Diclofenac, dexamethasone or laser phototherapy?

By Jan Tunér

In the May 2013 edition of Photomedicine and Laser Surgery, the editorial written by Tiina Karu has the title: Is it time to consider photobiomodulation as a drug equivalent? Well, is it? Let us have a look and see what the literature has to say about two very popular drugs:

NSAIDs (non steroidal anti-inflammatory drugs) are the best sold pharmaceuticals ever. The short term effects on pain and inflammation are obvious and very valuable. The long term effects, however, have been questioned and this is especially valid considering the many side effects of NSAIDs. Millions of patients are on long term medication with NSAIDs, and even life long. Indeed, many persons die from their medication. So an alternative option is required. I believe it is already available: laser phototherapy!

First, let us have a look at the strength of the scientific evidence for NSAIDs as such, and long term use of these in particular:

A Meta-analysis by Bjordal [1] on the effect of NSAIDs on knee osteoarthritis pain appears to become important for the recognition and future development of LPT. A research group summarises that nonsteroidal anti-inflammatory drugs (NSAIDs), including cyclo-oxygenase-2 inhibitors (coxibs), reduce short-term pain associated with knee osteoarthritis only slightly better than placebo, and long-term use of these agents should be avoided. Up for analysis were 23 placebo-controlled trials involving 10,845 patients, 7767 of whom received NSAID therapy and 3078 placebo therapy. All in all 21 of the NSAID-studies were funded by the pharmaceutical industry, and the results of 13 of these studies were inflated by patient selection bias as previous NSAID-users were excluded if they had not previously responded favourably to NSAID. Such an exclusion criterion for non-responders has never been seen in any controlled trial of LPT or other non-pharmacological therapies of osteoarthritis. In the remaining 10 unbiased NSAID-trials, the difference from placebo was only 5.9 mm on a 100 mm pain scale. This is far less than established data on differences that are considered minimally perceptible (9 mm) or clinically relevant (12 mm) for knee osteoarthritis patients. In addition, none of the trials found any effects beyond 13 weeks. This bleak support for long term use of NSAIDs is an excellent support for non-pharmaceutical methods, such as LPT.

Diclofenac is one of the best-selling NSAIDs. Several investigators have compared the effect of LPT and diclofenac:

The aim of a study by Marcos [2] was to evaluate the short-term effects of LPT or sodium diclofenac treatments on biochemical markers and biomechanical properties of inflamed Achilles tendons. Wistar rats Achilles tendons (n = 6/group) were injected with saline (control) or collagenase at peritendinous area of Achilles tendons. After 1 h animals were treated with two different doses of LPT (810 nm, 1 and 3 J) at the sites of the injections, or with intramuscular sodium diclofenac. Regarding biochemical analyses, LPT significantly decreased COX-2, TNF-alpha, MMP-3, MMP-9, and MMP-13 gene expression, as well as PGE2 production when compared to collagenase group. Interestingly, diclofenac treatment only decreased PGE2 levels. Biomechanical properties were preserved in the laser-treated groups when compared to collagenase and diclofenac groups.

Ramos [3] investigated the effects of LPT (810 nm) in rat-induced skeletal muscle strain. Male wistar rats were anaesthetised with halothane prior to the induction of muscle strain. Previous studies have determined that a force equal to 130% of the body weight corresponds to approximately 80% of the ultimate rupture force of the muscle tendon unit. In all animals, the right leg received a controlled strain injury while the left leg served as control. A small weight corresponding to 150 % of the total body weight was attached to the right leg in an appropriate apparatus and left to induce muscle strain twice for 20 minutes with 3 minute intervals. Walking index, C-reactive protein, creatine kinase, vascular extravasation and histological analysis of the tibial muscle were performed after 6, 12 and 24 hours of lesion induction. LPT in an energy dependent manner markedly or even completely reduced the Walking Index, leading to a better quality of movement. C-reactive protein production was completely inhibited by laser treatment, even more than observed with Sodium diclofenac inhibition (positive control). Creative Kinase activity was also significantly reduced by laser irradiations. In conclusion, LPT operating in 810 nm markedly reduced inflammation and muscle damage after experimental muscle strain, leading to a highly significant enhancement of walking activity.

