Causes of Joint Pain – Symptoms of Osteoarthritis?

Ahh the joy of joints…they bend, they move…and sometimes they hurt.   

If you suffer from joint pain you are not alone. Joint pain is actually so common it affects hundreds of thousands of people throughout Canada. There are many causes of joint pain, with the two most common being:  injury, and disease of the joint (or of the tissues that surround the joint). But, identifying joint pain is trickier than it sounds as you need to first truly determine if the pain you’re experiencing is actually in the joint.   

Joints, by definition, are areas where two bones meet to provide motion to a particular body part, for instance: knees, ankles, elbows, shoulders, hips and wrists.  The essential stuff (!) But joints are separated by cartilage and ligaments that attach the bones around the joint. Then there are tendons that helpfully attach muscle to the bone around the joint.  The problem is: cartilage, ligaments and tendons are ALL also prone to injury, so the sensation of pain in the joint region does not automatically mean you have injured the joint itself.   If you self-diagnose and try and treat the area the wrong way, you won’t be solving the problem.  

The causes of true joint pain are most frequently linked to disease, such as arthritis.  This used to be thought of as something our grandparents would get however that myth is quickly being corrected, as arthritis is one of the most common joint diseases today in people of various ages. The word arthritis actually means “joint inflammation”, and there are over 100 different types of arthritis. Osteoarthritis is very common and causes joint pain.   

At about this point many folks reading this who suffer from joint pain or pain in a joint area are starting to wonder “do I have osteoarthritis?” Good question.  Here’s what we can tell you:   

Osteoarthritis is a “non-inflammatory” type of arthritis, which means that inflammation is not the primary concern.  The most worrisome - although predictable - component to osteoarthritis is its degenerative nature.  Because osteoarthritis is caused over time by continual wear and tear of the joint (which is bound to happen in one’s lifetime someway, somehow) it becomes most prevalent in men and women over the age of 45.  The repetitive wear and tear is also a major reason why so many athletes (famous for overusing joints that are key excelling in the sport to which they are committed) are affected by osteoarthritis.

Osteoarthritis is a disease that develops over time, when the cartilage in the joint begins to break down, commonly during the aging process.  Osteoarthritis can also appear as a result of injury or infection to the joint, or as a result of a simple case of weak genetics. Obesity and weight are also blamed for contributing to osteoarthritis since the greater a person’s weight, the greater the strain put on his or her joints.

Osteoarthritis usually affects weight bearing joints like the knee.  

Some of the symptoms of osteoarthritis include:  aches, pains, stiffness, enlargement and/or swelling. Osteoarthritis sufferers often report one or more of these symptoms in the joint, which may occur when performing every day functions such as walking up the stairs, sitting or standing, and lifting objects around the house. Pain in the joint may not be experienced directly in the joint. Pain in the knee, thigh or groin could in fact be caused by osteoarthritis in the hip.  

Physicians who specialize in sports medicine often are experts in osteoarthritis, since the athletes are some of the most vulnerable to developing it.  They will review your medical history and perform imaging or lab tests to diagnose with certainty whether you do, in fact, have osteoarthritis. Seeking help for your osteoarthritis will help you reduce or eliminate symptoms, which in turn will significantly improve your overall quality of life.  Why would you wait? 

For more information about the causes of joint pain or to find out if you have osteoarthritis please call 416-800-0800 or visit www.aesm.ca today.

"The Anterior Cruciate Ligament - Stabilizing and Recovering from a Torn ACL"

A torn ACL sounds like a mystery – unless you’ve ever had one.  Described by those unfortunate to be stricken by one as “a loud popping sound followed by an intense and sharp pain in the knee”,  a torn ACL usually happens in an abrupt movement or sport, like shifting directions, weaving around guards while moving a basketball down court.  Shortly after tearing an ACL the knee joint will begin to swell, making it very difficult to straighten the leg or even walk.   ACL tears happen more frequently than you think. If you feel you may have injured your ACL take heart, you will heal, but not without some help.   Read on. 

The Anterior Cruciate Ligament is actually one of the most important ligaments to the human body.  Found behind the knee cap, extending through the middle of the knee joint between the shinbone and the thigh bone, this vital ligament prevents your thighbone from sliding backwards onto your tibia and also stabilizes the knee, preventing it from rotating.   

