Page 33 - Veterinary Laser Therapy in Small Animal Practice

Anti-inflammatory effect 19

long periods of time. The body has several protective leukocytes to burn wounds, [57] but most of them report
mechanisms, such as producing anti-inflammatory a decrease in polymorphonuclear cell infiltration after
cytokines, which inhibit iNOS, or increasing glutathi- LT and downregulation of lymphocytic proliferation
one, a radical scavenger that protects cells from toxicity during the healing process following experimental skin
caused by NO overproduction. But when NO escapes and mucosal wounds as well as burns. This correlates
control, things like cytotoxicity and SIRS can happen. with the anti-inflammatory effect of laser. [5, 43, 58–60] The
Yes, a bit of NO can be helpful on a wild Saturday night; story with mast cells is a bit more complex; they are
it actually may save your life if you are having a heart well known for their role in allergic reactions, and they
attack or stroke, but too much of it can kill you. Sounds are important in the early phenomena of burn healing,
familiar, after all. but a prolongation of their effects over time would per-
Since LT increases NO production, [53, 54] it could have petuate the inflammatory process and potentially the
a role in the treatment of myocardial infarction and discomfort associated with the injury. LT modulates
ischemic stroke, and this is being investigated (see sec- this; it increases the number of mast cells in the first 2
tions 5.3 and 9.8.3). LT delivered percutaneously in vivo weeks after second-degree burns in rats, but then in the
was able to successfully reverse experimentally induced fourth week (remodeling phase) the number of mast
arterial spasm in atherosclerotic Yucatan microswine. cells decreases in laser-treated animals. [61] In rats with
[55] The reason for this is that LT induces relaxation of experimental linear incisions, mast cells were increased
smooth muscle, as described in bronchoconstriction by day 4 but had decreased at day 10. [62] The different
models, [56] but also the smooth muscle that is present in experimental models may explain why, although both
the vascular wall. What is more interesting is that this studies indicate an early increase and later decrease in
increase in NO would be coming from eNOS, and LT mast cells in the wound, the shift happens at different
would actually be decreasing iNOS expression. [40] This times – later in the burn than in the incision model.
would be great news, since we could benefit from the But after all, you would expect an incision to heal faster
increased blood flow if needed, and still have an anti- than a burn.
inflammatory effect. Laser can also benefit mucosal inflammation: inter-
esting results have been published about its use in
3.2 The anti-inflammatory effect of laser radiotherapy- and chemotherapy-induced oral muco-
therapy on different cells, tissues, and sitis. LT provided analgesia and better resolution of
conditions the oral lesions, both in an experimental model and in
clinical studies with human patients, with associated
Inflammation shows particularities depending on the functional improvement and a better ability to eat. [63–67]
tissue and condition; some inflammatory cells are In models of pulmonary inflammation, asthma,
more predominant in acute inflammation and others and edema, LT also decreases leukocyte infiltration.
in chronification, and some specialized macrophages It has been proposed that this is because inhibition of
are exclusive to certain tissue types, such as the nerv- inflammatory mediators decreases intercellular adhe-
ous system microglia. As a general process, damage to sion molecule-1 (ICAM-1) expression. [68] Also both in
the endothelium, considered by many to be our largest vivo and in vitro studies have shown that the hyper-re-
organ, initiates the inflammatory cascade. The activa- sponsiveness of airway smooth muscle cells, as seen in
tion of certain molecules, such as integrins and vascular asthma and other respiratory disorders, can be signifi-
cell adhesion molecules (VCAMs), allows the adhesion cantly attenuated with LT. [56, 69] It also decreased the
(margination and rolling) of circulating neutrophils, number of eosinophils in the bronchoalveolar lavage
the first cell type to be recruited, which then migrate and the serum immunoglobulin E (IgE) levels in a
(diapedesis) through the endothelial wall and into the model of asthma. [45] A similar result was described in
inflammatory site. Neutrophils are the predominant a murine model of acute pleurisy, [44] in which inflam-
cell type in the first 24–48 h of acute inflammation, and matory mediators and exudate volume were decreased
are replaced by macrophages later on. after LT.
Wounds are the most studied field of LT, including The microglia, which make up the immune system
the inflammatory process (Figs 3.5 and 3.6). A few arti- of the brain and spine, also seem to respond to LT.
cles describe a stimulating effect on the chemotaxis of According to an in vitro study with neuronal cultures,

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