Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain

Prolotherapy is an injection-based complementary and alternative medicine (CAM) therapy for chronic musculoskeletal pain. The historical roots of therapeutic intervention that may have similar underlying mechanisms of action, however, extend to antiquity. Hippocrates anecdotally described the use of hot wires to create scar tissue (sclerotherapy, an early name for prolotherapy) in cases of severe shoulder dislocation in soldiers. Prolotherapy injections have been used for approximately 100 years by physicians practicing both conventional and complementary medicine. Modern applications can be traced to the 1950s when prolotherapy injection protocols were formalized by George Hackett, a general surgeon in the United States based on his clinical experience of more than 30 years. Although techniques and injected solutions vary by condition, clinical severity, and practitioner preferences, a core principle of contemporary prolotherapy is that a relatively small volume of an irritant or sclerosing solution is injected at sites on painful ligament and tendon insertions, and in adjacent joint space over the course of several treatment sessions. Prolotherapy is becoming increasingly popular in the United States and internationally, and is actively used in clinical practice. Increased quantity and quality of the scientific literature supporting prolotherapy, internet reports, and the use of prolotherapy by prominent sports personalities all contribute to a growing visibility and interest among physicians and patients. A 1993 survey sent to osteopathic physicians estimated that 95 practitioners in the United States were estimated to have performed prolotherapy on approximately 450,000 patients. However, this survey likely underestimated the true number of practitioners dramatically because only 27% of surveys were returned. No formal survey has been done since 1993. The current number of practitioners actively practicing prolotherapy is not known but is likely several thousand in the United States based on attendance at CME conferences and physician listings on relevant websites. Prolotherapy has been assessed as a treatment for a wide variety of painful chronic musculoskeletal conditions that are refractory to “standard of care” therapies. Although anecdotal clinical success guides the use of prolotherapy for many conditions, clinical trial literature supporting evidence-based decision-making for the use of prolotherapy exists only for low back pain, several tendinopathies, and osteoarthritis.

Nomenclature

Nomenclature surrounding prolotherapy has evolved. This procedure, now known most commonly as prolotherapy, has been identified using names consistent with existing hypotheses and understanding of possible mechanisms of action. Nomenclature has reflected practitioners’ perceptions of prolotherapy’s therapeutic effects on tissue. Historically, this injection therapy was called “sclerotherapy” because early solutions were thought to be scar-forming. “Prolotherapy” is currently the most commonly used name, and is based on the presumed “proliferative” effects on chronically injured tissue. It has also been called “regenerative injection therapy” (RIT) ; some contemporary authors identify the therapy according to the injected solution. The precise mechanism of action of the various injectants is not known, but is likely to be multifactorial.

Professional Status

No single national medical organization acts as a supervisory, credentialing, or guideline-generating capacity for prolotherapy or its practitioners. The National Institutes of Health identifies prolotherapy as a CAM therapy. The NIH National Center for Complementary and Alternative Medicine (NCCAM) has funded two ongoing clinical trials and two completed basic science studies on the mechanisms of prolotherapy. The Centers for Medicare and Medicaid Services and the Veteran’s Administration have reviewed the prolotherapy literature for low back pain and all musculoskeletal indications, respectively, and determined existing evidence to be inconclusive. Neither agency recommends third party compensation for prolotherapy. However, neither review included the most recent clinically positive studies or reviews in their evaluation. Private insurers are beginning to cover prolotherapy for selected indications and clinical circumstances; however, most patients pay “out-of-pocket”.

