Stress Fractures

Stress fractures account for 0.7% to 20% of all sports injuries, 80% to 90% of which occur in the lower limb and 1% to 2% occur in the pelvis.^1–3 Femoral neck stress fractures (FNSFs) occur more often on the compression (inferior) side than on the tension (superior) side, which is important due to differences in treatment protocols. There is a bimodal distribution of injury, with most occurring in those younger than 20 or older than 40 years of age, with higher rates in women and in sports such as cross-country and gymnastics⁴ (Fig. 29–1).

Wolf’s law states that through mechanisms of mechanotransduction, bone responds and adapts to the forces applied upon it by altering both its internal trabecular and outer cortical structures. Stress fractures result from repetitive submaximal forces occurring with enough frequency for the rate of bone destruction to exceed bone remodeling.⁵ Risk factors include a rapid increase in frequency, intensity, or duration of a repetitive activity; slower running speed; female gender; amenorrhea; muscle fatigue; strength imbalances; and biomechanical and gait abnormalities; a better overall fitness level is protective of stress fractures.^6–9

Diagnosis can be difficult and is often delayed up to 14 weeks, on average, due in part to vague symptoms, poorly sensitive and specific exam findings, and often unremarkable plain radiography early in the course of the disease process.¹⁰ The pain is often insidiously progressive, vague, and typically worse with activity and improved with rest. A thorough history and physical should be performed and include a dietary and menstrual history as well as biomechanical and gait analysis.

The physical exam typically reveals tenderness over the area, assuming the location is accessible for direct palpation. With FNSFs, one must rely on other exam findings, such as pain at the extreme ends of passive range of motion, log roll, heeltap, or single-leg standing or hopping.⁵ Definitive diagnosis is made through radiographic assessment. Plain films are often obtained first, but may take several weeks to demonstrate pathology. If plain films are unremarkable and clinical suspicion remains, bone scan, computerized tomography (CT), or magnetic resonance imaging (MRI) may be obtained, as they demonstrate pathology much earlier in the disease process.^11–14

Those looking to increase their physical activity should be counseled, and protocols should be developed, regarding preventive measures. However, once a stress fracture develops, treatment is often conservative, with activity modification to allow time for the bone to heal.¹⁵ Patients are typically made partial weight-bearing in lower-risk stress fractures (i.e., fibula) for up to 6 to 8 weeks, while in high-risk stress fractures (i.e., FNSF) they are made non–weight-bearing (NWB).¹⁶ This is followed by gradual progression through weight bearing as tolerated (WBAT) with progressive exercises emphasizing flexibility, core and pelvic girdle stability, muscular strength and endurance training, correction of biomechanical deficiencies, gait and proprioceptive retraining, and ultimately through unrestricted activity.² Pain can typically be managed with acetaminophen, but a short course of narcotics could be considered if pain is severe. Nonsteroidal anti-inflammatory drugs (NSAIDs) are typically avoided given concerns for potential interference with bone healing.¹⁷ Femoral shaft, sacral, and pubic rami stress fractures typically heal well with conservative management in 4 to 6 weeks.²

Compression-side FNSFs are typically more stable and may be managed with NWB status until asymptomatic; however, tension-side stress fractures have a higher risk of progression to fracture, delayed union, nonunion, avascular necrosis (AVN), and arthritis.² Because of this, management is with operative intervention via percutaneous pinning followed by WBAT. There are some studies suggesting safety with management of strict bedrest followed by partial weight bearing after several weeks; however, the risks of strict bedrest should be weighed carefully against surgical risk^5,18 (Fig. 29–2).

Femoroacetabular Dislocations

Hip dislocation can be associated with significant morbidity due to damage of the surrounding structures (such as the labrum, supporting ligaments, and muscles), neurovascular injury, fractures, and from longer-term complications such as posttraumatic arthropathy, heterotopic ossification, and AVN, which has been reported up to 12 years post injury.^19–22,28 It occurs posteriorly in the majority of cases and is more common in men.¹⁹ It occurs after total hip arthroplasty (THA) in approximately 2% to 3% of cases.^23,24 Factors affecting dislocation after THA include acetabular component orientation, surgeon experience, and prior surgery.²³

The hip joint is inherently stable due to the deep acetabular socket, the labrum, the angle of the femur, and significant ligamentous stabilization. As such dislocation occurs most often as a result of high-energy trauma, such as a motor vehicle accident (MVA), and in some high-energy sports such as basketball, football, rugby, snowboarding, or skiing.^21,25–27 Posterior hip dislocation occurs when a large longitudinal force strikes the distal femur with the knee and the hip flexed; the hip is usually adducted and internally rotated at the time of trauma, which creates a posterolaterally directed force through the femoral head. This is common with MVAs (Fig. 29–3). Anterior hip dislocation occurs when an anteriorly directed force acts on the limb held in hip flexion, abduction, and external rotation.