The aim of the study by de Almeida [4] was to analyse the effects of sodium diclofenac (topical application), cryotherapy, and LPT on pro-inflammatory cytokine levels after a controlled model of muscle injury. For such, we performed a single trauma in tibialis anterior muscle of rats. After 1 h, animals were treated with sodium diclofenac (11.6 mg/g of solution), cryotherapy (20 min), or LPT (904 nm; superpulsed; 700 Hz; 60 mW mean output power; 1.67 W/cm2; 1, 3, 6 or 9 J; 17, 50, 100 or 150 s). Assessment of interleukin-1 and interleukin-6 (IL-1 and IL-6) and tumour necrosis factor-alpha levels was performed at 6 h after trauma employing enzyme-linked immunosorbent assay method. LPT with 1 J dose significantly decreased IL-1, IL-6, and TNF-alpha levels compared to non-treated injured group as well as diclofenac and cryotherapy groups. On the other hand, treatment with diclofenac and cryotherapy does not decrease pro-inflammatory cytokine levels compared to the non-treated injured group. Therefore, the authors conlude that 904 nm LPT with 1 J dose has better effects than topical application of diclofenac or cryotherapy in acute inflammatory phase after muscle trauma.

The purpose of a study by Albertini [5] was to investigate the effect of LPT on the acute inflammatory process. Male rats were used. Paw oedema was induced by a sub-plantar injection of carrageenan, the paw volume was measured before and one, two, three and four hours after the injection, using a hydroplethysmometer. To investigate the action mechanism of the GaAlAs laser on inflammatory oedema, parallel studies were performed using adrenalectomised rats or rats treated with sodium diclofenac. Different laser irradiation protocols were employed for specific energy densities (EDs), exposure times and repetition rates. The rats were irradiated with laser for 80 s each hour. The EDs that produced an anti-inflammatory effect were 1 and 2.5 J/cm2, reducing the oedema by 27% and 45.4%, respectively. The ED of 2.5 J/cm2 produced anti-inflammatory effects similar to those produced by the cyclooxigenase inhibitor sodium diclofenac at a dose of 1 mg/kg. In adrenal-ectomised animals, the laser irradiation failed to inhibit the oedema. These results suggest that LPT possibly exerts its anti-inflammatory effects by stimulating the release of adrenal corticosteroid hormones.

The aim of a work by Meneguzzo [6] was to investigate the effects of infrared 810 nm on the acute inflammatory process by the irradiation of lymph nodes, using the classical model of carrageenan-induced rat paw oedema. Thirty mice were randomly divided into five groups. The inflammatory induction was performed in all groups by a sub-plantar injection of carrageenan (1mg/paw). The paw volume was measured before and 1, 2, 3, 4 and 6 hours after the injection using a plethysmometer. Myeloperoxidase (MPO) activity was analysed as a specific marker of neutrophil accu­mulation at the inflammatory site. The control group did not receive any treatment (GC); GD group received sodium diclofenac (1mg/kg) 30 minutes before the carrageenan injection; GP group received laser irradiation directly on the paw (1 Joule, 100 mW, 10 sec) 1 and 2 hours after the carrageenan injection; GLY group received laser irradiation (1 Joule, 100 mW, 10 sec) on the inguinal lymph nodes; GP+LY group received laser irradiation on both paw and lymph nodes 1 and 2 hours after the carrageenan injection. MPO activity was similar in the sodium diclofenac as well as in the GP and GLY groups, but significantly lower than the GC and GP + LY groups. Paw oedema was significantly inhibited in GP and GD groups when compared to the other groups. Interestingly, the GP+LY groups presented the biggest oedema, even bigger than in the control group. LPT showed an anti-inflammatory effect when the irradiation was performed on the site of lesion or at the correlated lymph nodes, but showed a pro-inflammatory effect when both paw and lymph nodes were irradiated during the acute inflammatory process.