Prolotherapy Technique

Like contemporary Western medical therapies, CAM therapies often follow directly from a particular way of understanding the patient’s normal and pathologic conditions. For example, acupuncture relies on an ancient tradition of energy meridians and physiologic correlations that inform the specific procedures of needle placement to improve overall balance. Meditation relies on an understanding of interaction between mind and body to influence the body using mental processes. The same is true of prolotherapy. In his clinical text on the practice of prolotherapy, George Hackett laid out the foundations of treating musculoskeletal injuries using prolotherapy. He developed a diagnostic and treatment strategy familiar to those with a detailed knowledge of conventional Western understanding of the effects of local trauma, healing, and pain referral patterns. His diagnostic and therapeutic techniques, developed in the 1950s, could be viewed as holistic before the term gained popularity in contemporary medicine. Hackett interpretated chronic pain and referred pain symptoms such as numbness, tingling, and weakness, and alteration in proprioception, as originating, in part, from poorly healed ligaments and tendons. As such, he preceded by several decades the current change in the understanding of chronic tendon and ligament pain. Formerly thought to be primarily inflammatory in nature (“tendon itis ), chronic tendon injury is now understood to be primarily a result of noninflammatory, degenerative tissue (tendin osis ). Injection protocols for a particular body part tend to treat not just the specific injured structure, but also the surrounding structures, in an effort to increase the integrity of the area as a whole.

During a prolotherapy session, therapeutic solutions are injected at sites of painful and tender ligament and tendon attachments, and into adjacent joint spaces. Prolotherapy treatment commonly consists of several injection sessions delivered every 2 to 6 weeks over the course of several months. Injections are often carried out in a joint-specific manner.

The actual prolotherapy procedure can be illustrated using a specific clinical scenario as an example discussed subsequently. In this section we describe a standard set of injections of the anterior knee. Prolotherapy is commonly performed by prolotherapists for patients with knee osteoarthritis who have one or more areas of anterior knee area tender to palpation. Injections are carried out in a “peppering” fashion throughout the tender tendon or ligament attachments with all injections done with the needle touching bone. This description is intended to demonstrate the overall process and anatomic detail with which a prolotherapist approaches a specific condition. It is not intended as a substitute for formal prolotherapy training.

Although there is no consensus regarding specific indications or procedural elements of prolotherapy, there is some consistency among prolotherapists concerning what constitutes appropriate injections of specific anatomic areas. The following example explains a set of injections for knee osteoarthritis and, in the authors’ view, can be viewed as a general approach for a majority of practicing prolotherapists.

Clinical Vignette

Patient Description

JM is a 55-year-old woman with knee pain for 3 years who is referred by her primary care physician for consideration of prolotherapy for knee osteoarthritis. Prior work-up revealed moderate joint space narrowing on plain radiograph. The patient denies prior knee trauma. Her knee pain worsens with activity but her knee does not “give out” or “lock”. Prior therapy has included rest, acetaminophen, and nonsteroidal antiinflammatory drugs (NSAIDs). Her examination reveals a noninflamed knee with crepitus on flexion and extension but without effusion. The knee is stable with near-normal range of motion and normal Lachman’s test. There is moderate tenderness to palpation of the pes anserine muscle group insertion, the medial popliteal attachments, and the proximal attachment of the medial collateral ligament.

Approach to the patient: Routine office evaluation has determined that the patient has moderate knee osteoarthritis and anterior knee pain without meniscal injury, posterior or anterior cruciate ligament injury, or other surgical issues. She seems to be a good candidate for prolotherapy. The overall clinical situation is discussed with the patient. She elects to proceed with a trial of prolotherapy.

Position: The patient may be positioned with the knee flexed at 90 degrees or extended while lying prone at 180 degrees. The flexed position is preferred because it is somewhat easier to inject relevant structures with the patient’s leg relaxed and leaning against the injector, and it allows better access to anterior knee structures.

Anatomic marking and local anesthesia: The major superficial anatomic landmarks are palpated and marked with skin marker of choice ( Fig. 15-1 ). Tender areas are injected with small intradermal skin wheals because this makes the deeper injections less painful. One percent buffered lidocaine is often used.