ACL Injuries are very common in athletes, but aren’t restricted to them. People that would describe themselves as simply “very active” can also experience an ACL tear.  High impact movement or contact sports such as hockey, football, soccer, and basketball are where many ACL injuries happen.  Sports like these – involving abrupt stopping and starting, or frequent jumping – are just the kind of thing that can put enough momentum and pressure on the knee joint which causes the ACL to tear.  

A torn ACL is considered an acute injury.  If you’ve ever had one you’ll agree! Tears to the Anterior Cruciate Ligament happen most often during rapid, sudden movement. So it makes sense that the injury itself also happens suddenly.   

If you are at all suspicious that you may have a torn ACL, do not put any weight on that leg and certainly do not continue the physical activity that you were involved in when the injury occurred.  

When you suffer from a torn ACL, the pain is considerable if not extreme.  To immediately reduce the knee from swelling, and slightly manage the pain, elevate and ice the area.  Immediate rest is the most important step you can take towards healing.  Rest will not only help you heal more quickly but also help you to ensure that you prevent further injury both before and after treatment – something you will wholeheartedly want to avoid! 

ACL injuries are equal-opportunists – they are not age specific.  People young and old can - without warning - end up with a torn ACL, though teens and young adults remain the demographic most frequently injured by them.  

Where your age plays a major role in ACL injury is in the treatment and recovery.  Most ACL injuries require surgery, and a knee that’s still growing is treated differently than one that isn’t, which in turn dictates the type of ACL surgery performed. Custom knee bracing and ongoing physical therapy will also be a part of the full recovery of a torn ACL.    

Once your ACL surgery has been performed, the knee needs stability and rest. Be patient. We can’t overemphasize how key to recovery patience through rest is. Recovery from this kind of physical injury, and surgery required to mend it, takes time. Trying to rush the healing process will not work, so commit early on to giving your ACL an ample period to recover without aggravation.    

Rehabilitation “rehab” from a torn ACL involves medically supervised physical therapy, several times a week.  Your physical therapist will guide you through important exercises that you can do at home. Athletes often speed up their ACL-tear recovery time through an accelerated program that involves more frequent therapy. Rehab also reduces pain, controls swelling and restores the knee’s full range of motion, balance and overall strength. If you play your cards right you will, one day, feel like new…. 

If you would like more information about recovering from an ACL injury please call 416-800-0800 or visit www.aesm.ca  today.

Lateral epicondylosis and calcific tendonitis in a golfer: a case report and literature review

Written by: Erik Yuill, Chiropractor, Athletic Edge Sports Medicine

Published in: The Journal of Canadian Chiropractors Association

ABSTRACT

Objective

To detail the progress of a young female amateur golfer who developed chronic left arm pain while playing golf 8 months prior to her first treatment visit.

Clinical Features

Findings included pain slightly distal to the lateral epicondyle of the elbow, decreased grip strength, and positive orthopedic testing. Diagnostic ultrasound showed thickening of the common extensor tendon origin indicating lateral epicondylosis. Radiographs revealed an oval shaped calcified density in the soft tissue adjacent to the lateral humeral epicondyle, indicating calcific tendonitis of the common extensor tendon origin.

Intervention and Outcome

Conventional care was aimed at decreasing the repetitive load on the common extensor tendon, specifically the extensor carpi radialis brevis. Soft tissue techniques, exercises and stretches, and an elbow brace helped to reduce repetitive strain. Outcome measures included subjective pain ratings, and follow up imaging 10 weeks after treatment began.

Conclusion

A young female amateur golfer with chronic arm pain diagnosed as lateral epicondylosis and calcific tendonitis was relieved of her pain after 7 treatments over 10 weeks of soft tissue and physical therapy focusing specifically on optimal healing and decreasing the repetitive load on the extensor carpi radialis brevis.

RESUME

Objectif

exprimer en détail la progression d’une jeune golfeuse de calibre amateur qui a développé une douleur chronique au bras gauche en jouant au golf 8 mois avant son premier traitement.

Caractéristiques cliniques

douleur légèrement distale à l’épicondyle latérale du coude, prise plus faible et test orthopédique positif. L’ultrason diagnostic a démontré l’épaississement du tendon extenseur commun, ce qui indique une épicondylose latérale. Les radiographies ont révélé une densité calcifiée de forme ovale dans les parties molles adjacentes à l’épicondyle humérale latérale, ce qui indique une tendinite du tendon extenseur commun.