The aim of a study by de Almeida [7] was to analyse the effects of sodium diclofenac (topical application) and LPT on morphological aspects and gene expression of biochemical inflammatory markers. We performed a single trauma in tibialis anterior muscle of rats. After 1 h, animals were treated with sodium diclofenac (11.6 mg g(-1) of solution) or LPT (810 nm; continuous mode; 100 mW; 1, 3 or 9 J; 10, 30 or 90 s). Histological analysis and quantification of gene expression (real-time polymerase chain reaction-RT-PCR) of cyclooxygenase 1 and 2 (COX-1 and COX-2) and tumour necrosis factor-alpha (TNF-alpha) were performed at 6, 12 and 24 h after trauma. LPT with all doses improved morphological aspects of muscle tissue, showing better results than injury and diclofenac groups. All LPT doses also decreased COX-2 compared to injury group at all-time points and to diclofenac group at 24 h after trauma. In addition, LPT decreased TNF-alpha compared both to injury and diclofenac groups at all-time points. LPT mainly with dose of 9 J is better than topical application of diclofenac in acute inflammation after muscle trauma.

Yet another study by Marcos [8] investigated if a safer treatment such as LPT could reduce tendinitis inflammation, and whether a possible pathway could be through inhibition of either of the two-cyclooxygenase (COX) isoforms in inflammation. Wistar rats (six animals per group) were injected with saline (control) or collagenase in their Achilles tendons. Then treated with three different doses of IR LPT (810 nm; 100 mW; 10 s, 30 s and 60 s; 3.57 W/cm2; 1 J, 3 J, 6 J) at the sites of the injections, or intramuscular diclofenac, a nonselective COX inhibitor/NSAID. It was found that LPT dose of 3 J significantly reduced inflammation through less COX-2-derived gene expression and PGE2 production, and less oedema formation compared to non-irradiated controls. Diclofenac controls exhibited significantly lower PGE2 cytokine levels at 6 h than collagenase control, but COX isoform 1-derived gene expression and cytokine PGE2 levels were not affected by treatments. As LPT seems to act on inflammation through a selective inhibition of the COX-2 isoform in collagenase-induced tendinitis, LPT may have potential to become a new and safer non-drug alternative to coxibs.

The aim of the study by de Paiva Carvalho [9] was to evaluate the effect of single and combined therapies (LPT, topical application of diclofenac and intramuscular diclofenac) on functional and biochemical aspects in an experimental model of controlled muscle strain in rats. Muscle strain was induced by overloading tibialis anterior muscle of rats. Injured groups received either no treatment, or a single treatment with topical or intramuscular diclofenac (TD and ID), or LPT (3 J, 810 nm, 100 mW) 1 h after injury. Walking track analysis was the functional outcome and biochemical analyses included mRNA expression of COX-1 and COX-2 and blood levels of prostaglandin E2 (PGE2). All treatments significantly decreased COX-1 and COX-2 gene expression compared with injury group. However, LPT showed better effects than TD and ID regarding PGE2 levels and walking track analysis. The author concludes that LPT has more efficacy than topical and intramuscular diclofenac in treatment of muscle strain injury in acute stage.

Crystalopathies are inflammatory pathologies caused by cellular reactions to the deposition of crystals in the joints. The anti-inflammatory effect of He-Ne laser and that of the nonsteroidal anti-inflammatory drugs (NSAIDs) diclofenac, meloxicam, celecoxib, and rofecoxib was studied in acute and chronic arthritis produced by hydroxyapatite and calcium pyrophosphate in rats. The presence of the markers fibrinogen, L-citrulline, nitric oxide, and nitrotyrosine was determined. In the study by Rubio [10] crystals were injected into the posterior limb joints of the rats. A dose of 8 J/cm2 of energy from a HeNe laser was applied for 3 d in some groups and for 5 d in other groups. The levels of some of the biomarkers were determined by spectrophotometry, and that of nitrotyrosine was determined by ELISA. In arthritic rats, the fibrinogen, L-citrulline, nitric oxide, and nitrotyrosine levels increased in comparison to controls and to the laser-treated arthritic groups. When comparing fibrinogen from arthritic rats with disease induced by hydroxyapatite with undiseased and arthritic rats treated with NSAIDs, the He-Ne laser decreased levels to values similar to those seen in controls. Inflammatory and oxidative stress markers in experimental crystalopathy are positively modified by photobiostimulation.