Injection of Ligamentous and Tendinous Attachments

Injections are performed through the skin wheal with the needle tip on bone with solution delivered in a peppering fashion approximately each square centimeter. A single skin puncture can be used to facilitate multiple placements of solution. After the initial needle positioning, the needle is either: (1) lifted slightly from the surface of the bone and repositioned, or (2) the skin is slid (skin sliding). Between 0.2 to 0.5 mL of solution is placed at each location. The order of injected anatomic sites injected is clinician-specific. The following order is used in the authors’ clinic.

1.

Medial knee: Injections begin at the superior aspect of the femoral condyle along the femur distally to the joint line. Injections are then made at the anterior tibia and the attachments of the pes anserine tendons. It is likely that these structures and not the much smaller bursa is the source of pain in this area. The popliteus muscle attachment is injected by displacing the medial calf musculature posteriorly; injections are done by directing the needle anteriorly onto the posterior tibia. Injections are then made on the joint line directed downward onto the top of tibia into attachments of the coronary ligaments, which attach the medial meniscus to the tibia. The patella is injected at the superior and inferior lateral and medial retinaculum.
2.

Lateral knee: The superior condyle of the femur is the first structure of the lateral knee to be injected. It is followed by the lateral collateral ligament, lateral joint line, and lateral coronary ligaments. The fibula is then palpated with thumb and forefinger over the head of fibula, and injections are done to top and anterior edge of the fibula and into tibiofibular ligament at the anterior portion of fibula.
3.

Intra-articular knee injection: An intra-articular injection is often performed as part of an anterior knee injection series; the most common access is the anteromedial port. The actual injection is consistent with that of a routine intra-articular steroid injection. Alterative access includes the lateral superior port, which can be palpated with the knee straight, and is located at the lateral patella, approximately 1 cm below the superior edge of the patella. Intra-articular access can be improved by applying pressure to the medial side of the patella and lifting its lateral border superiorly, thereby creating a wider port of entry ( Fig. 15-2 ).

Figure 15-2

Anatomic locations for prolotherapy injections at the anterior knee.

(Knee image courtesy Primal Pictures Ltd. www.primalpictures.com . Used by permission.)

Mechanism of Action

Injected solutions (“proliferants”) have historically been hypothesized to cause local irritation, with subsequent inflammation and tissue healing resulting in enlargement and strengthening of damaged ligamentous, tendinous, and intra-articular structures. These processes were thought to improve joint stability, biomechanics, function, and ultimately, to decrease pain.

The mechanism of action for prolotherapy is not clearly understood and, until recently, it received little attention. Supported by pilot-level evidence, the three most commonly used prolotherapy solutions have been hypothesized to act via different pathways: hypertonic dextrose by osmotic rupture of local cells, phenol-glycerine-glucose (P2G) by local cellular irritation, and morrhuate sodium by chemotactic attraction of inflammatory mediators and sclerosing of pathologic neovascularity associated with tendinopathy. The potential of prolotherapy to stimulate release of growth factors favoring soft tissue healing has also been suggested as a possible mechanism.

In vitro and animal model data have not fully corroborated these hypotheses. An inflammatory response in a rat knee ligament model has been reported for each solution, although this response was not significantly different from that caused by needle stick alone or saline injections. However, animal model data suggest a significant biologic effect of morrhuate sodium and dextrose solutions compared to controls. Rabbit medial collateral ligaments injected with morrhuate sodium were significantly stronger (31%), larger (47%), and thicker (28%), and had a larger collagen fiber diameter (56%) than saline-injected controls ; an increase in cell number, water content, ground substance amount, and a variety of inflammatory cell types were hypothesized to account for these changes. Rat patellar tendons injected with morrhuate sodium were able to withstand a mean maximal load of 136% (±28%)—significantly more than the uninjected control tendon. Interestingly, in the same study, tendons injected with saline control solution were significantly weaker than uninjected controls. Dextrose has been minimally assessed in animal models. Recent studies showed that injured medial collateral rat ligaments injected with 15% dextrose had a significantly larger cross-sectional area compared to both noninjured and injured saline-injected controls. P2G solution has received the least research attention; although it is in active clinical use, no animal or in vitro study has assessed P2G effect using an injury model. In research settings, most clinicians report using these solutions as single agents, although concentration of each one varies. In clinical practice, physicians sometimes mix prolotherapy solutions, or use solutions serially in a single injection session depending on experience and local practice patterns. The effect of varied concentrations or mixtures has not been assessed in basic science or clinical studies and no clinical trial has compared various solutions.

