Page 28 - Veterinary Laser Therapy in Small Animal Practice

CHAPTER 3

Anti-inflammatory effect

Our own genomes carry the story of evolution, written as the tissue’s own macrophages. A certain degree of
in DNA, the language of molecular genetics, and the activation of the inflammatory cascade is necessary
narrative is unmistakable. to achieve healing after trauma; the problem is that
— Kenneth R. Miller excessive or abnormal activation of the cascade, or
its prolongation, can have serious consequences for
The anti-inflammatory effect of laser therapy (LT) is the patient, from chronic pain to non-healing ulcers,
probably the second most reported effect, after wound autoimmune conditions, degenerative diseases, or even
healing. It can be so significant that in several experi- carcinogenesis (Fig. 3.1).
mental studies it achieves results similar to well-known
non-steroidal anti-inflammatory drugs (NSAIDs) such 3.1 Changing the flavor of the
as indomethacin, [22] meloxicam, [23] or diclofenac. [24] inflammatory soup
Let’s review what exactly we mean by inflammation
before we describe the effects of LT on this process. It makes sense to try to explain how can LT be anti-
When we talk about inflammation, the first things that inflammatory by breaking down inflammation into its
come to mind are probably the well-known signs of cellular and molecular components. I am not saying it’s
heat, tumefaction, redness, pain, and loss of function- fun – molecular biology is not as exciting as seeing a
ality. These are consequences of the phenomena that huge infected wound heal, of course, but it is what hap-
take place in order to isolate, destroy, and prevent the pens behind the scene.
propagation of noxious stimuli, because inflammation Macrophages, leukocytes, platelets, endothelial cells,
is actually part of the innate, natural, and non-specific fibroblasts – all of these cells produce inflammatory
defense mechanisms that enable an individual to fight mediators. These molecules are a substantial part of
and overcome an aggression. the language spoken by cells. The final clinical outcome
The response can be triggered by internal (vascular depends on the right amount of the right inflamma-
and immune) or external (trauma, temperature, radia- tory mediators at the right time, since their individual
tion, microorganisms and their toxins, etc.) factors. actions may vary according to their concentration and
Different types of cells (e.g. platelets, leukocytes, and time of release – again, like words making sense in a
endothelial cells) are involved, as well as a broad spec- language. There are different classifications of inflam-
trum of molecules called inflammatory mediators; an matory mediators, and new ones may be investigated
analogy can be made with the ingredients of a soup, as research progresses. This is going to get a bit hard
so this mixture is sometimes referred to as the inflam- core and if you are not in the mood, just have a look
matory soup. Among the inflammatory cells, which at Table 3.1 and jump to section 3.2. What follows is
include neutrophils, macrophages, lymphocytes, and a shortened description of the best known inflamma-
eosinophils, some are attracted to the injury site from tory mediators, with an explanation of how laser has
nearby locations and some are already present, such been reported to modulate them. Remember, though,

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