Hip dislocation should be suspected in the clinical setting of acute, severe hip pain with a history of high-energy trauma. As posterior hip dislocations are more common, the patient will often be found to have a shortened limb held in adduction and internal rotation, while with anterior dislocations, the limb is typically flexed, abducted, and externally rotated.²¹ When a hip dislocation is suspected or confirmed, it is crucial to evaluate the distal neurovascular status, given the high rate of concomitant injury.^20,21 Plain radiography is typically sufficient to confirm the diagnosis; however, CT should be considered if there is concern for concomitant fracture, trouble with reduction, or an asymmetric joint space on post-reduction plain films (Fig. 29–4). MRI may be considered post-reduction, or if there are persistent symptoms to assess for labral tears, chondral injuries, cartilaginous loose bodies, surrounding ligamentous or soft tissue damage, or AVN.^21,28

Prompt and proper management of hip dislocations is imperative to avoid significant associated complications and prevent long-term morbidity. Time to reduction is directly proportional to both neurologic injury and AVN. Uncomplicated hip dislocation is typically treated with closed reduction under anesthesia followed by WBAT for 6 to 8 weeks with posterior or anterior hip precautions.²¹ Dislocations not amenable to closed reduction or those with associated fractures are indications for emergent surgical intervention. After surgical intervention, most patients are made toe-touch weight bearing for 8 to 12 weeks with posterior or anterior precautions for 3 to 6 months.²¹ Acute pain management is typically controlled with a combination of ice, anti-inflammatories, and narcotics.

There is little high-quality evidence regarding rehabilitation protocols after a hip dislocation or for prevention of hip dislocation after THA. A recent Cochrane review found very low-quality evidence that hip precautions, with or without equipment, were effective in preventing dislocation and improving outcomes after THA. It also found insufficient evidence for or against post-THA rehab programs aimed at functional reintegration and education compared to conventional rehab strategies.²⁸ Despite this, it is common practice for post-THA and post-traumatic hip dislocation patients to undergo a community rehab program, with initial hip precautions, aimed at improved strength, functional range of motion (ROM), and neuromuscular control. Future studies are looking to help determine if current hip precaution strategies are superior to a less restrictive strategy with regard to subsequent dislocation risk and speed of recovery.²⁹

Myotendinous Injuries

Muscular injuries account for more than 30% of all athletic injuries.³⁰ The highest incidence of muscle strains tends to occur in the hamstrings, gastrocnemius, quadriceps, hip flexors, hip adductors, erector spinae, deltoid, and rotator cuff.

Myotendinous injuries typically occur via one of two mechanisms: either through direct trauma (i.e., a contusion) or through indirect trauma (i.e., overstretch or strong muscle activation) causing disruption of muscle fibers.³¹ The injury typically occurs a short distance from the myotendinous junction, as sarcomeres near the junction are less elastic than those at the center.^32,33 Factors that predispose to injury include crossing two joints, deceleration forces (eccentric contraction), having a higher percentage of type II fibers, prior injury, inadequate warm-up, poor flexibility, weakness, poor reciprocal control of agonist and antagonist muscles, and advancing age.^34,35

Diagnosis is often straightforward with a thorough history and physical exam. The patient will often describe a clear mechanism of injury and present with some combination of pain, swelling, ecchymosis, decreased ROM, tenderness with palpation, pain with muscle activation and/or stretch, and possible weakness and/or physical defect, depending on the severity of the injury. Plain radiography may show soft tissue swelling but is typically normal. Ultrasound is becoming increasingly prevalent and may demonstrate fiber disruption with a sonolucent area; however, it is limited by operator dependence and requires a skilled and experienced clinician.³⁶ Ultrasound’s greatest utility is that it allows for point-of-care assessment with dynamic visualization of the structures and readily identifies joint effusions, synovitis, tendinopathy, and bursitis and may be used for guided injections, should they be indicated.³⁷ MRI is helpful in the assessment of associated injuries but is often not necessary unless the diagnosis is uncertain or if there is need for specific determination of the underlying severity and prognosis, such as for a professional athlete.^33,37 Several grading scales have been proposed, but the most commonly used is a simple three-grade system as outlined in Table 29–1, with others expanding on those grades with more clinical or radiographic data, or even adding a fourth grade.³³

There is no specific consensus or criteria for management of myotendinous injuries, and treatment protocols should be individualized to the patient. Most injuries can be safely managed conservatively with the exception of complete tears, which will often require surgical repair.³³ Healing time is directly related to severity of injury, with minor injuries healing in roughly 1 week and severe injuries requiring anywhere from 4 to 8 weeks.³³ The general treatment of these injuries involves a gradual progression from initial management of acute inflammation through progressive increases in strength, flexibility, proprioception, agility, cardiovascular fitness, and eventual return to unrestricted activities. Initial management begins with relative rest, ice, compression, elevation (RICE) and analgesics.³³ NSAIDs may be used for the first few days; however, prolonged use should be avoided, as it may be associated with delayed healing.^38–40 Early mobilization with pain-free flexibility and strengthening promotes collagen fiber growth and realignment as well as enhanced proprioception while limiting adhesion formation.³³ Strengthening exercises should begin gradually and progress as tolerated to functional exercises, including progressive agility and trunk stabilization exercises.³⁵ Active warm-up should be encouraged, as it reduces muscle viscosity and activates neural pathways. In complete or recalcitrant injuries, surgical repair may be indicated, with a return to play time of 5 to 6 months.³⁵

