 Tooth buds are formed, as the epithelium cells interact with the messenchyme. This occurs at the sides of the dental placodes. Also, as opposed to the earlier Lamina stage, in the Bud stage, teeth may now only grow within the ectomesenchyme
(D) Cap Week 11 After folding, the bud takes upon the shape of an inverted cap
(E) Bell Week 14 The bud refolds once again, this time taking upon the shape of a bell



References

<pubmed>19266065</pubmed>| PMCID: PMC2651620

Int J Biol Sci. 2009; 5(3): 226–243. Published online 2009 February 24.

Copyright © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.

Some Recent Findings

Expression of caspase-14 and keratin-19 in the human epidermis and appendages during fetal skin development: Caspase-14 (CASP-14), a distinctive member of a unique family of cysteinyl aspartate-specific proteases has been exhibited via animal models to lack the typical caspase functions in apoptotic pathways however seems to actively participate in the developmental processes of terminal keratinocyte differentiation and cornification of fetal skin. Keratin- 19 (CK-19) is a type I keratin expressed from the early embryonic to the late fetal stages of human fetal skin development and functions as biochemical marker for cells of epithelial origin and potentially for epidermal stem cells. In recognition of the vital roles of CASP-14 and CK-19 in human skin development and maturation, the purpose of this study was to primordially investigate the expression of these two molecular factors throughout the stages of human fetal skin development from the gestational to postnatal period in order to evaluate their singular and collective functions in epidermal and associated appendage maturation and processes of differentiation and re-modelling of human fetal skin. The investigation was carried out as a retrospective immunohistochemical study observing the expression of CASP-14 and CK-19 in human skin samples collected at autopsy. Expression of CASP-14 was concentrated within the more differentiated fetal epidermal layers, progressively declining from the basal layer toward term. Expression within the epidermal appendages of the hair follicles and sebaceous glands were concentrated within layers of greater differentiation of the inner root sheath. CK-19 showed reduced expression with progressive epidermal development of the fetal stages and was a biochemical marker for epidermal stem cells nests of the stratum basale, showing marginal conservation in basal cell nests at term and postnatally. Expression within the epidermal appendages of the hair follicles and sebaceous glands were concentrated within the outer root sheath. Inconsistent patterns of expression of both molecules CASP-14 and CK-19 were demonstrated within eccrine sweat glands. Thus CASP-14 has demonstrated to be a biochemical marker of human epithelial differentiation during gestation, whilst CK-19 was a marker for epidermal stem cells nests of the stratum basale of the fetal epidermis and appendages.

<pubmed> 23377137</pubmed>

Figure 1: Hematoxylin/ eosin staining of embryonic skin sections and macroscopic view of external hair shafts of mouse. Cxcr4 receptor ablation in condensates and placodes show no effect on mouse HF morphogenesis. Hair follicle and shaft develop normally and in comparable numbers in both Tbx18cre (a) and Krt14-cre (b) Cxcr4fl/fl cKO mice.

Cxcr4 is transiently expressed in both epithelial and mesenchymal compartments of nascent hair follicles but is not required for follicle formation: Cellular signalling between mesencyhmal and epithelial layers of the developing skin initiate an assortment of morphogenetic events throughout embryogenesis, involving the formation of the skin and its related appendages. In particular, the development of hair follicles (HF) has been identified to be critically associated with the synchronized signalling exchanges between these two cellular layers and this interaction is understood to involve two specialised cell types- mesenchymal dermal condensate (DC) cells and epithelial placode cells. Expression of the chemokine receptor Cxcr4 has recently been detected in DC’s of budding HF’s however its function in supporting embryonic HF morphogenesis is currently unidentified. The aims of this study was to identify the specific signalling pathways associated with HF morphogenesis through investigating the precise expression patterns and subsequent role of the Cxcr4 receptor in both DC and epithelial placode cells during the primary stages of mouse hair follicle development. Expression patterns of the Cxcr4 receptor were identified via immunofluoresent staining on back skin sections of mouse embryos aged 14.5 days during the three main HF developmental stages. Subsequent analysis of staining patterns revealed Cxcr4 receptor expression in budding HF is concentrated within epithelial placode cells and later DC cells in developing HF’s, signifying a shift of expression between epithelial and mesenchymal layers during HF morphogenesis. The functionality of the Cxcr4 receptor was tested using a separate cre/loxP recombination system in genetically altered mice to conditionally ablate this gene in both the mesenchymal and epithelial layers of the developing embryonic mouse skin. To target DC’s a cross was made between Tbx18cre and Cxcr4 floxed mice and epithelial placodes were targeted via the crossing of Krt12-cre with Cxcr4 floxed mice. Cxcr4 receptor ablation in conditional knockout mice (cKO) was verified through immunofluorescence. Normal HF development was still induced despite the absence of Cxcr4 expression in the skin of the cKO mice and numbers were comparable to those found in the wild-type (WT) control group in embryonic and postnatal skin groups showed that the Cxcr4 receptor and the associated chemokine signalling through this receptor is inessential for normal early HF development.

