Biology Forums - Study Force

Hi! I know that there are only 2 questions per topic, but I feel like this comes under the same umbrella as one question.. Hopefully? I'm not sure if I should split this into two topics! But here goes!

Bart and Homer were riding their motor bikes through the hills when they skidded on
some oil on the road. Bart sustained some superficial abrasions to his elbows. Homer
sustained a large deep gash to his right knee and the palm of his left hand along with a
scrape to his head that resulted in the removal of his last remaining hairs.
(25 marks in total)

a) List the five layers of the epidermis and discuss how each layer contributes to the
effectiveness of this structure? (10 marks)

b) Bart sustained superficial abrasions to his elbows, affecting only the epidermis,
although his head hair was damaged in the fall, and took on a serrated
appearance. Discuss how the epidermis undergoes wound healing. (5 marks)

c) Superficial injuries generally heal without scar tissue, but the healing process of
Homer’s deeper injuries is more complex would likely result in scarring. Explain
how the scarring occurs and how it differs from normal skin. (5 marks)

d) The injuries to Bart and Homer’s skin involved various thicknesses of skin.
Compare and contrast thin and thick skin. (5 marks)

(http://upload.wikimedia.org/wikipedia/commons/2/20/Skinlayers.png)

a. The stratum basale (basal layer) is the deepest epidermal layer and is the site of mitosis.

b. The stratum spinosum (prickly layer) is several cell layers thick and contains keratinocytes, melanin granules, and the highest concentration of epidermal dendritic cells.

c. The stratum granulosum (granular layer) contains keratinocytes that are undergoing a great deal of physical changes, turning them into the tough outer cells of the epidermis.

d. The stratum lucidum (clear layer) is found only in thick skin and is composed of dead keratinocytes.

e. The stratum corneum (horny layer) is the outermost protective layer of the epidermis composed of a thick layer of dead keratinocytes.


Skin is composed of two distinct layers, the epidermis and the dermis. In partial thickness epidermal wounds, only the epidermis is damaged, leaving the basement membrane intact along with hair follicles and sweat and sebaceous glands. Because only the epidermal surface needs to be replaced and epithelial progenitor cells remain intact below the wound, the synthesis and deposition of collagen is not required. To repair a surface lesion such as a “paper cut,” the site must only be reepithelialized by migration of keratinocytes from below the wound and at the wound edge. The degree of reepithelialization depends on the amount of tissue loss and the depth and width of the wound.

Reepithelialization begins within 24 to 48 hours as uninjured keratinocytes detach from the basal lamina to bore through or underneath the fibrin clot, crawling into and across the wound—a process termed lamellopoidial crawling. Migration starts as keratinocytes at the wound edge upregulate their production of matrix metalloproteinases (MMPs), releasing the cells from their tethers to the basal lamina. Keratinocytes resting on the basal lamina migrate across the wound site at a rate of 1 to 2 mm/day, attaching to fibronectin and vitronectin contained within the clot by upregulating their expression of a5ß1 and aVß6 integrins. While moving through the dense fibrin clot, keratinocytes dissolve the dense fibrin matrix through the upregulation of several proteases such as tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA), activating the fibrinolytic enzyme plasmin.

Keratinocyte locomotion occurs through the contraction of actinomyosin filaments of the cytoskeleton. Because of changes in integrin expression and actinomyosin filament assembly as keratinocytes attach to the clot’s provisional matrix, there is a delay of several hours before the migration of basal keratinocytes is observed. Once migration begins, keratinocytes move one by one over the wound site until the wound is covered by a complete layer of keratinocytes. After migration is complete, the cells behind the wound edge undergo a proliferative burst to replace keratinocytes lost resulting from injury while also forming additional keratinocyte layers over the basal layer. It is believed that epidermal growth factor (EGF), keratinocyte growth factor (KGF), and transforming growth factor (TGF-a) may drive cell proliferation and wound closure. Migration and proliferation continue until keratinocytes receive a stop signal, likely due to contact inhibition. At this time, MMP expression is interrupted, and a new basement membrane is produced whereby new cell-matrix adhesions are established.


This is a very *scientific* explanation, but I hope it gives some insight.

(http://www.ncbi.nlm.nih.gov/books/NBK3938/bin/ch1f7.jpg)

Wound remodeling of different tissue types. (A) At the site of injury, the fibrin clot and necrotic tissue is removed by microglia and macrophages. Unlike nonneural tissue, lost tissue is not replaced, leaving a lesion with a cerebral spinal fluid– filled cyst. Astrocytes become more dense surrounding the cyst to form a glial scar, protecting the uninjured tissue from further injury. (B) In partial thickness wounds, little or no remodeling is required because no ECM is produced during repair. (C) In the PNS, the tissue regains function as the axon successfully innervates its target while Schwann cells produce new myelin to insulate the regenerated axons. (D) Remodeling of cutaneous tissue involves contraction by fibroblasts to close the wound site, aligning the collagen matrix in response to lines of stress, and reepithelialization of the epidermis by keratinocytes. After contraction, fibroblasts within granulation tissue undergo apoptosis, leaving an acellular collagenous scar.


You'll need to discuss the stratum lucidum.