Iliopsoas Injury

There is wide variation in the reported incidence of iliopsoas injury, ranging from 0.66% to 30% in acute groin injuries, and 12% to 36% in chronic groin injuries.^37,41 While various pathologies are associated with the iliopsoas complex, such as internal snapping hip syndrome and iliopsoas syndrome, only iliopsoas strain and tendinopathy will be discussed here.

The iliopsoas is a complex of the iliacus and the psoas major, with some authors including the psoas minor. Collectively the iliopsoas acts to flex and externally rotate the hip. The psoas major and iliacus are innervated by the ventral rami of L1–L3 and femoral nerve (L1–L2), respectively.³⁷

Given the significant time spent sitting, iliopsoas tightness is a ubiquitous problem, which may predispose it to injury. Acute iliopsoas strain is usually associated with a history of abrupt onset of pain, while iliopsoas tendinopathy or bursopathy is typically more insidious in onset and associated with an increase in intensity or frequency of training. Diagnosis of iliopsoas pathology is largely clinical and based on a thorough history and physical exam. The Thomas or iliopsoas test can be used to assess for muscle tightness or spasm. An obturator test may indicate an inflammatory process over the obturator muscle, such as ruptured appendix or abscess. Imaging is complementary and may help assess for associated injuries. Management follows the same principles of other myotendinous injuries (Fig. 29–5).

Abscesses in the pelvis may be localized by demonstrating irritation of the more lateral iliopsoas or the medial obturator internus muscles. Provocative maneuvers include the iliopsoas and the obturator tests. With the Iliopsoas test, the supine patient keeps the knee extended and is asked to flex the thigh against the resistance of the examiner’s hand. Pain in the pelvis indicates irritation of the iliopsoas. The obturator test is performed when the supine patient flexes the ipsilateral thigh to 90 degrees. The examiner moves the hip in internal and external rotation. Pelvic pain indicates an inflamed muscle. One should examine the patient from the side of the limb being tested.

Piriformis Syndrome

The piriformis originates from the anterolateral aspect of the sacrum and inserts on the superior medial aspect of the greater trochanter. It is innervated by the nerve to the piriformis (L5–S2) and acts as a lateral hip rotator when the hip is in extension and as a hip abductor when the hip is in flexion (Fig. 29–6). Piriformis dysfunction, through mechanical effects on local structures, may result in groin, pelvic, and radicular-type pain. Piriformis syndrome occurs when the piriformis compresses the sciatic nerve resulting in radicular-type symptoms. It most frequently occurs during the fourth and fifth decades, with incidence ranging from 5% to 36%. Women are disproportionally affected, which may be related to the larger Q angle in women.⁴²

Piriformis syndrome results from the intimate anatomic relationship between the piriformis and the sciatic nerve and may be a result of primary anatomy or secondary to trauma or ischemia. In up to 22% of the population, the sciatic nerve may pierce the piriformis muscle, pass between two muscle bellies in a split piriformis, or both. Occasionally the sciatic nerve itself may split, sending part (often the fibular portion) through the piriformis muscle belly, while the other portion courses superiorly or inferiorly around the piriformis.⁴²

Most patients with piriformis syndrome complain of increasing pain with sitting, standing, or lying longer than 15 to 20 minutes. They may complain of pain or paresthesia radiating down the posterior thigh, typically terminating proximal to the knee, pain with rising from a seated position, limited internal rotation, contralateral sacroiliac (SI) joint pain, dyspareunia, or pain with defecation.⁴² Exam may reveal a palpable “sausage-shaped” mass in the buttock, ipsilateral hip external rotation, and restricted internal rotation.⁴² There is no single test specific to piriformis syndrome, but the Lasègue and Freiberg signs, as well as pain in the FADIR position, have been used to assist in the diagnosis.^42,43 Electrodiagnostics can be helpful in differentiating piriformis syndrome from radiculopathy or other peripheral neuropathy. Imaging studies, including x-rays, CTs, and MRIs, are helpful for ruling out other conditions.