Although the above studies indicate that LPT is as effective, or more effective as diclofenac, a potentiation of the effect of diclofenac by adding LPT is suggested in the following study:

The aim of the study by Markovic [11] was twofold: (1) to evaluate the postoperative analgesic efficacy, comparing long-acting and intermediate-acting local anaesthetics; and 2 to compare the use of laser irradiation and the non-steroid anti-inflammatory drug diclofenac, which are claimed to be among the most successful aids in postoperative pain control. A twofold study of 102 patients of both sexes undergoing surgical extraction of LTM was conducted. In the first part of the study, 12 patients with bilaterally impacted lower molars were treated in a double-blind crossover fashion; local anaesthesia was achieved with 0.5% bupivacaine plain or 2% lidocaine with 1:80.000 epinephrine. In the second part of the study, 90 patients undergoing lower molar surgical extraction with local anaesthesia received postoperative laser irradiation (30 patients) and a preoperative single dose of 100 mg diclofenac (30 patients), or only regular postoperative recommendations (30 patients). The results of the first part of the study showed a strikingly better postoperative analgesic effect of bupivacaine than lidocaine/epinephrine (11 out of 12; 4 out of 12, respectively, patients without postoperative pain). In the second part of the study, LPT irradiation significantly reduced postoperative pain intensity in patients premedicated with diclofenac, compared with the controls. Provided that basic principles of surgical practice have been achieved, the use of long-acting local anaesthetics and LPT irradiation enables the best postoperative analgesic effect and the most comfortable postoperative course after surgical extraction of lower molars.

Dexamethasone is a corticosteroid, thus not an NSAID, but the issue of replacing pharmaceuticals with long term negative effects with a treatment with no side effect is urgent here as well.

A rabbit model of endophthalmitis was established by Ma [12] to evaluate the antiinflammatory effect of LPT as an adjunct to treatment for Staphylococcus epidermidis endophthalmitis. Rabbits were randomly divided into three groups to receive intravitreal injections into their left eye: group A received 0.5 mg vancomycin (100 μl), group B received 0.5 mg vancomycin + 0.2 mg dexamethasone (100 μl), and group C received 0.5 mg vancomycin (100 μl) and laser irradiation (10 mW, 632 nm) focused on the pupil. Slit lamp examination and B-mode ultrasonography were conducted to evaluate the symptoms of endophthalmitis. Polymorphonuclear cells and tumour necrosis factor alpha (TNF-α) in aqueous fluid were measured at 0 h, and 1, 2, 3, 7 and 15 days. A histology test was conducted at 15 days. B-mode ultrasonography and histology revealed that groups B and C had less inflammation than group A at 15 days. Groups B and C had fewer polymorphonuclear cells and lower levels of TNF-α in aqueous fluid than group A at 2, 3 and 7 days. There was no significant difference between groups B and C. There was no significant difference between groups A, B and C at 15 days. As an adjunct to vancomycin therapy to treat S. epidermidis endophthalmitis, LPT has an antiinflammatory effect similar to that of dexamethasone.

Castano [13] tested LPT on rats that had zymosan injected into their knee joints to induce inflammatory arthritis. The author compared illumination regimens consisting of a high and low fluence (3 and 30 J/cm2), delivered at high and low irradiance (5 and 50 mW/cm2) using 810 nm daily for five days, with the positive control of conventional corticosteroid (dexamethasone) therapy. Illumination with a 810 nm laser was highly effective (almost as good as dexamethasone) at reducing swelling, and a longer illumination time (10 or 100 minutes compared to 1 minute) was more important in determining effectiveness than either the total fluence delivered or the irradiance. LPT induced reduction of joint swelling correlated with reduction in the inflammatory marker serum prostaglandin E2 (PGE2).