Intervention et résultat

les soins conventionnels visaient à diminuer la charge répétitive sur le tendon extenseur commun, particulièrement le muscle court extenseur radial du carpe. Les techniques des parties molles, les exercices et les étirements, ainsi qu’un support de coude ont contribué à réduire la tension répétitive. Les niveaux de douleur subjectifs ont été établis, et une imagerie a eu lieu 10 semaines après le début du traitement.

Conclusion

une jeune golfeuse de calibre amateur souffrant d’une douleur chronique au bras a reçu un diagnostic d’épicondylose latérale et de tendinite calcifiante et fut guérie de sa douleur après 7 traitements répartis sur une période de 10 semaines de thérapie physique et des parties molles axée sur la guérison optimale et la réduction de la charge répétitive sur le muscle court extenseur radial du carpe.

INTRODUCTION

The sport of golf has grown in popularity over recent years, especially in North America. In any sport, with an increase in popularity comes an increase in injury incidences. Golfers commonly report injuries to the lower back, lower extremity, and upper extremity. The most common upper limb area to be injured in amateur golfers is the elbow.¹ The term “golfer’s elbow” has traditionally been used as a common expression to describe medial epicondylosis. A much more widespread elbow problem in golfers is in fact lateral epicondylosis (LE). Among amateur golfers, lateral elbow pain was found to be 5 times more common than medial elbow pain.² In golfers, LE results from repetitive forearm extension and excessive gripping of the club during the swing. Additional identified risk factors that can contribute to elbow injuries in golfers include poor swing mechanics, poor conditioning, inadequate warm-up, inappropriate equipment, overuse, age, and preexisting pathological conditions.^1,2

The diagnosis of LE was first recorded in the literature by Runge in 1873.³ It is the most common cause of lateral elbow pain affecting approximately 1–3% of adults each year, and is more commonly seen in the dominant arm.^4,6,7 Men and women are affected with an equal prevalence, typically in their 4^th to 5^th decade of life.^5–7 Though special imaging is rarely ordered for cases of LE, the most common radiographic finding is calcification along the lateral epicondyle within the common extensor tendon.⁸

Calcified tendinopathy or calcific tendonitis (CT) is a chronic condition where deposits of calcium phosphate crystals accumulate in the midsubstance of the tendon fibers.^9–11 Epidemiological studies report that the prevalence of CT is highly variable (3–22% in the general population) depending on the location within the body.^10,11 CT has been shown to worsen tendinopathy conditions causing increased rupture rates, slower recovery times, and high frequencies of complication after surgery.^9,14 Women are affected slightly more often than men, with patients typically between 30 and 60 years of age.^12,15

This case report will describe an amateur female golfer who experienced lateral arm pain while playing golf and during her activities of daily living. Imaging revealed an oval shaped calcific density in the soft tissue adjacent to the lateral epicondyle of the humerus. The patient underwent a simple non-invasive conservative treatment plan using soft tissue techniques, an elbow brace, as well as stretching and strengthening exercises.

CASE REPORT

In this case, a 27-year old female amateur golfer developed left arm pain while playing. The pain first occurred for a short duration 8 months prior to the patient’s initial visit. She also recalls starting a new job one month later, where typing on a laptop re-aggravated her symptoms. Hitting golf balls at the driving range was described to be extremely painful at that time. The patient reported trouble picking up heavy objects with her left hand. The symptoms then subsided for a period of 6 months, until an acute exacerbation 1 week prior to her initial visit. At that time the patient found it difficult to move her elbow and experienced shooting pains down her forearm. Rest, ice, an elbow brace, and medication (ibuprofen taken 4 times a day) were self administered by the patient but failed to improve her condition. She rated her pain as 4/10 on a Visual Analog Scale (VAS). The patient reported no previous history of trauma or injury and a systems review was unremarkable.