Piriformis syndrome typically has a great prognosis, with more than 79% of patients improving with rest, NSAIDs, muscle relaxants, and ice.⁴³ Physical therapy to increase strength and flexibility, as well as acupuncture, trigger point injections, correction of biomechanical deficiencies, and various manual medicine techniques to address related somatic dysfunctions, may also be helpful.⁴² Use of adjunctive modalities such as heat therapy, cold therapy, iontophoresis, phonophoresis, botulinum toxin injection, and ultrasound have proven helpful.⁴² If conservative treatment fails, the final treatment option is surgical decompression.⁴²

Quadriceps Injury

The rectus femoris is the most commonly strained quadriceps muscle, as it crosses two joints (Fig. 29–7). Contusions are the second most frequent injury after strains, and in sports without padding for the thigh, they can be a major disabling injury.⁴⁴ One possible complication is myositis ossificans (MO), a non-neoplastic heterotopic ossification in the area of contusion, which occurs in 9% to 17% of cases. It should be suspected if symptoms worsen after 2 to 3 weeks and is associated with loss of ROM and persistent swelling. Risk factors for MO include previous injury, delay in treatment longer than 3 days, ipsilateral knee effusion, knee flexion less than 120 degrees, and if the injury occurred during football.⁴⁵

The pathophysiology of myositis ossificans is incompletely understood but is thought to occur via inappropriate differentiation of fibroblasts into osteogenic cells due to dysregulation of local stem cells from injury and inflammation.⁴⁶

An accurate history and physical are typically sufficient to diagnose strains and contusions. In the case of MO, plain radiographs may demonstrate heterotopic bone formation in the muscle belly, but this is typically not evident until several weeks from injury. CT and MRI can better characterize the development of MO⁴⁶ (Fig. 29–8).

Treatment of strains and contusions generally follows the same basic principles as for in other locations. The main difference between the management of strains and contusions is the recommendation to keep the knee in a hinged knee brace at 120 degrees of knee flexion for the first 24 hours in an attempt to limit hematoma formation in the setting of contusion. NSAIDs have been used for MO prevention after severe contusions based on studies demonstrating a decrease in heterotopic bone formation after THA in those patients given indomethacin for at least 7 days. Surgical intervention may be required if MO develops and is recalcitrant to conservative measures, which is often the case. However, surgical excision should be delayed until the ectopic bone has fully matured, typically in 12 to 24 months, as early excision before bone maturity may result in more severe local recurrence.

Hamstring Injury

Hamstring injuries are very common as they are two-joint muscles, with the exception of the short head of the biceps femoris (SHBF). Prevalence generally ranges from 8% to 25%; however, it has been reported up to 50%, with recurrence rates exceeding 30%, and often results in 2 to 6 weeks of sporting absence.³⁵

The hamstring muscle group consists of the biceps femoris, semitendinosus, and semimembranosus. Collectively they act to extend the hip and flex the knee. Pathophysiology, risk factors, diagnosis, and management are similar to the other myotendinous injuries previously discussed (Fig. 29–9).

Adductor Injury

Adductor strains are common, with approximately 30% of groin pain attributed to adductor injuries.⁴⁷ The adductor longus is involved in 62% to 90% of cases.^48,49 These injuries occur in many sports, including football, soccer, hockey, basketball, tennis, figure skating, baseball, horseback riding, karate, and softball.⁵⁰ These injuries can be problematic and linger, with up to 42% of athletes with groin myotendinous injuries unable to return to their activity after more than 20 weeks.⁴⁸

The adductor muscle group consists of the adductor magnus, minimus, longus, and brevis, as well as the gracilis and pectineus (see Fig. 29–9). The obturator nerve (L2–L4) innervates all muscles of the adductor group except for the pectineus, which is innervated by the femoral nerve (L2–L4). The adductor magnus is also partly innervated by the tibial nerve (L4–S3). The mechanism of injury is often an abrupt change of direction or forceful kicking.⁴⁹ The pathophysiology, diagnosis, and management are similar as for other myotendinous injuries.

Iliotibial Band Friction Syndrome

Iliotibial band (ITB) friction syndrome (ITBFS) is the most common cause of lateral knee pain in runners.^51,52 It has a reported incidence of between 1.6% and 12% and accounts for 15% to 24% of overuse injuries.⁵²

The ITB is a large fascial band originating from the gluteus maximus and tensor fascia lata (TFL) and extending down the lateral thigh to insert on Gerdy’s tubercle on the proximal lateral tibia. The pathophysiology of ITBFS is incompletely understood but is felt to be multifactorial, ultimately resulting in rubbing of the ITB across the lateral femoral condyle as the knee flexes and extends beyond 30 degrees.^51–54 Predisposing factors include excessive internal tibial rotation, genu varum, increased foot pronation, overtraining, eccentric TFL and gluteus medius contraction, long-distance running, slow-paced running, downhill running, and weakness of the hip abductors resulting in poor pelvic stability.^51,52,54

