Partial thickness wound: Does mechanism of injury influence healing?

Wound healing is a complex multistep process which is temporally and spatially controlled. In partial thickness wounds, regeneration is possible from the stem cells in the edges of the wound and from the remnants of the epidermal appendages (such as hair follicles and sebaceous glands). This study examines whether the mechanism of injury influences healing of wounds of similar depth. Burn and excisional wounds were created on the back of Hampshire pigs and harvested at 7, 14, 28, 44, 57 and 70days after injury and processed for histology and immunohistochemistry. Quantitative analysis of re-epithelialisation, inflammatory response and thickness of the scar and semi-quantitative analyses of the architecture of the resultant scar were performed and subjected to statistical analysis. Results demonstrated a higher number of neutrophils, macrophages and lymphocytes present in the burn on day 7 compared to the excisional wounds. The inflammatory profile of burn wounds was higher than that of excisional wounds for the first month after injury albeit less marked than on day 7 after injury. Re-epithelialisation was markedly advanced in excisional wounds compared to burn wounds at day 7 after injury, corresponding to the higher number of hair follicles in the underlying dermis of excisional wounds at this time point. The thickness of the neo-epidermis increased with time and at day 70 after wounding, the neo-epidermis of the burn was significantly thicker than the neo-epidermis of the excisional scar. Interestingly, following partial thickness excision of skin, there was neo-dermal reformation albeit with an altered architecture, lacking the normal basket-weave pattern of collagen. The thickness of the dermis of partial thickness excisional scar was greater than that of the adjacent unwounded skin. The neo-dermis of the burn scar was even thicker, with the collagen arranged more compactly and disorganised compared to excisional scar and normal skin. This study provides evidence that the mechanism of injury does influence wound healing and the resultant scarring.

Longitudinal changes in plasma Transforming growth factor beta-1 and post-burn scarring in children.

Transforming growth factor beta1, a multifunctional growth factor, plays a pivotal role in wound healing and has been shown to accelerate impaired wound healing. However, high systemic levels of Transforming growth factor beta1 have generally been associated with fibrotic disease processes such as myelofibrosis and pulmonary fibrosis. Hypertrophic scarring occurring during childhood interferes with growth, impairs the function and causes immense psychological and aesthetic problems. Burns is the leading cause of hypertrophic scarring. We studied the longitudinal relationship between plasma Transforming growth factor beta-1 and post-burn wound healing and scarring in children. We discovered that the plasma levels of Transforming growth factor beta-1 rapidly increased to significantly higher levels in the first two weeks post-injury and fell thereafter, in patients who healed with good quality scars post-burn. By contrast, the increase in plasma TGFbeta1 levels in the early stages after-burn, was noticeably absent in patients who developed hypertrophic scarring. We propose that this change in the systemic levels of TGFbeta1 early after the burn may be used as an indicator of patients at risk of developing hypertrophic burn scars. This group of patients could then be targeted for early pharmacological/physical interventions to reduce/prevent scar-related morbidity in burn survivors.

Supramolecular organization in streptococcal pericellular capsules is based on hyaluronan tertiary structures.

Supramolecular organization involving a polyanionic glycan in a bacterial capsule (hyaluronan, HA, in streptococcal capsules) is revealed, for the first time, by electron-histochemical methodology previously used to elucidate ultrastructure in extracellular matrix. Capsular HA filaments thereby revealed closely resemble aligned linear structures demonstrated by similar technology in HA solution. These parallel arrays, spontaneously formed, are based on HA tertiary structures (beta sheet-like) which are stabilized by hydrophobic and hydrogen bonds. HA tertiary structures in aqueous solutions resist shear stress as shown by rheo-NMR. Thus, supramolecular HA wrapping covering many cells probably stabilizes chains of bacteria. Streptococci possibly templated the ordered structures since eukaryotic B6 cell HA did not produce similarly organized envelopes. Supramolecular organization in streptococcal and pneumococcal capsules are compared. Their glycans are very similar but the potential for HA-like tertiary structures is not present in the pneumococcal type 3 polysaccharide and chains of cells are not formed to the same extent by pneumococci. We suggest that the streptococcal capsule exemplifies a simple extracellular matrix analogous to those in animal connective tissues, which contain glycans (chondroitin, keratan, and dermochondan sulfates) of the HA family, capable of undergoing aggregation to similar tertiary structures.