Clinical Evidence

Early Research

Since its inception, prolotherapy has been primarily performed outside of academia. Research has been primarily done by clinicians who perform prolotherapy themselves. This has lead to a pragmatic orientation of existing prolotherapy studies and a relative paucity of large, rigorous, clinical trials in spite of significant clinical activity. Although the first randomized controlled trial (RCT) did not appear until 1987, clinicians have enthusiastically reported the results of more modest, pilot-level nonrandomized clinical trials since the 1930s ( Tables 15-1 and 15-2 ).

Table 15-1

Description of Case Reports and Case Series

Study	Indication	Subjects	Injectant	Outcome Measures	Results
Gedney et al., 1937	Knee OA pain, knee instability, LBP, SI dysfunction	1 F, age 68 yrs; 1 M, age 45 yrs	Neoplasmoid ^∗and MacDonald’s Solution ^∗injection	Subjective pain and mobility	Improved mobility, decreased pain
Shuman et al., 1941	Recurrent shoulder dislocation	1 F, age 23 yrs; 3 M, ages 17, 18, 24 yrs	AC joint capsule injections using one or more of the following: Sodium Linsoleate ^∗, Alparene ^∗, Sylnasol ^∗, Neoplasmoid ^∗	Subjective pain, recurrence of dislocation	No recurrence of dislocation, decreased pain
Bahme et al., 1945	SI dysfunction	30 F, 70 M; ages 12-75 yrs; pain for 0.5-45 yrs	OM and SI ligament Sylnasol ^∗injections	Subjective pain	50%-100% pain relief
Gedney et al., 1951	LBP	3 M, ages 19, 32, 34; pain for 0.5-16 yrs	Sylnasol ^∗injections	Work status, subjective pain	Ability to return to work, decreased pain
Gedney et al., 1952	SI dysfunction, LBP	1 F, age 23 yrs; 1 M, age 30 yrs; pain for 1 yr	SI ligament Sylnasol ^∗injections	Subjective pain	Resolution of pain
Hackett et al., 1953	SI dysfunction, LBP	9 M, 8 F; ages 15-52 yrs; pain for 4 mos-20 yrs	Sylnasol ^∗injections	Subjective pain	Resolution of pain through 2 yr follow-up Occasional exacerbation resolved with retreatment
Hackett et al., 1953	SI dysfunction	119 M , 134 F; ages 15 to 70; pain for up to 30 yrs	Not given	Subjective pain	Pain-free for 2-14 yrs (long-term follow-up questionnaire)
Shuman et al., 1954	LBP, knee pain, shoulder separation, other joint pain	93 adults	Not given	Return to work	95% (88) able to return to work, 5% (5) unable to return to work
Hackett et al., 1954	SI dysfunction	3 F, ages 40, 56, and 58 yrs	Not given	Subjective pain	Resolution of pain
Neff et al., 1960	LBP, SI dysfunction	3 adults	Sylnasol ^∗injections	Subjective pain	Resolution of pain
Myers et al., 1961	LBP	267 adults	Sylnasol/pontocaine ^∗solution or Zinc/phenol ^∗solution injections	Subjective pain	Resolution of pain in 82% of subjects
Hackett et al., 1962	SI dysfunction, other joint pain	1857 subjects (1516: SI dysfunction, 284: other indications); ages 15-88 yrs; pain/disability for 3 mos to 65 yrs	Sylnasol ^∗or P2G injections	Subjective pain	“Satisfactory cure” in 82% (1489) subjects for up to 19 yrs
Hackett et al., 1962	Head-neck strain	82 subjects	P2G injections	Subjective pain	“Good to excellent” results in 74 subjects
Kayfetz et al., 1963	Traumatic (whiplash) or nontraumatic (tension) headache	102 M, 162 F subjects (206 traumatic, 58 nontraumatic headache); pain (average) for 4 yrs	Sylnasol ^∗, zinc sulfate ^∗or P2G injected during 1-20 sessions	4-point pain scale: from excellent (no pain or symptoms) to poor (no relief of pain or symptoms)	Pain improvement during 6 mos to 5 yrs follow-up: excellent: 145; good: 43; fair: 41; poor: 33; lost to follow-up: 2