Reis [14] investigated the role of extracellular matrix elements and cells during the wound healing phases following the use of LPT and anti-inflammatory drugs. Thirty-two rats were submitted to a wound inflicted by a 6-mm-diameter punch. The animals were divided into four groups: sham treated, those treated with the GaAlAs laser (4 J/cm2, 9 mW, 670 nm), those treated with dexamethasone (2 mg/kg), and those treated with both LPT and dexamethasone. After three and five days, the cutaneous wounds were assessed by histopathology using polarised light and ultrastructural assessments by transmission electron microscopy. Changes seen in polymorphonuclear inflammatory cells, oedema, mononuclear cells, and collagen fibre deposition were semi-quantitatively evaluated. The laser-treated group demonstrated an increased collagen content and a better arrangement of the extracellular matrix. Fibroblasts in these tissues increased in number and were more synthetically active. In the dexamethasone group, the collagen was shown to be non-homogenous and disorganised, with a scarcity of fibroblasts. In the group treated with both types of therapy, fibroblasts were more common and they exhibited vigorous rough endoplasmic reticulum, but they had less collagen production compared to those seen in the laser group. Thus, LPT alone accelerated post-surgical tissue repair and reduced oedema and the polymorphonuclear infiltrate, even in the presence of dexamethasone.

In a study by Jajarm [15] thirty patients with erosive-atrophic OLP were randomly allocated into two groups. The experimental group consisted of patients treated with the 630 nm laser. The control group consisted of patients who used dexamethason mouth wash. Response rate was defined based on changes in the appearance score and pain score (VAS) of the lesions before and after each treatment. Appearance score, pain score, and lesion severity was reduced in both groups. No significant differences were found between the treatment groups regarding the response rate and relapse. The study demonstrated that LPT was as effective as topical corticosteroid therapy without any adverse effects and it may be considered as an alternative treatment for erosive-atrophic OLP in the future.

The aim of a study by Aimbire [16] was to investigate if LPT can modulate formation of haemorrhagic lesions induced by immune complex, since there is a lack of information on LPT effects in haemorrhagic injuries of high perfusion organs, and the relative efficacy of LPT compared to anti-inflammatory drugs. A controlled animal study was undertaken with 49 rats, randomly divided into seven groups. Bovine serum albumin i.v. was injected through the trachea to induce an immune complex lung injury. The study compared the effect of irradiation by a 650 nm laser with doses of 2.6 J/cm2 to celecoxib, dexamethasone, and control groups for haemorrhagic index (HI) and myeloperoxide activity (MPO) at 24 h after injury. The HI for the control group was 4.0. Celecoxib, laser, and dexamethasone all induced significantly lower HI than in the control animals at 2.5, 1.8 and 1.5, respectively. Dexamethasone, but not celecoxib, induced a slightly, but significantly lower HI than laser (p = 0.04). MPO activity was significantly decreased at 1.6 in groups receiving celecoxib at 0.87, dexamethasone at 0.50, and laser at 0.7 when compared to the control group, but there were no significant differences between any of the active treatments. In conclusion, LPT at a dose of 2.6 J/cm2 induces a reduction of HI levels and MPO activity in haemorrhagic injury, which is not significantly different from that obtained by celecoxib. Dexamethasone is slightly more effective than LPT in reducing HI, but not MPO activity.