The diagnosis of ITBFS is largely based on history and physical exam. The patient typically presents with insidiously progressive lateral knee pain and/or that is worse with activity and improves with rest. Ober’s test is used to determine ITB tightness, which may predispose to ITBFS, while Noble’s test demonstrates tenderness as the ITB crosses over the lateral femoral condyle. Imaging studies are reserved for recalcitrant cases and are primarily used to rule out other pathology. MRI being the study of choice, however, clinicians will often start with plain radiographs or utilize ultrasound given its dynamic examination ability.⁵⁵

Management of ITBFS is largely symptomatic and similar to strains and tendinopathy, with most patients fully recovering by 6 weeks with conservative management.⁵⁴ During the acute phase, treatment includes activity modification, ice, physical therapy, and nonsteroidal anti-inflammatory and analgesic medications.^51,56 Therapy progresses with an emphasis on stretching the ITB, resolving myofascial adhesions, improving hip abductor strength and neuromuscular control of the hip and knee, and increasing frequency and intensity of exercises with gradual return to activities.^51,57 Certain adjuvant modalities have been shown useful, including phonophoresis, combined analgesic and corticosteroid injection, and extracorporeal shockwave therapy.^58–60 Open bursectomy or arthroscopic lateral synovial recess resection may be considered in cases refractory to conservative treatment.^51,61,62

Bursitis (Bursopathy)

Bursa are potential spaces that are either formed during normal embryologic development or as a result of myxoid degeneration of fibrous tissue due to friction between adjacent structures.⁶³ Bursitis may be somewhat of a misnomer, as there is often no associated bursal inflammation.⁶⁴ Histopathologic findings have shown tendinopathy and bursopathy often coexist.⁶⁵

As with most musculoskeletal disorders, the diagnosis is often made with a thorough history and physical exam. Patients typically present with insidiously progressive pain in the location of a known bursa, which is often worse with activity and improved with rest. There may be associated swelling and erythema. Local anesthetic block can be diagnostically confirmatory. Imaging modalities may be complementary. Plain radiographs are often obtained initially but are typically unremarkable. Imaging with ultrasound, CT, or MRI will reveal a cystic mass with a localized fluid collection surrounded by a thin wall and may demonstrate reproducible pain with sonopalpation.⁶³ Ultrasound is useful, as it provides accurate point-of-care assessment of bursal inflammation and allows for dynamic assessment of surrounding musculature to investigate for concomitant tendinopathy and enthesopathy. MRI also provides excellent visualization for diagnosis and assessment of surrounding structures.^66,67

The vast majority of cases resolve with conservative therapies such as physical therapy, weight loss, corticosteroid and local anesthetic injections, nonsteroidal anti-inflammatory drugs, and behavior modification.^68–70 However, comorbid osteoarthritis and low back pain are associated with prolonged symptomatology.^71,72

Greater Trochanteric Bursitis (Greater Trochanteric Pain Syndrome)

Because of the multiple possible pain generators in the area of the greater trochanter, a potentially more appropriate proposed terminology is greater trochanteric pain syndrome (GTPS).^{65,66,68,72,73–76} GTPS is estimated to affect between 10% and 25% of the population in industrialized societies, and is more common in females.^68,73

Three to four bursae have consistently been described surrounding the greater trochanter, providing cushioning for the gluteus tendons, ITB, and TFL.⁶⁸ Risk factors include female gender, coexisting low back pain, osteoarthritis, ITB tenderness, obesity, THA, and having trochanters wider in relation to iliac wings, all of which likely result in altered lower-limb biomechanics.^69,71,73,77

Most cases respond favorably with conservative therapy (i.e., hip abductor stretching and strengthening, cold packs, and steroid injections) but may require surgical intervention, such as longitudinal release of the ITB combined with subgluteal bursectomy.⁷⁸ According to one systematic review, efficacy among surgical techniques varied depending on the clinical outcome measure, but all were superior to corticosteroid therapy and physical therapy in refractory cases.⁷⁹ The review found that traditional conservative therapy helped most patients, shockwave therapy was a good alternative, and surgery was effective in refractory cases.

Iliopsoas (Iliopectineal) Bursitis

The iliopsoas bursa is the largest in the human body.⁷⁰ Iliopsoas bursitis is a relatively rare pathology associated with rheumatoid arthritis (RA), osteoarthritis, osteonecrosis, infections, trauma, overuse, impingement syndromes, and hip replacement.⁸⁰ While the exact pathomechanisms are poorly understood, it may become irritated from local repetitive trauma or due to intra-articular pathology via communication with the femoroacetabular joint.³⁷ This potential communication is an important consideration when interpreting effects of diagnostic injections, as it can make it difficult to differentiate bursal from intra-articular pathology. Symptoms may arise from direct pressure on local structures, and it has even been reported to cause femoral neuropathy and lymphedema, especially when associated with RA.⁸¹

Plain radiographs are obtained initially and may demonstrate underlying destructive arthropathy. Definitive diagnosis can be made by observation of bursal opacification with a hip arthrogram, assuming the patient has a joint-bursal communication.⁷⁰ Other useful diagnostic aids include ultrasound, CT, and MRI.