Kayfetz et al., 1963	Occipitocervical injury (whiplash)	87 M, 102 F; ages 10-61 yrs; pain for >1 mo in 78%, pain for >1 yr in 21% of subjects	Sodium psylliate ^∗, tetradecyl sulfate ^∗, zinc sulfate ^∗injected in 1-20 sessions over 1 to 6 mos	4-item pain scale: from excellent (no pain or symptoms) to poor (no relief of pain or symptoms)	Pain improvement: excellent: 113; good: 15; fair: 34; poor: 27
Peterson et al., 1963	LBP	136 adults	P2G injections	Pain improvement (percentage of improvement)	Pain improvement: excellent (>75%): 106; good (50-75%): 114; fair (25-50%): 5; poor (<25%): 11
Barbor et al., 1964	LBP	153 adults; pain for 6 mos-20 yrs	P2G injections	Subjective pain relief	Pain relieved to subject’s satisfaction: 111; Pain relief failure: 17; Lost to follow-up: 25
Blumenthal et al., 1974	Headache	3 adults	P2G injections	Subjective pain	Resolution of pain
Leedy et al., 1976	LBP	50 adults; ages 25-72 yrs; pain for 1 mo to >10 yrs	Not given	Subjective pain at 5-yr follow-up	Pain resolution with: 0 exacerbation: 26 1 exacerbation: 18 2 exacerbations: 5 >2 exacerbations: 1
Leedy et al., 1977	Shoulder pain, LBP, costochondritis, epicondylitis	4 M, 4 F	Farnsworth formula 61 ^∗injections	Subjective pain	Symptom resolution
Leedy et al., 1982	SI dysfunction	4 M, 18-55 yrs; 1F, 82 yrs	Not given	Subjective pain	Symptom relief
Bourdeau et al., 1988	LBP	11 M, 13 F; ages 19-82 yrs; pain for 2 mos to 30 yrs	12.5% dextrose injections in 3-10 treatment sessions	4-point pain scale at 5-yr follow-up	Excellent (little or no pain for 5 yrs): 7; Very good (little or no pain for 2-5 yrs): 10; Good (little or no pain for 1 yr): 2; Poor (pain control for less than 6 mos): 5
Ongley et al., 1988	Knee pain, knee laxity	4 subjects	30-40 mL P2G “peppered” into PCL, ACL, LCL, MCL insertions	Laxity measured with “Genucom” knee analysis system; subjective pain and function	Improvement for 90° A-P ^hdraw, 90° A-P draw with internal rotation, 30° A-P draw, and 80° internal-external rotation (P < .05); Complete pain resolution: 2 Partial pain improvement: 2 Function improvement: 4
LaCourse, et al., 1990	LBP	8 adults	P2G injections; subjects also received lidocaine and steroid injection, and exercise advice	Pelvic inclination as measured by inclinometer	Decreased pelvic inclination
Dorman, et al., 1991	Low-back, mid-back and neck pain	40 F, 40 M adults	P2G injections; subjects also received lidocaine and steroid injection, and exercise advice	Pain severity, functional capacity, sleep	Decreased pain severity, improved functional status and sleep
Schwartz et al., 1991	SI dysfunction	43 adults; ages 20-70 yrs	3 injections with SM each 2 weeks apart	Pain relief scale at 2-week follow-up	Pain relief: 95%: 20; 75%: 11; 66%: 4; 33%: 1; 0%: 3
Hirschberg et al., 1992	Iliocostal friction syndrome	6 M, 6 F; ages 38-82 yrs	12.5-25% dextrose injections and use of rib compression belt and Hoek corset	Subjective pain	Resolution of pain
