Vertebral compression fracture
In this article we will discuss the research on stem cell therapy in treating vertebral compression fracture and treatment options including the use of Prolotherapy.
New research from a combined team of researchers representing the United States, South Korea and Israel, summarized recent findings in the treatment of vertebral compression fracture:
- The most common type of injury in osteoporotic patients is vertebral compression fracture.
- Current surgical, and nonsurgical, interventions for vertebral compression fracture do not provide appropriate clinical responses to repair and induce new bone formation, frequently leaving patients in pain and/or disability.
- Bone formation and fracture repair are dependent on the appropriate number and function of stem cells already in the injured area.
- This has inspired investigators to utilize stem cells in a number of preclinical animal models to increase the number of functional stem cells and thereby enhance bone regeneration.1
Doctors at the California Institute for Regenerative Medicine also reported patients success with a combined treatment of stem cells and parathyroid hormone to enhance bone remodeling.2
The use of stem cell therapy for the healing of osteoarthritic bone disease is discussed at length in our companion article Stem cell therapy and bone repair in osteoarthritis patients, and our article on the role of stem cells, inflammation and bone repair.
Treating pain from a vertebral compression fracture
Since a vertebral compression fracture can be quite painful, anti-inflammatory medications are typically recommended. However, in the long run, they can do more damage than good, especially if injured ligaments are involved in the fracture, or may even have contributed to susceptibility to a fracture.
Although anti-inflammatory drugs have been shown to produce short-term pain benefit, they result in long-term loss of function and even more chronic pain by actually inhibiting the healing process of soft tissues and accelerating cartilage degeneration.
Another treatment option is orthotic support in the form of a brace to properly position the back while the fracture heals. More recently, vertebroplasty and spine balloon therapy have been added as treatment options. Both essentially “cement” the fracture. The problem with these treatment approaches, even if exercise and non-steroidal anti-inflammatory agents are added to the mix, is that they do nothing to address the potential problem of ligament and tendon laxity.
Prolotherapy for post-fracture pain
Osteoporosis affects the incidence of vertebral compression fractures as follows:
- Weakened bones, which are a result of osteoporosis, cause a weakness in the fibro-osseous junction, contributing to ligament and tendon laxity.
- This laxity decreases the stability of the bones, especially around the vertebrae.
- Eventually, because of the osteoporosis and the weakened ligaments, the vertebrae can no longer support the weight of the body and are compressed, resulting in a painful fracture.
- Prolotherapy helps stabilize the fracture site by causing the growth of ligamentous tissue at the fibro-osseous junction and strengthens the vertebral ligaments to eliminate the pain.
Prolotherapy, in strengthening the fibro-osseous junction – where the ligaments attach to the bone – stabilizes the compressed vertebral segment. The strengthening of the ligament and formation of new bone can realign the area, resulting in improved posture.
Prolotherapy, however, is not a complete treatment for osteoporosis compression fractures. The underlying cause must be corrected or the osteoporosis-induced compression fracture will recur.
1 Pelled G, Sheyn D, Tawackoli W, et al. BMP6-Engineered MSCs Induce Vertebral Bone Repair in a Pig Model: A Pilot Study. Stem Cells International. 2016;2016:6530624. doi:10.1155/2016/6530624.
2 Littman N, Abo A. Proceedings: Using Stem Cell Therapies to Reestablish Osteogenic Capability for Bone Regeneration. Stem Cells Translational Medicine. 2015;4(11):1247-1250. doi:10.5966/sctm.2015-0202.