On physical examination, postural observation revealed mild anterior head carriage, and slight anterior rolling of the left shoulder. No swelling or discoloration was noted. Palpation reproduced pain and tenderness over the left lateral epicondyle, wrist extensor muscles, and radiocapitellar joint. The left extensor carpi radialis brevis was particularly tight, as was the sternocleidomastoid, levator scapulae, and scalenes. The chief complaint was reproduced with resisted wrist extension and passive wrist supination. Resisted wrist supination and finger extension were both pain free. Orthopedic testing found Cozen’s test and Varus stress test to be positive for left elbow pain (Table 2). A cervical spine screen was negative and an upper limb neurological exam was within normal limits. Grip strength was found to be weaker on the left when compared to the right.

Table 2 Orthopedic tests regularly used to aid in the diagnosis of lateral epicondylosis.6,7

The patient was diagnosed with left lateral epicondylosis. Due to the acute nature of the patient’s pain and the extreme difficulty moving her elbow, she was referred for ultrasound and radiographic imaging to rule out more sinister differentials (osteochondritis dissecans of the capitellum or radiocapitellar arthritis). Diagnostic ultrasound showed thickening of the origin of the common extensor tendon from the lateral humeral epicondyle, indicating LE. Radiographs revealed an oval shaped calcified density in the soft tissue adjacent to the lateral humeral epicondyle, indicating CT of the common extensor tendon origin (Figure 1).

Figure 1 Imaging results for the patients left elbow. A) Diagnostic ultrasound showing thickening of the origin of the common extensor tendon, indicating lateral epicondylosis. B) Anterior to posterior radiograph showing an oval shaped calcified density in the (more ...)

TREATMENT

The patient was treated with 7 sessions over 10 weeks. Passive treatment consisted of NSAIDs (Naprosyn taken as required) and ice to help decrease inflammation. A fitted tennis elbow brace was prescribed to help reduce the repetitive load on the common extensor origin. Soft tissue techniques in the form of forearm interosseous release and light massage of the extensor muscles, specifically to the extensor carpi radialis brevis (ECRB) muscle, were performed during each session for 3 to 5 minutes. The wrist extensors and flexors were stretched. Isometric bicep curls and triceps extensions were prescribed. Postural strengthening exercises included scapular setting, chin retraction, and wall angels. Wall-clocks were given as a shoulder girdle proprioceptive exercise. Additionally, active care consisted of the patient being given plasticine crunches to increase grip strength. See Table 1 for a complete list of exercise progression.

Table 1 Exercises and stretches prescribed to improve strength, flexibility and grip endurance of the forearm musculature.

After 10 weeks the patient had fully recovered. She was able to return to playing golf pain free. Follow up imaging studies showed that the common extensor tendon thickening and calcification had resolved. This patient was not considered a surgical candidate, as a trial course of conservative care was successful in allowing her to return to sport pain free.

DISCUSSION

Calcific tendonitis

The pathogenesis of CT is still not fully understood. Suggestions as to the origin of calcification include vascular or mechanical trauma, hypoxia, extracellular matrix vesicle organelles, metaplasia of tendon cells, and metabolic endocrine disorders.^12,13 In CT, calcium phosphate (hydroxyapatite) deposits within the tendon cause inflammation and painful symptoms. These deposits may trigger an inflammatory reaction through the up regulation of inflammatory mediators. The potential for crystals to elicit an inflammatory reaction is reported to depend on their morphology. Surface area, size, density, and calcium phosphate ratio of the crystal all display positive correlations with clinical symptoms.¹⁶ Asymptomatic patients tend to have calcific deposits that appear granular with sharply defined and well-circumscribed borders. Alternatively, acutely painful patients have enlarged deposits with liquefied, poorly circumscribed borders.¹⁷ The condition itself has 4 well-defined phases. The first, formative phase, initiates from one of the causes listed above. During this phase the tendon undergoes fibrocartilaginous transformation. Then the calcific phase occurs, in which the calcific deposit enlarges producing pain and mechanical symptoms. Next, the resorptive phase involves macrophages and multinuclear giant cells absorbing the deposit and is often very painful. Finally, the reparative phase consists of fibroblasts restoring the collagen pattern back to normal tendon tissue.^12,15

As mentioned in the introduction, there is strong evidence that suggests CT worsens the clinical manifestations of tendinopathy. Tendon biology can also be influenced by age, gender, previous injury, and hormonal variations (especially thyroxine). Furthermore, endocrine and connective tissue conditions may be implicated in the development of CT. With this in mind, the presence of an endocrine co-morbidity could alter the natural history of CT and lead to a chronic symptomatic state.¹⁰ For example, it is known that hypothyroidism causes a build up of glycosaminoglycans in the extracellular matrix of tendons, which could predispose the tendons to develop calcific deposits. Tendinitis is often found as a presenting complaint in patients with hypothyroidism, and symptom resolution is frequently obtained with treatment of the underlying deficiency.¹⁰