Reeves et al., 1994	Fibromyalgia	31 adults; pain (average) for 7-8 yrs	12.5% dextrose injected at 16 fibromyalgia sites an average of 3.5 times	Average pain (0-10 Likert scale); subjective functional status	Average pain improvement of 16%; Improved functional status
Dorman et al., 1995	LBP	9 adults	Proliferant and protocol not given	Oxygen consumption efficiency while walking	Improved oxygen consumption efficiency while walking
Mathews, 1990	SI dysfunction	16 subjects	3 series of P2G injections	5-item pain scale	At 4-mos follow-up: no pain: 11; slight pain: 1; much better: 1; slightly better: 1; no better: 1; Lost to follow-up: 1
Reeves et al., 1997	Recurrent knee dislocation	1 F, age 72 yrs	5% dextrose injections	Subjective pain; dislocation	Decreased pain Joint relocation
Reeves et al., 2003	Knee pain, flexion and laxity	16 adults	10% and 25% dextrose injections	Pain scale; knee laxity	At 3-yr follow-up: pain at rest, stair, and walk decreased by 35-45%; subjective swelling (P < .05) and ROM (P < .01) improved, ligament laxity decreased by 71% (P < .01).
Hooper et al., 2004	Cervical, thoracic and lumbar pain	126 F, 51 M subjects; average age 39.5 yrs; pain for 3 mos-27 yrs (average: 4.8 yrs)	20% dextrose injections; weekly set of injections for 3 sessions with repeated set of 3 sessions if pain control incomplete	Subjective pain, function and ability to work on three 5-item scales	At mean 9 mos follow-up: Pain reduction: 91% of subjects; function improvement: 84.8% of subjects; improved ability to work (for those working outside the home): 84% of subjects
Hooper et al., 2005	Cervical pain	1 M subject; neck pain (MVA-related) for 2 yrs	Intra-articular 20% dextrose injected under fluoroscopic guidance at zygapophyseal joints C2-C6	Neck disability index score (NDI)	NDI score decreased from 24/50 preinjection to 9/50 at 1 yr, and 2/50 at 3 yrs
Lazzara et al., 2005	Full-thickness Achilles tendon rupture	1 F, 26 yrs; pain and inability to bear weight; MRI proven right Achilles tendon rupture 4.3 cm proximal to the calcaneus and 1.1 cm gap	Injections of 20 mL solution (SM, dextrose, 2% lidocaine and bacteriostatic water) at the Achilles tendon, anterior talofibular and calcaneofibular ligaments, and ankle joint biweekly for 8 sessions over 3 mos	Subjective pain, disability, ultrasound and MRI	No subjective pain at rest or while jogging and has normal gait. MRI showed no defect at 10 weeks, ultrasound at 14 weeks showed tendon significantly larger than unaffected side
Topol et al., 2005	Groin pain (osteitis pubis and/or adductor tendinopathy)	24 M rugby and soccer players pain (average) for 15.5 mos	12.5% dextrose injected at the pubis symphysis and ischiopubic ramus at 4-week intervals for 2-6 injection sessions (mean 2.8)	VAS, Nirschl Pain Phase Scale	Improvement in both outcome measures (P < .05); 22/24 subjects plying at full capacity at mean 17 mos follow-up (6 to 32 mos)
Maxwell et al., 2007	Achilles tendinopathy (insertional and midportion)	11 F, 25 M adults ages 23-82 yrs (mean: 52.6 yrs); pain for 3 mos-120 mos (average: 28.6 mos)	25% dextrose injected into anechoic and hypoechoic areas of the tendon every 6 weeks for mean of 4 sessions (2-11)	100 mm VAS for pain at rest, with activity and during sport; tendon thickness; degree of neovascularity, hypoechogenicity	Sustained at 12 mos follow-up: VAS pain at rest: 81% improvement; VAS pain with activity: 84% improvement; VAS pain during sport: 78% improvement; Decrease in tendon thickness, hypoechogenicity and neovascularity.
