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By Jeffery J. Ericksen, MD
Musculoskeletal conditions make up two percent of the global disease burden and are currently the most common cause of chronic disability (www.dcp2.org). The most common musculoskeletal dysfunctions include:
- Osteoarthritis
- Inflammatory arthritis
- Back pain
- Musculoskeletal injuries
- Crystal arthritis
- Metabolic bone disease
Many of these conditions occur later in life. With the elderly population increasing, it is likely that older adults will suffer from one or more of these conditions. Some patients may benefit from participating in physical therapy or moderate exercise to improve functionality and decrease pain. For patients with specific musculoskeletal pain syndromes, however, they may find that prolotherapy treatment provides better results.
Prolotherapy (PrT) is an injection treatment for musculoskeletal pain syndromes that stem from connective tissue injuries or damage from chronic degenerative conditions and overuse syndromes. PrT derives its name from proliferant therapy and was formerly known as sclerotherapy although research has demonstrated that PrT, done using solutions that induce a localized inflammatory or healing response, are stimulating organized connective tissue regeneration and not scar formation. Most practitioners stopped using the term sclerotherapy in the 1950s. The term “ligament and tendon regenerative injection therapy” has been suggested, but is not yet widely accepted in clinical use.
PrT was championed in the 1950s by Dr. George Hackett who extensively used this treatment in his general surgical practice that focused on treating chronic pain conditions. He injected small volumes of proliferant solutions into painful tendon and ligament insertion sites known as entheses (fibro-osseus junctions) serially, typically for 3-6 treatment sessions over monthly intervals. Dr. Hackett’s book remains the premier discussion of PrT for chronic pain management with proliferant injections [1].
Early History
PrT has a historical basis dating back to early Egyptian use of hot cautery to treat horse lameness. Hippocrates used applied heat for unstable joints in humans. It is likely that applied heat induced scar formation and provided joint stability when injury or disease led to instability from joint connective tissue laxity. Later discussion of proliferant injections is traced to Velpeau in 1835; Hall & Frazier in 1929 described using the process in animals; and, in 1937, Dr. Earl Gedney described sclerosing injections in ligaments.
The American Academy of Sclerotherapy (www.acopms.com) was formed in 1940 and is still active. Today, the Hackett-Hemwall Foundation (www.HackettHemwall.org) conducts research and physician education in PrT. The American Association of Orthopaedic Medicine (http://aaomed.org) provides education and information on non-surgical management of musculoskeletal disorders with PrT as the primary focus for many conditions.
Rationale for PrT
 The use of PrT for musculoskeletal conditions is based on the growing understanding that most conditions are not due to active inflammation. Histological study, MRI, and ultrasound imaging methods have demonstrated that these tissues manifest few if any inflammatory cells. Instead, degenerative connective tissue fibrils with collagen thinning, fraying, and disruption with immature non-functional blood vessels (neovascularization) has been noted in tendon structures. In general, the biomedical literature supports the use of the terms “tendinosis,” “tendinopathy,” and “enthesopathy” to describe these tissues rather than the terms suffixed by “-itis,” such as tendonitis or bursitis that imply inflammation. Thus, the focus of treatment has shifted away from inhibiting inflammation and toward the direction of stimulating tissue recovery or regeneration.
Mechanism of Action
The theory behind PrT is that injections cause local tissue injury, which triggers the release of inflammatory mediators. Ongoing debate centers on the role of the specific solution vs. the role of the tissue injury caused by the needle penetrating tissues that advocates of dry needling argue as the necessary event. Inflammatory mediators then stimulate granulocytes and macrophages to begin activity from growth factors released. Fibroblasts are then stimulated that synthesizes collagen at the injury site followed by maturation of the collagen fibrils to tighten and strengthen the tissue. Recruitment of circulating stem cells is possible from the growth factor release seen in PrT treatment.
Traditional PrT solutions are classified based on their effect on local tissues. Irritant solutions include:
- Phenol
- Particulate solutions (such as ground pumice flour)
- Phenol-quinone urea
These solutions damage cells by oxidizing and alkylating surface proteins which potentially renders cells as antigenic and immediately stimulates the inflammatory cascade and recruits macrophages that secrete growth factors.
Osmotic shock agents include:
- Dextrose
- Glycerin
- Zinc sulfate
Osmotic shock agents create cells via osmotic pressure gradients, glycosylation of surface proteins, and metallation of proteins. This leads to granulocyte and macrophage attraction. Chemotactic agents, such as sodium morrhuate (cod liver oil salt), directly attract inflammatory cells plus fibroblasts. Sodium morrhuate is rich in arachidonic acid acting as a precursor for prostaglandins, leukotrienes, and thromboxanes necessary for inflammation.
Blood can also serve as an injection solution since it is the natural proliferant used by the body during injury. More recent development of platelet rich plasma (PRP) systems has enabled routine injection of autologous platelets and growth factors in high concentration as a proliferant solution. The PRP development work has been followed by the use of autologous bone marrow derived from stem cell harvesting (BMAC) to provide concentrated stem cell volumes for injection into more significant tissue injuries for robust healing stimulation.
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