Pulsed ultrasounds accelerate healing of rib fractures in an experimental animal model: an effective new thoracic therapy?
OBJECTIVE
Rib fractures are a frequent traumatic injury associated with a relatively high morbidity. Currently, the treatment of rib fractures is symptomatic. Since it has been reported that pulsed ultrasounds accelerates repair of limb fractures, we hypothesized that the application of pulsed ultrasounds will modify the course of healing in an animal model of rib fracture.


METHODS
We studied 136 male Sprague-Dawley rats. Animals were randomly assigned to different groups of doses (none, 50, 100, and 250 mW/cm(2) of intensity for 3 minutes per day) and durations (2, 10, 20, and 28 days) of treatment with pulsed ultrasounds. In every subgroup, we analyzed radiologic and histologic changes in the bone callus. In addition, we examined changes in gene expression of relevant genes involved in wound repair in both control and treated animals.


RESULTS
Histologic and radiologic consolidation was significantly increased by pulsed ultrasound treatment when applied for more than 10 days. The application of 50 mW/cm(2) was the most effective dose. Only the 100 and 250 mW/cm(2) doses were able to significantly increase messenger RNA expression of insulin-like growth factor 1, suppressor of cytokine signaling-2 and -3, and vascular endothelial growth factor and decrease monocyte chemoattractant protein-1 and collagen type II-alpha 1.


CONCLUSIONS
Our findings indicate that pulsed ultrasound accelerates the consolidation of rib fractures. This study is the first to show that pulsed ultrasound promotes the healing of rib fractures. From a translational point of view, this easy, cheap technique could serve as an effective new therapeutic modality in patients with rib fractures.
Santana-Rodríguez
Norberto
N
Experimental Surgery Unit, Research Unit, Hospital Universitario Dr Negrín, Las Palmas de Gran Canaria, Spain. norbesr@terra.es
Clavo
Bernardino
B
Fernández-Pérez
Leandro
L
Rivero
José C
JC
Travieso
María M
MM
Fiuza
María D
MD
Villar
Jesús
J
García-Castellano
José M
JM
Hernández-Pérez
Octavio
O
Déniz
Antonio
A
D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics; D024061:Collagen Type III / Q000235:genetics; D004195:Disease Models, Animal; D017102:Fracture Healing / Q000235:genetics; D005786:Gene Expression Regulation; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D011859:Radiography; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012253:Rib Fractures / Q000000981:diagnostic imaging / Q000235:genetics / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics; D013997:Time Factors; D014464:Ultrasonic Therapy; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics
C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D024061:Collagen Type III; D012333:RNA, Messenger; C491408:Socs2 protein, rat; C491410:Socs3 protein, rat; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D042461:Vascular Endothelial Growth Factor A; C548904:insulin-like growth factor-1, rat; C467498:vascular endothelial growth factor A, rat; D007334:Insulin-Like Growth Factor I