Background: Healing of a tendon graft in a bone tunnel depends on
bone ingrowth into the interface between tendon and bone. Excessive
osteoclastic activity may contribute to bone resorption, tunnel widening, and
impaired healing. We hypothesized that inhibition of osteoclastic activity by
osteoprotegerin (OPG) would increase bone formation around a tendon graft in
anterior cruciate ligament reconstruction in a rabbit model, while increased
osteoclastic activity due to the aplication of receptor activator of nuclear
factor-kappa B ligand (RANKL) would impair bone ingrowth.
Methods: Sixty skeletally mature, male New Zealand White rabbits
underwent bilateral anterior cruciate ligament reconstruction. OPG (100 µg
per tunnel) or RANKL (10 µg per tunnel) was delivered to the tendon-bone
interface with use of a synthetic calcium phosphate carrier vehicle. Twenty
animals were killed at two, four, and eight weeks after surgery. Two rabbits
from each group were prepared for histological evaluation, and the other
rabbits were used for biomechanical testing.
Results: A significantly greater amount of bone surrounded the
tendon at the healing tendon-bone interface in the OPG-treated limbs compared
with the controls and the RANKL-treated limbs at all time-points (p <
0.05). There were significantly fewer osteoclasts in the OPG-treated limbs
compared with the controls and the RANKL-treated limbs (p < 0.05). The
average tunnel area in the OPG group was significantly smaller than that in
the RANKL group (p = 0.003 at two weeks and p = 0.004 at four weeks). The
femur-anterior cruciate ligament-tibia complex of the OPG-treated limbs had
significantly increased stiffness compared with RANKL-treated limbs at eight
weeks (p = 0.04).
Conclusions: Osteoprotegerin significantly improves bone formation
around the grafted tendon and improves the stiffness at the healing
tendon-bone junction in a rabbit model.
Clinical Relevance: Inhibition of excessive osteoclastic activity
may improve tendon-to-bone healing.