Most cases respond to conservative measures; however, if this is unsuccessful, if bursal distension recurs, or if it is complicated by infection or neurovascular compromise, surgical bursectomy with or without capsulotomy or hip joint synovectomy may be considered.⁷⁰ If associated with internal snapping hip syndrome, iliopsoas release or resection, or resection of osseous prominences, may be considered.⁷⁰

Ischial Bursitis

The ischial bursa is an adventitious bursa that has been noted to be inconsistent in its presence, but is typically located between the gluteus maximus and ischial tuberosity.⁶³ Ischial bursitis typically occurs due to direct trauma, such as a fall on the ischial tuberosity.⁸²

Diagnosis is based on history and physical exam. Patients with ischial bursitis typically complain of localized pain, which may radiate to the thigh or lower leg and which typically worsens with hill running, sprinting, or prolonged sitting. Exam demonstrates localized tenderness over the ischial tuberosity that is worsened with resisted hamstring stretch.⁸⁵ Imaging is complementary. Management is similar to other bursopathies.

Acetabular Labral Injuries

Isolated lesions tend to occur in younger patients, typically associated with significant hip trauma, whereas they are often associated with degenerative changes in the older population. The prevalence of labral injuries has been reported anywhere from 22% to 55%.⁸³ They are noted to be most associated with femoral acetabular impingement (FAI), capsular laxity, hip hypermobility, dysplasia, and degeneration, although most are not associated with any specific event.⁸⁶

The femoroacetabular joint is a ball-and-socket joint surrounded by the acetabular labrum, a firm fibrocartilaginous structure that functions in shock absorption, stability, pressure distribution, and joint lubrication. Injuries are associated acutely with trauma and hip dislocation but more often are insidious in nature and associated with repeated hip external rotation and occur frequently in sporting activities such as soccer, hockey, golf, and ballet.⁸⁶ Repeated rotational movements also result in increased stress on the capsular tissue, resulting in attenuation of the iliofemoral ligament that ultimately leads to rotational instability of the hip and subsequent increased forces on the labrum (Fig. 29–10A and B).

Due to the large list of differential diagnoses, diagnosis can be quite difficult and may be delayed up to 2 years.⁸⁶ Patients typically complain of anterior hip or groin pain, often with mechanical symptoms of clicking, locking, catching, giving way, and occasionally with buttock pain.⁸⁶ Multiple exam maneuvers can assist in the diagnosis, including the anterior hip impingement test, the posterior hip impingement test, FABER (Patrick’s test), resisted straight-leg raise test (Stinchfield’s test), log-roll test, and apprehension test; however, they are limited in their specificities.⁸⁶ Fluoroscopically guided diagnostic hip injections are highly sensitive and specific for localizing groin pain as intra-articular in origin.⁸⁴

Radiographic assessment should begin with plain films to rule out osseous abnormalities such as degenerative joint disease, heterotopic ossification, dysplasia, etc. MR arthrography is the best imaging modality, as conventional MRI and CT are unreliable. Diagnostic accuracy of imaging modalities improves with joint distension.⁸⁵ However, arthroscopy remains the gold standard for labral injury diagnosis.⁸⁶

Management typically begins conservatively with relative rest, NSAIDs, analgesics, and focused physical therapy for 10 to 12 weeks with limitations in pivoting movements and may require reduced weight bearing.⁸⁶ Aquatic therapy may be of value initially, as it creates an exercise environment in which weight bearing over the hip joint is decreased. Range-of-motion exercises are helpful to increase nutrient flow and promote healing.⁸⁶ Gait analysis and retraining should be performed along with therapy focused on enhancing proprioception and balance.⁸⁶ However, while this approach typically results in initial improvement, physical therapy remains controversial, and pain frequently returns with activity resumption; surgical correction with arthroscopic debridement and surgical repair is often necessary.^86,87 A course of postoperative NSAIDs may be considered to prevent the development of heterotopic ossification.

Osteitis Pubis

Osteitis pubis is a less common cause of groin pain in the athletic population. It tends to occur in sports that require a lot of kicking, twisting, and cutting, such as soccer, ice hockey, rugby, football, and running.^88,89 It has been reported that osteitis pubis is the cause of groin pain in 3% to 5% of soccer players, with a higher prevalence noted in males.⁹¹ It is often self-limiting but may take up to a year to improve.⁹¹

It is an overuse syndrome from repetitive strain and microtrauma on the pubic bones, pubic symphysis, and surrounding soft tissues from the abdominal and adductor muscles.⁹¹ Pregnancy, reduced hip internal rotation, infection, immobility of the sacroiliac joint, and rheumatologic disorders such as ankylosing spondylitis, rheumatoid arthritis, and osteoarthritis have been reported as predisposing factors.⁹¹