<pubmed>25066162</pubmed>

The ventral proximal nail fold: stem cell niche of the nail and equivalent to the follicular bulge--a study on developing human skin:

<pubmed>22804461</pubmed>

More Recent Papers

<pubmed>23826487</pubmed> <pubmed>22342389</pubmed> <pubmed>24911066</pubmed> <pubmed>25143675</pubmed>

Historic Findings

Skin


Glands

Sebacious glands

Sweat glands

Hair

Technology

The

<pubmed>5656140</pubmed>

The development of hair was noted to be a cycling phenomenon in 1959 from Chase and Eaton's experiments on the.

In 1953 Chase, Montagna and Malone concluded that with the development of the hair follicle the surrounding skin goes under. They determined the mechanism of hair follicle development.

Downwards growth of the follicle from the level of the dermis during the quiecent phase thought he adipose layer during gowth and differntiation.

They also established that upward movement of hair inovlves the addition of ne cells from the matrix of the follicle and an enlargement of each cell.

Furthermore their research also showed that the epidermal and dermal layers were dynamic and interacting with each other.

The most significant developments in the understanding of hair follicle development came from studies investigating the differentiation pattern of cells as the follicle develops.


<pubmed>4097391</pubmed>

Nail

Teeth

Abnormalities

Aplasia Cutis Congenita

Aplasia cutis congenita at the scalp

Aplasia cutis congenita (ACC) is a rare skin abnormality, characterised by the absence of all layers of the skin. It is most common to occur on the scalp (70%), specially the vertex. In severe cases, the defect can go as deep as the bone or the dura. Other sites of ACC include the skin of the limb regions. “ACC occurs in approximately 1 in 10000 live births, with a female-to-male ratio of 7:5.” The specific aetiologic agent for ACC is still unknown. It has been suggested to be genetic and/or environmental. The damage to the vertex is suggested to be the result of the biomechanical stretch at this area when the fetal brain is growing.[1]

Presently, ACC is managed via conservative treatments or surgical treatments. Conservative treatments refer to basic wound treatments and preventing infection with the use dressings and antibiotics. Surgical treatments, specifically scalp reconstruction procedures, aim to reconstruct the damage to the skin through skin grafts, local scalp flaps, and pericardial scalp flaps. Large defects are often treated using surgical treatments.[2]

Harlequin Ichthyosis

A baby with harlequin ichthyosis.[3]

Congenital ichthyosis is an autosomal recessive disease of the skin, characterised by visible and excessive scaling of the skin and hyperkeratosis, i.e. thickening of stratum corneum layer of the epidermis and in some cases, hypohidrosis, i.e. the lack of ability to sweat. [4] Harlequin ichthyosis (HI) occurs only in 1 in 1,000,000 babies. It is life-threatening in the first few weeks and/or months of the neonate.[4] The thick skin can restrict movement of the baby and sometimes constrict extremities and lead to necrosis then autoamputation.[5] Babies with HI are also characterised by bilateral ectropion (everted eyelids), eclabium (everted lips), and underdeveloped nose.[5] In 50% of HI cases, respiratory failure is often the cause of death.[6] This disease is caused by a nonsense mutation in the ATP-binding-cassette A12 (ABCA12) gene, which is responsible for encoding a lipid transporter essential for the regulation of lamellar bodies. [4][5][6]

