Received date: February 07, 2021, Manuscript No. IPARS-22-13024; Editor assigned date: February 09, 2021, PreQC No. IPARS-22-13024 (PQ); Reviewed date: February 23, 2021, QC No. IPARS-22-13024; Revised date: February 28, 2021, Manuscript No. IPARS-22-13024 (R); Published date: March 07, 2022, DOI: 10.36648/2472-1905.8.2.9
Citation: Nioen D (2022) Proliferative Phase of Glucocorticoid Steroids Systemic Glucocorticoids. J Aesthet Reconstr Surg Vol.8 No.2:009.
The wound-healing process consists of four highly integrated and overlapping phases: hemostasis, inflammation, proliferation, and tissue remodeling or resolution. These phases and their bio physiological functions must occur in the proper sequence, at a specific time, and continue for a specific duration at an optimal intensity. There are many factors that can affect wound healing which interfere with one or more phases in this process, thus causing improper or impaired tissue repair.
Wounds that exhibit impaired healing, including delayed acute wounds and chronic wounds, generally have failed to progress through the normal stages of healing. Such wounds frequently enter a state of pathologic inflammation due to a postponed, incomplete, or uncoordinated healing process. Most chronic wounds are ulcers that are associated with ischemia, diabetes mellitus, venous stasis disease, or pressure. Non-healing wounds affect about 3 to 6 million people in the United States, with persons 65 years and older accounting for 85% of these events. Non-healing wounds result in enormous health care expenditures, with the total cost estimated at more than $3 billion per year.
Glucocorticoid steroids systemic glucocorticoids, which are frequently used as anti-inflammatory agents, are well-known to inhibit wound repair via global anti-inflammatory effects and suppression of cellular wound responses, including fibroblast proliferation and collagen synthesis. Systemic steroids cause wounds to heal with incomplete granulation tissue and reduced wound contraction. Glucocorticoids also inhibit production of Hypoxia-Inducible Factor-1 (HIF-1), a key transcriptional factor in healing wounds. Beyond effects on repair itself, systemic corticosteroids may increase the risk of wound infection. While systemic corticosteroids inhibit wound repair, topical application produces quite different effects. Topical low-dosage corticosteroid treatment of chronic wounds has been found to accelerate wound healing, reduce pain and exudate, and suppress hyper granulation tissue formation in 79% of cases.
The proliferative phase generally follows and overlaps with the inflammatory phase, and is characterized by epithelial proliferation and migration over the provisional matrix within the wound (re-epithelialization). In the reparative dermis, fibroblasts and endothelial cells are the most prominent cell types present and support capillary growth, collagen formation, and the formation of granulation tissue at the site of injury. Within the wound bed, fibroblasts produce collagen as well as glycosaminoglycans and proteoglycans, which are major components of the Extracellular Matrix (ECM). Following robust proliferation and ECM synthesis, wound healing enters the final remodeling phase, which can last for years. In this phase, regression of many of the newly formed capillaries occurs, so that vascular density of the wound returns to normal. One critical feature of the remodeling phase is ECM remodeling to an architecture that approaches that of the normal tissue. The wound also undergoes physical contraction throughout the entire wound-healing process, which is believed to be mediated by contractile fibroblasts (myo fibroblasts) that appear in the wound.
In summary, the proper oxygen level is crucial for optimum wound healing. Hypoxia stimulates wound healing such as the release of growth factors and angiogenesis, while oxygen is needed to sustain the healing process. One therapeutic option that can sometimes overcome the influence of tissue hypoxia is hyperbaric oxygen therapy. While HBOT can be an effective treatment for hypoxic wounds, its availability is limited.
Infections once skin is injured, micro-organisms that are normally sequestered at the skin surface obtain access to the underlying tissues. The state of infection and replication status of the micro-organisms determines whether the wound is classified as having contamination, colonization, local infection/critical colonization, and/or spreading invasive infection. Contamination is the presence of non-replicating organisms on a wound, while colonization is defined as the presence of replicating micro-organisms on the wound without tissue damage. Local infection/critical colonization are an intermediate stage, with micro-organism replication and the beginning of local tissue responses. Invasive infection is defined as the presence of replicating organisms within a wound with subsequent host injury.
Stressors can lead to negative emotional states, such as anxiety and depression, which may in turn have an impact on physiologic processes and/or behavioral patterns that influence health outcomes. In addition to the direct influences of anxiety and depression on endocrine and immune function, stressed individuals are more likely to have unhealthy habits, which include poor sleep patterns, inadequate nutrition, less exercise, and a greater propensity for abuse of alcohol, cigarettes, and other drugs. All of these factors may come into play in negatively modulating the healing response.
Drugs Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) such as ibuprofen are widely used for the treatment of inflammation and rheumatoid arthritis and for pain management. Low-dosage aspirin, due to its anti-platelet function, is commonly used as a preventive therapeutic for cardiovascular disease, but not as an anti-inflammatory drug. There are few data to suggest that short-term NSAIDs have a negative impact on healing. However, the question of whether long-term NSAIDs interfere with wound healing remains open. In animal models, systemic use of ibuprofen has demonstrated an anti-proliferative effect on wound healing, resulting in decreased numbers of fibroblasts, weakened breaking strength, reduced wound contraction, delayed epithelialization, and impaired angiogenesis. The effects of low-dose aspirin on healing are not completely clear. Clinical recommendations suggest that, to avoid anti-platelet effects, individuals should discontinue NSAIDs for a time period equal to 4 to 5 times the half-life of drugs before surgery. Thus, the majority of surgical patients do not have significant NSAID activity at the time of wound repair.
The increase in pressure ulcers or pressure-related injuries in obese individuals is also influenced by hypo vascularity, since poor perfusion makes tissue more susceptible to this type of injury. In addition, the difficulty or inability of obese individuals to reposition them further increases the risk of pressure-related injuries. Moreover, skin folds harbor micro-organisms that thrive in moist areas and contribute to infection and tissue breakdown. The friction caused by skin-on-skin contact invites ulceration. Together, these factors predispose obese individuals to the development of impaired wound healing.