Effect of low-energy laser (HeNe) irradiation on the process of bone repair in the rat tibia

The effect of low-energy laser (HeNe) irradiation on bone repair in the tibia of the rat after hole injury was investigated using biochemical and quantitative histomorphometrical methods. The activity of alkaline phosphatase (ALP) showed a sharp peak at 6 days post-injury and a lower peak at 12 days. The overall kinetics of tartrate-resistant acid phosphatase (TRAP) activity coincided with that of ALP but with the higher peak at 12 days postoperatively. Calcium accumulated progressively at the site of injury, peaking at 11 days and then declining. The histological evaluation revealed filling ofthe intramedullary canal with woven bone at the site of injury at 6 days after surgery, and progressive filling of the hole-injury gap in the cortical bone by membranous ossification. Direct irradiation of the hole injury with HeNe laser at 5 and 6 days after injury altered the osteoblast and osteoclast cell populations, as reflected by the significant 2.2-fold increase in ALP enzymatic activity over control, nonirradiated rats at 10 days post-injury, and a significant decrease of 40% in TRAP activity at 11 days. Histomorphometrical analysis revealed a more rapid accumulation of reparative new bone in the hole injury of the laser-irradiated rats. The volume fraction (percent of total volume of the injured zone) of the new reparative compact bone was 27 ± 9%, 88 ± 9%, and 94 ± 6% at 10, 13, and 15 days after injury, respectively, in the laser-irradiated rats; respective control values were 9 ± 7%, 44 ± 9%, and 58 ± 5% for the same time intervals. The volume fraction of the trabecular bone in the hole injury decreased more rapidly with time in the laser-irradiated tibiae than in controls. We conclude that HeNe laser irradiation at the proper time, energy, and frequency after injury probably affects the population of osteoblasts and osteoclasts in the injured site, as demonstrated by alterations in ALP and TRAP activities. It also caused approximately twofold enhancement in bone repair in the hole injury of the rat tibia as revealed by histomorphometry.