Lateral Epicondylosis

The lateral epicondyle has a pyramidal morphology, with each of the three sides (anterior, posterior, and inferior) serving as a specific attachment site. The anterior surface contains attachments for the ECRB and extensor digitorum communis muscles, which are in fact part of the common extensor tendon origin. Posteriorly the anconeus muscle originates, while the apex and inferior surface are attachments for the lateral collateral ligament.⁴ Important anatomical consideration must also be given to the radial nerve (Figure 2). The posterior interosseous nerve (PIN) branch is commonly entrapped in the supinator muscle at the radial tunnel, causing symptomotology similar to LE. Thus PIN entrapment is an important differential that should be considered in longstanding cases of LE.⁴

Figure 2 The most common mechanism for lateral epicondylosis is caused by repetitive eccentric contraction of the extensor carpiradialisbrevis (ECRB) muscle. This causes microtears within the common extensor tendon origin. A) ECRB muscle at proximal lateral epicondyle (more ...)

Epicondylitis is a term that implies the presence of inflammation, however, it is only the very early stages of LE that demonstrate this histological trait. Investigations have shown the disease process to be a degenerative tendinopathy, thus tendinosis or lateral epicondylosis is cited as the preferred terminology.^3,6 However, biochemical analysis has shown increased levels of the neurotransmitter glutamate and substance P receptors within the common extensor origin of patients with LE. These findings suggest a mechanism for neurogenic pain generation and provide a potential explanation for pain relief from steroid injection into a condition that is largely absent of inflammation.⁴

Biomechanical assessment shows that LE is primarily caused by excessive ECRB eccentric contraction causing a microtraumatic tear in the common extensor tendon origin (Figure 2).³ Extensor carpi radialis longus attaches to the lateral supracondylar ridge of the humerus, not the lateral epicondyle, and thus is not involved in LE. Other hypothesized causes of LE include direct trauma, hypovascularity of the region, and anatomical predispostion.^3,6,7 Identified risk factors associated with LE include a history of heavy tool use, and significant forearm strain while performing repetitive tasks.⁴

During the clinical encounter, patients with LE will present with pain localized to the lateral aspect of the elbow that radiates down the forearm with certain movements or carrying items in their hand.^3,6 Symptoms are usually exacerbated by resisted wrist extension or passive wrist flexion. There will often be more pain in the morning or after the elbow has been held in a flexed position for a prolonged period of time.^4,7

The physical exam should start with screens of the cervical spine and shoulder to rule out any radicular or referred pain from these structures.³ As was reported with the amateur golfer, palpation will typically discover a point of maximal tenderness just distal and anterior to the lateral epicondyle over the origin of the ECRB muscle.⁴ Several orthopedic tests are regularly positive with this condition; these include Cozen’s test, Mill’s test, Thomson test, Bowden test, and the Chair test (Table 2).^6,7 Grip strength should be tested and compared with the opposite hand to determine if there is a significant difference.^3,6,7 Two important differentials to rule out during the physical exam are PIN entrapment and posterolateral rotatory instability. Approximately 5% of LE patients simultaneously have PIN entrapment. This condition is indicated by pain on resisted supination with the elbow flexed (entrapment in the supinator muscle) or pain with resisted long finger extension (Maudsley’s test) when the elbow is extended (entrapment in the ECRB muscle).^3,6 Abnormal sensation to the web of the thumb also suggests injury to the PIN.² Posterolateral rotatory instability is caused by injury and laxity in the lateral collateral ligament of the elbow. It is important to evaluate the integrity of this structure with a Varus stress test. This condition should be considered if patients have undergone treatment for LE and continue to have persistent symptoms.⁶

