Not another clinical dilemma is more challenging and no other substrate is more hard to work with than irradiated tissue. In the new millennium, more than 50% of cancer patients receive some form of radiotherapy. A functional understanding of the tissue effects of radiation and current approaches to the rising epidemic of radiation injury is essential for every plastic surgeon.
Ionizing radiation exerts its effects by the energy transference to biologic material, which ends in excitation of tissue electrons. Radiation exists principally in three forms: X-rays (short wavelength rays produced by an electrical device), gamma rays (short wavelength rays emitted from unstable isotopes) and particulate radiation (rays produced by electrons, protons, a-particles, neutrons and p-mesons).
Those clinically relevant are from the X-ray and gamma varieties. These rays have both direct (alteration of intracellular DNA/RNA) and indirect (generation of oxygen free radicals) mechanisms of cell toxicity. The former effect confers its therapeutic benefit on rapidly dividing cancer cells, but indirect mechanisms really are a detriment to rapidly dividing, normal tissue such as skin and also the lining from the gastrointestinal tract.
Therapeutic radiation is typically delivered locally at a low-dose rate (brachytherapy) or high-dose rate through megavoltage devices (external beam or tele-therapy). In either case, radiation administered is measured since the radiation absorbed dose (rad) or more recently, the Gray (Gy) unit. 1 Gray equals 100 rads. Each type of radiation has a characteristic depth of penetration that can be used to establish its impact on a lesion.
The treatment parameters therefore have influence on the overall radiation-induced damage: (1) total dose; (2) dose fraction size; (3) total amount of tissue treated; (4) elapsed time during irradiation. Dose fractionation regimens happen to be created by radiation therapists to minimize problems for normal tissue. Standard dose regimens in practice today occur for a price of 100-200 cGy each minute.
Overall, the extent of radiation damage continues to be categorized as lethal (irreversible), sub-lethal (reversible/correctable by cellular repair mechanisms) and potentially lethal (modifiable by cellular environment). Toxic effects can manifest as an acute injury (<6 months) or chronic injury (>6 months). On the cellular level, the toxic manifestations are multiple. Keratinocytes, being the most superficial and proliferative cell type in the skin, are the most radiosensitive.
Erythematous reactions, which signal epidermal damage, are considered trimodal. The first, often not clinically evident, occurs just 1-24 hours post radiation and it is probably due to activation of proteolytic enzymes and increased local capillary permeability. This is typically followed by a more intense reaction appearing approximately one week after therapy; this phase is brought on by problems for the basal layer on the skin. Inflammatory and immune reaction to this injury result in a third phase of erythema, which may occur 6-7 weeks after radiation.
Complete destruction of the epidermal layer results in the characteristic moist desquamation seen in early radiation damage. Owing to the turnover time of the epidermis (59-72 days), the daily rate of epidermal loss in irradiated tissue occurs at 2.6% ± 0.2%. Other epidermal residents are also suffering from radiotherapy.
Exposure of melanocytes to ionizing radiation results in increased melanin transfer to keratinocytes and thus hyperpigmentation of your skin. This really is seen early in treatment, whereas at a later time, melanocyte death results in patches of hypopigmentation characteristic of chronic cases.
From the cells in the dermis, the fibroblast is the primary target in radiation injury. Fibrotic response to multiple radiation insults ("reactive" fibrosis) can be mainly because of alterations in the physiology of the cell type. Overexpression of collagen, differentiation of fibroblast progenitors into myofibroblasts and increased production of TGF-B1, a profibrotic cytokine, all appear to contribute to clinically evident fibrosis.
Paradoxically, long-term radiation leads to fibroblast depletion and thus the poor wound healing potential and compromised tensile strength inherent in chronic wounds. Reconstitution of chronic wounds with nonirradiated fibroblasts or with platelet-derived growth factor-BB (PDGF-BB), which indirectly stimulates fibroblasts via activated macrophages, restores normal wound breaking strength and time to healing.
Our website is not responsible for the information contained by this article. Webworldarticles.com is a free articles resource thus practically any visitor can submit an article. However if you notice any copyrighted material, please contact us and we will remove the article(s) in discussion right away.
This article was sent to us by:
Ralph C. Bennett at
02092011
1. Breast reconstruction and general types of free flaps
All articles in this directory are property of their respective authors. Additionally, read our Privacy Policy
© 2010 WebWorldarticles.com - All Rights Reserved. Partners: Gunblade Saga