2014 Group Project 5

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.

Development Overview

Skin

Week	Description	Phase Diagram
Week 4-5	Example	Example
Week 5-6	Example	Example
Week 8-10	Example	Example
Week 12	Example	Example
Week 40 (birth)	Example	Example
Adult	Example	Example

Teeth

<pubmed>19701759</pubmed>

Current Research

• Fetal skin wound healing:
• Biology and function of fetal and pediatric skin:
• Selective D2-40 lymphatic endothelium immunoreactivity in developing human fetal skin appendages:

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.

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.

Harlequin Ichthyosis

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. 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. The thick skin can restrict movement of the baby and sometimes constrict extremities and lead to necrosis then autoamputation. Babies with HI are also characterised by bilateral ectropion (everted eyelids), eclabium (everted lips), and underdeveloped nose. In 50% of HI cases, respiratory failure is often the cause of death. 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.

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.
• Mechanical removal of excess scales from the skin
• Bathing to remove excess scales from the skin
• Topical therapy - to reduce hyperkeratosis.
• Use of oral retinoids - known to have high rates of survival.

Hypohidrotic Ectodermal Dysplasia

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. Patients with ectodermal dysplasia often have sparse hair and oligodontia, which is a condition where teeth are missing and are poorly developed. 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. 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.

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.

Congenital Alopecia Areata

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. 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. High frequencies of catagen and telogen hair follicles are also present in areas affected by AA.

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. 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.