The differential diagnosis list for LE also includes synovial plica, cervical radiculopathy, osteochondritis dissecans of the capitellum, and radiocapitellar arthrosis,^3,4,6 several of which require special imaging in order to rule out. In fact, imaging studies are often more helpful in ruling out a differential cause of elbow pain than in making a diagnosis of LE.³ Radiological examination of LE patients is usually normal.⁵ Occasionally intra-articular pathology or calcifications within the surrounding soft tissue structures are observed.⁴ As was demonstrated in the case report, calcifications have been associated with persistent LE and are reported to be present in approximately 7–25% of patients.^3,4,6,8 Ultrasound examination of LE patients can identify thickening of the common extensor tendon, intrasubstance tendon tears, focal hypoechoic regions within the tendon, adjacent bony irregularity, and calcifications.^4,6,7,12 Magnetic resonance imaging is generally not indicated for LE patients. Its main usefulness is in the exclusion of osteochondral defects, identifying non-displaced physeal fractures, quantifying the extent of tendon tearing, and preoperative planning.^3,4,6

The success rate for conservative treatment of LE patients is around 90%.^2,3 It can include several interventions used either alone or in combination. Ice should be applied several times throughout the day during the acute phase of LE. Once the subacute phase begins, heat can be applied to help promote increased blood flow to the area and reduce muscle spasm.² Ultrasound therapy can also be useful to influence blood flow and tissue extensibility while decreasing pain.² Medications suggested for pain control include acetaminophen as well as oral or topical NSAIDs.⁴ Acupuncture was also shown to display a trend of shortening pain symptoms in LE patients.^6,18 Low-level laser therapy at 904 nm wavelength has demonstrated positive results for tendon pathology through stimulation of fibroblast activity.⁶ Additionally, counter-force wrist extension braces have been shown to be helpful. The brace is believed to decrease the repetitive load on the elbow by preventing the forearm muscles from fully contracting, leading to decreased tension within the common extensor origin.^2,4,6 It is important to note that braces placed just distal to the lateral epicondyle reduce loads greater than braces placed directly over the lateral epicondyle.^3,18 Shock wave therapy has produced contradicting evidence in terms of its efficacy for treating LE. Some investigators have found patients improved, while others have reported a lack of effectiveness.^3,19 Osteopathic and chiropractic manipulation of the elbow has been effective in certain cases of LE. The goal of manipulation is to release adhesions within joint articulations, promote realignment, and normalize function.^2,18 Injections of various substances have also been used to decrease pain and promote healing in numerous tendonopathies including LE. See Table 3 for a complete list of substances used for injection and proposed mechanisms of action.^3,4,6 Regarding physical therapy, exercises are generally aimed at strengthening the wrist extensors and flexors, but supinator, pronator, and grip strength exercises should also be included in an effort to prevent re-injury. Stretching exercises and eccentric training for the forearm extensor and flexor muscles can also aid in recovery.^3,4 Theoretically, eccentric training induces hypertrophy in the musculotendinous junction, increasing tensile strength to the area and reducing the amount of strain on the tendon. Eccentric contractions may also stimulate tendon cells to produce collagen and decrease neovascularization that contributes to pain.⁴ There has been some research done on injury prevention programs for golfers. These tend to focus more on developing muscular endurance and motor control of the lower back and shoulder areas.²⁰

Table 3 Substances commonly used for injection of tendonopathies and the proposed mechanisms by which they mediate their actions.3,4,6

There are several poor prognostic factors to successful conservative treatment of LE patients. These include dominant arm involvement, high baseline pain levels of long duration, poor coping mechanisms, and manual labor occupation.⁴ A wide variety of surgical treatment options exist for LE patients. Both open and arthroscopic techniques have high success rates of 84–97%. However, only 4–11% of LE patients who seek medical care will require surgery.^3,4 Operative management is indicated for patients with: 1) Persistent pain. 2) Functional disability. 3) After 6 to 12 months of failed conservative therapy.^3,4,6 Complications that may arise from elbow surgery include peripheral nerve injury, heterotropic ossification of soft tissues, and posterolateral rotatory instability from overly aggressive debridement.⁴

SUMMARY

Injuries in amateur golfers have been widely reported.^1,2 Some of the more common injuries to be discussed in the literature include the lower back, wrist, elbow, and stress fractures.^1,21,22 The cause of injury to LE patients is believed to be multi-factorial and include repetitive microtrauma to the ECRB of the common extensor tendon as well as significant forearm strain during repetitive tasks, such as swinging a golf club. Conservative treatment is aimed at physical therapy featuring stretching and strengthening exercises along with several other possible co-interventions. In this case, a young female amateur golfer with elbow pain diagnosed as LE and CT was relieved of her pain after 7 treatments over 10 weeks.