Miller et al., 2006	Chronic degenerative discogenic leg pain	35 F, 41 M ages 21-90 yrs (mean 55 yrs) with pain for 2-240 (mean 39 mos) who failed physical therapy; had substantial but temporary relief with two fluoroscopically guided epidural steroid injections and had CT-proven multiple grade IV or V tears of the annulus fibrosis	3 mL 25% dextrose; biweekly disc space injection for mean of 3.5 injection sessions	0-10 VAS pain scale	43.4% of subjects had sustained improvement with a mean of 71% improvement at mean follow-up of 18 mos compared to baseline status. 43.4% (33/76) of subjects showed a sustained treatment response of 71% Baseline VAS for responders was 8.9 (±1.4), 2.5 (±2.0) at 2 mos, and 2.6 (±2.2) at 18 mos
Khan, et al., 2008	Refractory coccygodynia	23 F, 14 M adults (mean 36 yrs) with > 6 mos of pain	25% dextrose injected to tender coccyx points in 1-3 injections depending on initial pain level.	0-10 VAS pain scale	At 2 mos, reduction of VAS from 8.5 at baseline to 2.5. 30/37 achieved “good” pain improvement; 7/30 “not improved”.
Cusi et al., 2008	SI joint pain with failure of load transfer (disability) at the SI joint	20 F, 5 M adults ages 26-67 (mean 40.4 yrs); at least 6 mos of LBP who failed 3 mos PT	Computer tomography-guided injection of (1.8 mL/5 mL 50% dextrose to dorsal interosseous ligament each 6 weeks for 3 sessions and continued to perform PT program	Quebec Back Pain Scale, Roland Morris 24, Roland Morris Disability Scale	At 26 mos average (range 6-39 mos): Improvement compared to baseline status in all pain and disability measures (P < .01)
Ryan et al., 2008	Plantar fasciitis	17 F, 3 M adults mean age 51 (SD 13) yrs; at least 6 mos of symptoms of plantar fasciitis who failed one or more conservative treatments	Ultrasound-guided injection of 25% dextrose with lidocaine; abnormal hypoechoic areas and anechoic clefts/foci in the thickened portion of the plantar fascia were targeted	0-100 VAS pain levels and percentage pain reduction at rest, activities of daily living, and activity Ultrasound assessed tendon thickness, number of tendons with anechoic clefts or foci, and degree of neovascularity	At 12 mos follow-up, subjects reported a mean change on VAS of 12.1 (21.0), 21.6 (29.5), and 35.1 (41.4) points at rest, activities of daily living, and physical activity, respectively They also reported pain reduction of 88%, 84%, and 78% at rest, activities of daily living, and physical activity Structurally, there was a mean reduction in tendon thickness, number of tendons with anechoic clefts or foci, and degree of neovascularity

ACL , Anterior cruciate ligament; A-P, Anterior-posterior; LBP, Low back pain; LCL, Lateral collateral ligament; MCL, Medial collateral ligament; mos, Months; OA, Osteoarthritis; OM , Osteopathic manipulation; P2G , Phenol-glucose-glycerine; PCL, Posterior cruciate ligament; SI, Sacroiliac; SM, Sodium morrhuate; VAS, Visual analog scale; yrs, Years. (Elements of table used in: Rabago D, Best T, Beamsley M, Patterson J. Systemic review of prolotherapy for chronic musculoskeletal pain. Clin J Sport Med, 15(5): 376-380; 2005.)

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