2015 ISAKOS Biennial Congress ePoster #1275

Mechanoreceptor Re-Innervation Following Allograft Versus Autograft Anterior Cruciate Ligament Reconstruction

Simon W. Young, MD, FRACS, Auckland NEW ZEALAND
Roberto Valladares, MD, Palo Alto, CA UNITED STATES
Jason L. Dragoo, MD, Englewood, CO UNITED STATES

Stanford University, Palo Alto, CA, USA

FDA Status Not Applicable

Summary: We present comparative data demonstrating reduced concentration of mechanoreceptors in both ACL allografts and autografts. This may explain the continued proprioceptive deficit even following ACL reconstruction.

Rate:

Abstract:

Introduction

Functional instability following anterior cruciate ligament (ACL) rupture is due to both loss of mechanical restraint and loss of proprioception, which restricts the ability of coordinated muscle activity to compensate and stabilize the knee joint. This lack of coordinated muscle control is thought to be due to diminished or absent sensory feedback from the ACL mechanoreceptors to the neuromuscular system.
Clinical, motor and proprioceptive function is known to improve following ACL reconstruction but does not return to normal. While histological studies of human ACL allografts have been unable to demonstrate mechanoreceptor re-innervation, animal data suggests re-innervation occurs when an autograft is used. The aim of this study was to compare the presence or absence of mechanoreceptors in allograft versus autograft in following ACL reconstruction in humans.

Methods

Eleven patients with previous ACL reconstruction presenting for either revision ACL surgery or knee arthroscopy for other reasons were enrolled in a prospective, comparative study. Six patients had a previous autograft ACL and five patients had an allograft. In the case of revision patients, the previous ACL graft tissue was excised within 6 weeks of ligament rupture, and in arthroscopy patients 2mm biopsies of the ACL graft were taken from the tibial and femoral insertions. ACL tissue was also taken from 2 additional patients within 6 weeks following acute primary ACL rupture to act as controls.

The specimens were fixed with 10% buffered formalin solution and frozen section was performed. Specimens were stained with hematoxylin-eosin (H-E) and monoclonal antibodies against S-100 and neurofilament protein (NFP). Immunohistochemical examination was performed using Freeman and Wyke’s criteria to morphologically classify mechanoreceptors.

Results

The average time between original graft and biopsy was 10.7 years (range 0.5 – 27). Ruffini corpuscles and free nerve endings were shown to be present in control group specimens with reduced concentration of neural tissue seen in graft specimens.
Histological examination for mechanoreceptors using NFP staining showed significantly less mechanoreceptors in allograft and autograft patients than controls (mean number of NFP positive mechanoreceptors per high power field: 0.67+/-0.9 allograft and 0.49+/-0.8 autograft versus 4.7+/-0.9 controls, p<0.0001, Figure 2.) There was no significant difference in the number of mechanoreceptors between autograft and allograft tissue.

Conclusion

We present comparative data demonstrating reduced concentration of mechanoreceptors in ACL grafts compared to native ACL tissue. This may explain the continued proprioceptive deficit even following ACL reconstruction. This deficit appears to persist irrespective of graft choice and time since surgery.