REFERENCES

1. Bayes MC, Wadsworth LT. Upper extremity injuries in golf. Phys Sportsmed. 2009;37(1):92–6.[PubMed]
2. Stockard AR. Elbow injuries in golf. J Am Osteopath Assoc. 2001;101(9):509–16.[PubMed]
3. Van Hofwegen C, Baker CL, 3rd, Baker CL., Jr Epicondylitis in the athlete’s elbow. Clin Sports Med. 2010;29(4):577–97.[PubMed]
4. Calfee RP, Patel A, DaSilva MF, Akelman E. Management of lateral epicondylitis: current concepts. J Am AcadOrthop Surg. 2008;16(1):19–29.
5. Matthews P, Leyshon R. Acute calcification in tennis and golfer’s elbow. Rheumatol Rehabil. 1980;19(3):151–3.[PubMed]
6. Scher DL, Wolf JM, Owens BD. Lateral epicondylitis. Orthopedics. 2009;32(4):276–282.
7. Levin D, Nazarian LN, Miller TT, O’Kane PL, Feld RI, Parker L, McShane JM. Lateral epicondylitis of the elbow: US findings. Radiology. 2005;237(1):230–4.[PubMed]
8. Pomerance J. Radiographic analysis of lateral epicondylitis. J Shoulder Elbow Surg. 2002;11(2):156–7.[PubMed]
9. Lui PP, Chan LS, Lee YW, Fu SC, Chan KM. Sustained expression of proteoglycans and collagen type III/type I ratio in a calcified tendinopathy model. Rheumatology (Oxford) 2010;49(2):231–9.[PubMed]
10. Harvie P, Pollard TC, Carr AJ. Calcific tendinitis: natural history and association with endocrine disorders. J Shoulder Elbow Surg. 2007;16(2):169–73.[PubMed]
11. Holt PD, Keats TE. Calcific tendinitis: a review of the usual and unusual. Skeletal Radiol. 1993;22(1):1–9.[PubMed]
12. Siegal DS, Wu JS, Newman JS, Del Cura JL, Hochman MG. Calcific tendinitis: a pictorial review. Can Assoc Radiol J. 2009;60(5):263–72.[PubMed]
13. Hayes CW, Rosenthal DI, Plata MJ, Hudson TM. Calcific tendinitis in unusual sites associated with cortical bone erosion. Am J Roentgenol. 1987;149(5):967–70.[PubMed]
14. Gohr CM, Fahey M, Rosenthal AK. Calcific tendonitis: A model. Connect Tissue Res. 2007;48(6):286–91.[PubMed]
15. Mouzopoulos G, Stamatakos M, Mouzopoulos D, Tzurbakis M. Extracorporeal shock wave treatment for shoulder calcific tendonitis: a systematic review. Skeletal Radiol. 2007;36(9):803–11.[PubMed]
16. Chiou HJ, Hung SC, Lin SY, Wei YS, Li MJ. Correlations among mineral components, progressive calcification process and clinical symptoms of calcific tendonitis. Rheumatology (Oxford) 2010;49(3):548–55.[PubMed]
17. Wainner RS, Hasz M. Management of acute calcific tendinitis of the shoulder. J Orthop Sports Phys Ther. 1998;27(3):231–7.[PubMed]
18. Valen PA, Foxworth J. Evidence supporting the use of physical modalities in the treatment of upper extremity musculoskeletal conditions. Curr Opin Rheumatol. 2010;22(2):194–204.[PubMed]
19. Sems A, Dimeff R, Iannotti JP. Extracorporeal shock wave therapy in the treatment of chronic tendinopathies. J Am Acad Orthop Surg. 2006;14(4):195–204.[PubMed]
20. Lehman GJ. Resistance training for performance and injury prevention in golf. J Can Chiropr Assoc. 2006;50(1):27–42. [PMC free article][PubMed]
21. McHardy AJ, Pollard HP. Golf and upper limb injuries: a summary and review of the literature. Chiropr Osteo. 2005;25:13–7.
22. Lee AD. Golf-related stress fractures: a structured review of the literature. J Can Chiropr Assoc. 2009;53(4):290–9. [PMC free article][PubMed]