Accelerated bone repair after plasma laser corticotomies.
OBJECTIVE
To reveal, on a cellular and molecular level, how skeletal regeneration of a corticotomy is enhanced when using laser-plasma mediated ablation compared with conventional mechanical tissue removal.


BACKGROUND
Osteotomies are well-known for their most detrimental side effect: thermal damage. This thermal and mechanical trauma to adjacent bone tissue can result in the untoward consequences of cell death and eventually in a delay in healing.


METHODS
Murine tibial corticotomies were performed using a conventional saw and a Ti:Sapphire plasma-generated laser that removes tissue with minimal thermal damage. Our analyses began 24 hours after injury and proceeded to postsurgical day 6. We investigated aspects of wound repair ranging from vascularization, inflammation, cell proliferation, differentiation, and bone remodeling.


RESULTS
Histology of mouse corticotomy sites uncovered a significant difference in the onset of bone healing; whereas laser corticotomies showed abundant bone matrix deposition at postsurgical day 6, saw corticotomies only exhibited undifferentiated tissue. Our analyses uncovered that cutting bone with a saw caused denaturation of the collagen matrix due to thermal effects. This denatured collagen represented an unfavorable scaffold for subsequent osteoblast attachment, which in turn impeded deposition of a new bony matrix. The matrix degradation induced a prolonged inflammatory reaction at the cut edge to create a surface favorable for osteochondroprogenitor cell attachment. Laser corticotomies were absent of collagen denaturation, therefore osteochondroprogenitor cell attachment was enabled shortly after surgery.


CONCLUSIONS
In summary, these data demonstrate that corticotomies performed with Ti:Sapphire lasers are associated with a reduced initial inflammatory response at the injury site leading to accelerated osteochondroprogenitor cell migration, attachment, differentiation, and eventually matrix deposition.
Leucht
Philipp
P
Department of Surgery, Stanford University, Stanford, CA
Lam
Kentson
K
Kim
Jae-Beom
JB
Mackanos
Mark A
MA
Simanovskii
Dmitrii M
DM
Longaker
Michael T
MT
Contag
Christopher H
CH
Schwettman
H Alan
HA
Helms
Jill A
JA
D000818:Animals; D001861:Bone Regeneration / Q000502:physiology*; D016923:Cell Death; D049109:Cell Proliferation; D004247:DNA / Q000235:genetics; D005500:Follow-Up Studies; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D020287:In Situ Nick-End Labeling; D053685:Laser Therapy; D008156:Luciferases / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D010011:Osteocytes / Q000166:cytology / Q000378:metabolism; D010027:Osteotomy / Q000379:methods*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000235:genetics / Q000378:metabolism; D019707:Receptors, Chemokine / Q000235:genetics / Q000378:metabolism; D013977:Tibia / Q000166:cytology / Q000378:metabolism / Q000601:surgery*; D014945:Wound Healing / Q000502:physiology*
C503133:Gr-1 protein, mouse; D018840:HSP70 Heat-Shock Proteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D018809:Proliferating Cell Nuclear Antigen; D019707:Receptors, Chemokine; D004247:DNA; D008156:Luciferases