WOUNDS and dermatology issues represent perhaps the widest variety of ailments in veterinary practice, both in origin and complication.
From an acute burn to a chronic lick granuloma, from an ischaemic ulcer to a dehiscent surgical site, no two wounds will be alike. Compound this variation with different histologies and enzyme over/underexpressions; then throw bacterial or fungal infections on top of all that; now plan for a dog gnawing at it constantly or a horse sleeping in a dirty stable.
Needless to say, having one modality that functions well throughout this gauntlet of variation is invaluable. Laser therapy has documented success treating each corner of this wound healing domain, with particular success (over other modalities) in contaminated wounds and infections.
Through increased cellular oxygenation and metabolism, lasers promote fibroblast proliferation, collagen regulation and a host of positive enzymatic changes that lead to faster and stronger wound closure. Simultaneously bringing more oxygen to anaerobic fungi and bacteria, lasers can provide anti-microbial protection.
Unfortunately, the job is not finished when the wound has been disinfected and closed. Scarring, both internal and external, can lead to a host of problems for the animal.
In joints, for example, a postsurgical scar can lead to limited range of motion as well as chronic arthritis. A scar on an internal organ can affect the functional recovery. Fortunately, the fundamental nature of laser therapy can reduce this risk.
At the core of every wound there is a region that has a very high concentration of collagen, through which there is minimal blood flow. After a time, the fibrotic cross-linking of this collagen matrix denies any nutrients to the central cells, and they become dormant, never to be fully healed. Laser therapy counteracts this process in two ways.
First, laser will increase the microcirculation via angiogenesis through the matrix, vasodilation and increased overall blood perfusion.
Dozens of papers have demonstrated this effect, some through histology reports of mast cell degranulation and prostaglandin increases, others through thermography and laser speckle flowmetry, but most notably Kubota [Lasers Med Sci (2002) 17: 146-153] and Uozumi et al. [Lasers Surg Med (2010) 42: 566-576]. These papers, among others, have shown an immediate as well as a lasting increase in localised blood flow.
With this increase of blood flow and nitric oxide concentration comes a subsequent increase in cellular oxygenation. This phenomenon alone is well-known to speed up the wound closure and repair processes (in fact, the entire negative-pressure modality is based on this) but laser therapy goes one step further.
There is profound evidence that laser’s interaction with cytochrome oxidase in the mitochondria leads to more rapid redox cycle and ultimately an increase of ATP synthesis [Karu et al. Photomed Las Surg (2008) 26 (6): 593-599].
Once the cell is introduced to and has burned its oxygen-fuel into chemical energy, all of the cellular compartments will begin to function, and the cells that were previously nutrient-poor and dormant will selfregulate their collagen, reducing the breadth and rigidity of the scar.
Of course other modalities are specifically suited to aid in the healing process of a particular type of wound based on the histological and enzymatic profile of a given patient. But the fundamental action of laser therapy makes it perhaps the most versatile piece of equipment a general practitioner can have.
Neither the origin of nor the complications that arise from any wound a veterinarian faces (malignant cancers aside) will exclude the potential benefits of laser therapy.