Diagnosis is based on a thorough history and physical exam. Patients typically present with pelvic and anterior or medial groin pain that may radiate into the lower abdomen, perineum, inguinal region, scrotum, or medial thigh. It is exacerbated by walking, pelvic motion, rising from a seated position, adductor or abdominal muscle activation, or stretching.⁹¹ Exam demonstrates tenderness over the pubic symphysis. Special maneuvers include the lateral compression test, cross-leg test, and pubic symphysis gap test with isometric adductor contraction. Palliation of pain with local corticoid and/or anesthetic injections in the pubic symphysis is also suggestive of osteitis pubis; however, this would also be palliative in proximal adductor tendinopathy, enthesopathy, bursopathy, etc. Radiographic assessment typically begins with plain films. Ultrasound and MRI may be helpful to differentiate osteitis pubis from local soft tissue pathology. MRI may reveal subchondral plate marrow edema with anterior to posterior extension.⁹¹

It is often self-limiting, and treatment typically begins with conservative measures such as relative rest, NSAIDs and analgesics, and an individualized progressive rehabilitation program to improve strength, flexibility, and proprioception. A recent review found that a structured rehabilitation program resulted in successful return to pre-injury participation between 4 and 30 weeks with successful long-term follow-up reported at 6 and 48 months.⁹⁰ Other potential modalities include osteopathic manipulative techniques, proprioceptive neuromuscular facilitation, prolotherapy, and local injections with steroid and anesthetic.^90,91 If conservative therapies fail, surgery may need to be considered, including arthroscopic or open symphysis curettage, wedge or total resection of the pubic symphysis, polypropylene mesh placement, and pubic fusion.⁹¹

Avascular Necrosis

There are between 20,000 and 30,000 new cases of AVN annually, with most occurring in those between 20 and 40 years of age. It occurs bilaterally in 70% of cases and accounts for approximately 10% of annual THAs.⁹¹ AVN is associated with alcohol abuse in 20% to 40% of cases, corticosteroid therapy in 35% to 40%, and is idiopathic in 20% to 40% of cases.

While the etiology and pathogenesis remain uncertain, AVN ultimately results from decreased blood flow and subsequent cellular death, fracture, and collapse of the articular surface. Most studies cite the effects of local factors affecting blood supply such as vascular damage, intraosseous pressure, and mechanical stress combined with metabolic factors and genetic predisposition.⁹⁴ High doses of glucocorticoids, as well as excessive alcohol intake, have been demonstrated to result in alterations in circulating lipids with subsequent microemboli.⁹² Systemic illnesses such as antiphospholipid antibody syndrome, inherited thrombophilia, hypofibrinolysis, sickle cell disease, inborn errors of metabolism, and decompression sickness have been associated with AVN, as has direct vascular or cellular trauma.⁹⁴

Due to the high morbidity and significant percentage of cases that progress, early diagnosis is crucial. Clinically, patients are asymptomatic early in the disease process but progress to develop groin pain that may radiate into the ipsilateral buttock, medial thigh, or knee. Exam may reveal decreased range of motion and pain at the extremes of range of motion, particularly in internal rotation.⁹⁴ Plain radiography is typically normal early in the disease process, but when they do become remarkable, they demonstrate cystic and sclerotic changes in the femoral head that are best viewed in frog-leg lateral radiographs. Other changes that may be noted in plain radiography include the crescent sign that implies delamination of the cartilage from the underlying bone.⁹³ However, MRI is the most accurate diagnostic method and will demonstrate a smooth, concave, well-circumscribed band with serpiginous lesions, which may be enhanced with gadolinium⁹⁴ (Fig. 29–11).

Unfortunately, there is no uniform treatment algorithm for AVN. Medication classes used to slow progression include anticoagulants, lipid-lowering agents, bisphosphonates, and certain vasoactive medications such as prostacyclin.⁹⁴ Other adjuvant therapies include extracorporeal shockwave therapy, pulsed electromagnetic therapy, and hyperbaric oxygen.⁹⁴ However, most patients ultimately go on to require surgical intervention, as 67% of asymptomatic patients and 85% of symptomatic patients progress to collapse of the femoral head.⁹⁴ Total hip arthroplasty is most often performed in those with femoral head collapse, while core decompression is often performed in those with symptoms prior to femoral head collapse. Because AVN affects younger patients, joint preservation is often considered through vascularized and nonvascularized bone grafts, hemiarthroplasty, osteotomy, and arthrodesis.⁹⁴

Degenerative Joint Disease

Femoroacetabular osteoarthritis (OA) is a common and disabling ailment, largely of the elderly population. There is variability in the reported prevalence; however, up to 10% of those over 60 and 25% of those over 85 years of age may suffer from hip OA, with a 10% risk of requiring THA.^95,96