In an effort to clarify the molecular based mechanism of the anti-inflammatory effects of laser irradiation, Abiko [17] used a rheumatoid arthritis (RA) rat model with human rheumatoid synoviocytes (MH-7) challenged with IL-1, treated with laser  or dexamethasone (DEX), monitored by gene expressions and analysed by the signal pathway database. RA rats were generated by the immunisation of type-II collagen, after which foot paws and knee joints became significantly swollen. The animals were laser treated and the swelling rates measured. MH-7 was challenged with IL-1ß and gene expression levels monitored, using the Affymetrix Gene Chip system, and the signal pathway database analysed using the Ingenuity Pathway Analysis (IPA) tool. LPT significantly reduced swellings in the rats’ foot paws and knee joints and made it possible for them to walk on their hind legs. LPT altered many gene expressions of cytokines, chemokines, growth factors and signal transduction factors in IL-ß induced MH-7. IPA revealed that LPT as well as DEX kept the MH7A at a normal state to suppress mRNA levels of IL-8, IL-1ß, CXC1, NFkB1 and FGF13, which were enhanced by IL-1ß treatment. However, certain gene expression of inflammatory factors were reduced by LPT, but were enhanced by DEX. LPT reduced inflammatory factors through altering signal pathways by gene expression levels. Interestingly, LPT altered useful targeted gene expressions, whereas DEX randomly altered many gene expressions, including the unwanted genes for anti-inflammation. Dexomethasone is a steroid known for having a long range of serious side effects. Thus, genome based gene expression monitored by the Gene Chip system together with a signal pathway based database provide unprecedented access to elucidate the mechanism of the biostimulatory effects of LPT.

It has been suggested that LPT acts on pulmonary inflammation. Thus, Mafra de Lima [18] investigated in a work if LPT (650 nm, 2.5 mW, 31.2mW/cm2, 1.3J/cm2, spot size of 0.08 cm2 and irradiation time of 42s) can attenuate oedema, neutrophil recruitment and inflammatory mediators in acute lung inflammation. Thirty-five male Wistar rats (n=7 per group) were distributed in the following experimental groups: control, laser, LPS, LPS+laser and dexamethasone+LPS. Airway inflammation was measured 4h post-LPS challenge. Pulmonary microvascular leakage was used for measuring pulmonary edema. Bronchoalveolar lavage fluid (BALF) cellularity and myeloperoxidase (MPO) were used for measuring neutrophil recruitment and activation. RT-PCR was performed in lung tissue to assess mRNA expression of tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin (IL-10), cytokine-induced neutrophil chemoattractant-1 (CINC-1), macrophage inflammatory protein-2 (MIP-2) and intercellular adhesion molecule-1 (ICAM-1). Protein levels in both BALF and lung were determined by ELISA. LPT inhibited pulmonary edema and endothelial cytoskeleton damage, as well as neutrophil influx and activation. Similarly, LPT reduced the TNF-α and IL-1β, in lung and BALF. LPT prevented lung ICAM-1 up-regulation. The rise of CINC-1 and MIP-2 protein levels in both lung and BALF, and the lung mRNA expressions for IL-10, were unaffected. Data suggest that the LPT effect is due to the inhibition of ICAM-1 via the inhibition of TNF-α and IL-1β.

Steroids are frequently used to treat inflammation. Some studies report a reduced effect of LPT in the presence of steroids, while others have found positive results of LPT even in the presence of steroids. However, steroids are known to delay wound healing through a reduction of leukocyte migration and a suppression of interleukins, while LPT is known to stimulate wound healing. In a study by Pessoa [19], 48 rats were used, and after the execution of a wound on the dorsal region of each animal, they were divided into four groups (n = 12), receiving the following treatments: G1 (control), wounds and animals received no treatment; G2, wounds were treated with laser; G3, animals received an intraperitoneal injection of sodium phosphate of dexametasone, dosage 2 mg/kg of body weight; G4, animals received steroids and wounds were treated with laser. The laser emission device used was a 904 nm unit, in a contact mode, with 2.75 mW gated with 2.900 Hz during 120 sec. After a period of 3, 7 and 14 days, the animals were sacrificed. The results showed that the wounds treated with steroid had a delay in healing, while laser accelerated the wound healing process. Additionally, wounds treated with laser in the animals also treated with steroids, presented a differentiated healing process with a larger collagen deposition as well as a decrease in both the inflammatory infiltrated and in the delay on the wound healing process. Laser accelerated healing, delayed by the steroids, acting as a biostimulative coadjutant agent, balancing the undesirable effects of the steroids on the tissue’s healing process. The effect of LPT is almost as potent as dexametasone but, again, without side effects.