There is currently no known cure for this disease. Management techniques include:

  • Monitoring in neonatal intensive care units.
-Temperature within the incubator is controlled to avoid fluctuation in body temperature and to stop sweating. [4]
  • Mechanical removal of excess scales from the skin [4]
  • Bathing to remove excess scales from the skin[4]
  • Topical therapy - to reduce hyperkeratosis. [4][6]
  • Use of oral retinoids - known to have high rates of survival.[6]

Hypohidrotic Ectodermal Dysplasia

Oligodontia: a clinical manifestation of HED.[7]

Hypohidrotic ectodermal dysplasia (HED) is the most of all ectodermal dysplasias, caused by an abnormality in the development of ectodermal tissues, which inlude skin, hair, teeth, sweat glands, and nails.[8][9] Patients with ectodermal dysplasia often have sparse hair and oligodontia, which is a condition where teeth are missing and are poorly developed.[8][9] Sweating is a very important function in the body in terms of thermoregulation. HED is mainly characterised by hypohidrosis due to the lack of sweat glands in the skin, which could lead to hyperpyrexia and sometimes death. In neonates, the mortality rate of HED reaches up to 30%, with the first year of life having the highest risk. [8] HED is caused by a genetic abnormality of the ectodysplasin A gene (EDA) and passed on by X-linked inheritance. The mutations of this gene results in the poor sweating ability or none at all in a person. The effects of this abnormality is usually more severe in males than in females. [10][9]

There is currently no pharmacological therapies for HED but there are methods applied to prevent the disease from aggravating. Neonates with HED are placed in incubators and monitored to prevent them from overheating. Management of this disease gets easier as the patient ages. Adults with HED can control their thermoregulation by staying in cool environments or drinking cold drinks to lower the body temperature. Currently, there are studies that aim to find a cure for this abnormality, e.g. gene replacement therapy in animal models.[9]

Congenital Alopecia Areata

Patches of hair loss: a sign of alopecia areata.[11]

Alopecia areata (AA) is an abnormality of the hair affecting anagen hair follicles, characterised by well-demarcated patches of hair loss. It is non-scarring and can occur on the scalp and/or the body. 90% of AA cases occur on the scalp. 5%-10% of patients with AA lose all hair on their scalp; this is called alopecia totalis. While others lose all of their body hair, this is called alopecia universalis. [12] Its pathogenesis is considered to be both genetic and autoimmune. There is an abnormality with the genes related to the immune system and to the hair follicles. And histopathology shows signs of lymphatic infiltration of the hair follicles and the loss of these scalp lymphocytes allow hair follicles to recover.[13] High frequencies of catagen and telogen hair follicles are also present in areas affected by AA.[12]

There is currently no cure for AA. There are several treatments to combat AA but none of these have led to remission of the disease, the most effective being corticosteroids and topical immunotherapy.[12] A new method of treating alopecia areata is currently being studied. Transepidermal drug delivery (TED) is a new treatment that functions by creating micro-channels in the epidermis. By doing so, drug delivery to the skin is improved. This treatment was highly effective and had lower rates of side effects, e.g. pain, compared to previous treatments.[14]

References

  1. <pubmed>22549580</pubmed>
  2. <pubmed>23147310</pubmed>
  3. <pubmed>24520234</pubmed>
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 <pubmed>19824737</pubmed>
  5. 5.0 5.1 5.2 <pubmed>23419760</pubmed>
  6. 6.0 6.1 6.2 6.3 <pubmed>24124810</pubmed>
  7. <pubmed>21165248 </pubmed>
  8. 8.0 8.1 8.2 <pubmed>20682465</pubmed>
  9. 9.0 9.1 9.2 9.3 <pubmed>24678015</pubmed>
  10. <pubmed>21357618</pubmed>
  11. <pubmed>23960401</pubmed>
  12. 12.0 12.1 12.2 <pubmed>17269961</pubmed>
  13. <pubmed>16338213</pubmed>
  14. <pubmed>25260052</pubmed>