The Non-Angioblastic Cellular Contribution to Human Meniscal Healing; An Ex vivo Study
Author(s): Lanny L. Johnson, M.D., Gretchen Flo, D.V.M., David A. Detrisac, M.D., P. Linden Dillin, M.D.
Objective: The objective of this study was to identify the non-angioblastic sources of cellular contributions to meniscal repair.
Background: Preservation of the knee joint meniscus is a time honored need to prevent osteoarthritis. The vascular supply of the meniscus is limited to the outer one-third. Successful repairs are limited to this area. Repairs in the avascular portion are limited to selected cases. Independent of the region the common denominator of a successful surgical repair of the meniscus is the secure fixation and contact of the two portions. Therefore, multiple biological adjuncts have been advanced to enhance success of meniscus repair. Independent of these ideas healing remains based upon the innate biological tissue and fluids response to injury and surgery. Following bleeding the blood clot is populated with cells. Cellularity presence in the joint is a main contributor to healing. The purpose of this ex vivo study was to identify the source of the non-angioblastic cellular contribution using the same human’s meniscus and fluids.
Methods: Human meniscus and patient blood and synovial fluid from the same person were harvested at time of meniscectomy. The meniscus was cut into five sections. Each section had a core lesion in the center replicating a vascular access channel. Each of the five specimens was placed in separate container with one of the following fluids, normal saline, patient’s plasma, patient’s blood, patient’s synovial fluid aspirate and mixture of blood and synovial fluid. They were cultured for 12 weeks. The specimens were then subject to histological examination.
Results: There was no contribution of cells to from the normal saline or plasma. Meniscal cells remained viable, but no proliferation was observed. The patient’s synovial fluid and blood contributed to the cellularity on the cut edges of the meniscus specimens. The core lesion resulted in loss of meniscal substance and cells in the adjacent area. No meniscal cells were seen to be released or proliferated from the disrupted meniscus. Most of the cellularity was observed from the application of the aspiration of the normal response to injury, a spontaneous mixture of blood and synovial fluid. The host meniscus cells did not appear to contribute any new cellularity.
Conclusions: This human ex vivo study showed the potential for the patient’s body fluids of blood and synovial fluid from the same patient to be potential cellular contributors to meniscal healing and resultant preservation.