In a study by Lara [20], 44 rats were treated with fluorouracil and, in order to mimic the clinical effect of chronic irritation, the palatal mucosa was irritated by superficial scratching with an 18-gauge needle. When all of the rats presented oral ulcers of mucositis, they were randomly allocated to one of three groups: group I was treated with laser (GaAlAs), group II was treated with topical dexamethasone, and group III was not treated. Excisional biopsies of the palatal mucosa were then performed, and the rats were killed. Tissue sections were stained with haematoxylin and eosin for morphological analyses, and with toluidine blue for mast-cell counts. Group I specimens showed higher prevalence of ulcers, bacterial biofilm, necrosis and vascularisation, while group II specimens showed higher prevalence of granulation tissue formation. There were no significant statistical differences in the numbers of mast cells and epithelial thickness between groups.  For the present model of mucositis, rats with palatal mucositis treated with laser showed characteristics compatible with the ulcerative phase of oral mucositis, and rats treated with topical dexamethasone showed characteristics compatible with the healing phase of mucositis. Topical dexamethasone was more efficient in the treatment of rats’ oral mucositis than the laser.

The stud by Marchionni [21] aimed to assess the effect of LPT associated with and without dexamethasone on inflammation and wound healing in cutaneous surgical wounds. Background: Limited studies are directed at the possible interference of laser photobiomodulation on the formation of myofibroblasts, associated with an antiinflammatory drug. Standard skin wounds were performed on 80 Wistar rats, distributed into four groups: no treatment (sham group), laser only (670 nm, 9 mW, 0.031 W/cm2, 4 J/cm2, single dose after surgery), dexamethasone only (2 mg/kg 1 h before surgery), and laser with dexamethasone. Tissue was examined histologically to evaluate oedema, presence of polymorphonuclear, mononuclear cells, and collagen. The analysis of myofibroblasts was assessed by immunohistochemistry and transmission electron microscopy. The intensity was rated semiquantitatively. The results showed that laser and dexamethasone acted in a similar pattern to reduce acute inflammation. Collagen synthesis and myofibroblasts were more intense in the laser group, whereas animals treated with dexamethasone showed lower results for these variables. In a combination of therapies, the synthesis of collagen and actin and desmin-positive cells was less than laser group. Laser was effective in reducing swelling and polymorphonuclear cells and accelerated tissue repair, even in the presence of dexamethasone.

It has been suggested that LPT and dexamethasone in combination do not bring about any advantages. But the following study suggests that LPT works even in an environment with DEX.

The aim of a study by Garcia [22] was to compare LPT as adjuvant treatment for induced periodontitis with scaling and root planing (SRP) in dexamethasone-treated rats. One-hundred twenty rats were divided into groups: D group (n = 60), treated with dexamethasone; ND group (n = 60) treated with saline solution. In both groups, periodontal disease was induced by ligature at the left first mandibular molar. After 7 days, the ligature was removed and all animals were subjected to SRP and were divided according to the following treatments: SRP, irrigation with saline solution (SS); SRP + LPT, SS and laser irradiation (660 nm; 24 J; 0.428 W/cm2). Ten animals in each treatment were killed after 7 days, 15 days and 30 days. The radiographic and histometric values were statistically analysed. In all groups radiographic and histometric analysis showed less bone loss (P < 0.05) in animals treated with SRP + LPT in all experimental periods. SRP + LPT was an effective adjuvant conventional treatment for periodontitis in rats treated with dexamethasone.

From the above papers it is clear that LPT has an effect similar to that of dexamethasone. Possibly not as strong as dexamethasone, but without the side effects. Thus, a promising alternative, especially for long term use.


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