Osteoarthritis has often been referred to as a “wear and tear” disease. While physiologic biomechanical loading is crucial to maintaining joint and bone homeostasis, pathologic stress results in disruption of this homeostatic balance. It has been shown that repetitive articular shear stress results in decreased type II collagen and proteoglycan expression in articular cartilage as well as increased pro-inflammatory mediator release resulting in increased cellular apoptotic changes.⁹⁹ This results in focal areas of cartilage loss with associated areas of bony hypertrophy with osteophytes and subchondral sclerosis as well as capsular thickening.⁹⁸ Risk factors for developing hip OA include abnormal hip joint morphology (such as developmental dysplasia or FAI), slipped capital femoral epiphysis, Legg–Calvé–Perthes disease, weakness or poor control of deep stabilizing hip musculature, prior joint or labral injury, increasing age, increasing body mass index (BMI), family history, high-impact occupation, poor diet, ethnicity, and possibly female gender.⁹⁹

The diagnosis of hip OA may be made with a good history and physical exam; however, radiographic confirmation is often helpful or required. The American College of Rheumatology has set forth diagnostic criteria as displayed in Table 29–2. It is important to note that the presence or absence of radiographic features suggestive of OA does not correlate well with the presence or absence of symptoms⁹⁸ (Fig. 29–12).

Many of the treatment guidelines for hip OA are extrapolated from research on knee OA. Management is aimed at symptom palliation rather than reversal of the pathophysiologic changes. However, there is a growing emphasis on primary prevention by addressing modifiable risk factors such as obesity through education regarding healthful diet and exercise. Surgical techniques to restore normal patterns of joint loading in developmental hip dysplasia and FAI have been developed to prevent or delay the development of hip OA; however, their efficacy is still to be elucidated.⁹⁹ Conservative measures consisting of education, weight management, NSAIDs, analgesics (such as Tramadol), serotonin-norepinephrine reuptake inhibitors (SNRIs) (such as duloxetine), disease-modifying osteoarthritis drugs (DMOADs), intra-articular steroid injections, and physical therapy are attempted first.⁹⁹ While initial preclinical trials were promising, later-phase trials of DMOADs (such as glucosamine sulfate, chondroitin sulfate, doxycycline, bisphosphonates, and matrix metalloprotease inhibitors) have been less convincing.^98,99 There is conflicting evidence regarding the efficacy of hyaluronic acid, and current guidelines do not recommend its use.⁹⁹ Intra-articular platelet-rich plasma has been gaining popularity but requires further clinical studies.⁹⁹ While there is no particular exercise shown to be superior to another, individualized treatment plans aiming to improve flexibility, strength, cardiovascular endurance, and neuromuscular coordination have been shown to reduce pain, improve function, and possibly postpone need for THA; however, there is a paucity of data to demonstrate formal physical therapy is superior to a self-guided exercise program.⁹⁹ Cases that are unresponsive to conservative measures require surgical intervention with THA. It has been shown that improved preoperative function imparts improved long-term outcomes, thus suggesting earlier surgical intervention when conservative measures clearly are not proving effective may be helpful.⁹⁹ Hip resurfacing may be an option only for very select patients (typically young, active males), as this is associated with a higher rate of revision and reoperation.⁹⁹

Neurovascular

Obturator Neuropathy

Obturator neuropathy is an uncommon problem but has been reported as a cause of chronic groin pain and should be considered on the differential for groin and medial thigh pain.⁹⁹ Obturator neuropathy may occur from compression within the obturator canal; where the nerve perforates the obturator externus muscle; or within fascial planes between the pectineus, adductor brevis, and obturator externus.¹⁰⁰ It may also result from surgery, hemorrhage, tumor compression, and sports-related injury.¹⁰²

Patients typically present with a clinical pattern of exercise-induced medial thigh paresthesias, sensory loss, or pain that radiates distally along the medial thigh.^101,102 Physical exam may be notable to decreased sensation to the medial thigh, weakness in adduction, loss of the adductor reflex, and possible atrophy, and gait analysis may be notable for excessive hip external rotation and abduction resulting in a wide base of support.¹⁰²

Plain radiography is often obtained to investigate for osseous abnormalities, but is most often unremarkable. MRI may be obtained to assess for other soft tissue pathologies and those in whom surgery is being considered. Ultrasound can be useful to assess for entrapment of the obturator nerve and will demonstrate swelling of the nerve proximal to the site of entrapment, decreased echogenicity, and increased vascularity.¹⁰¹ Local obturator nerve block may also be helpful in suggesting the diagnosis. Definitive diagnosis is with electrodiagnostic studies, including nerve conduction studies and electromyography, which will help rule out radiculopathy or other peripheral mononeuropathies as the cause for the patient’s symptoms.

Initially, conservative measures include relative rest, NSAIDs, acetaminophen, an obturator nerve block, physical modalities such as therapeutic ultrasound, soft tissue massage, and physical therapy with adductor muscle and pelvic strengthening and stretching (Fig. 29–13). Acute-onset obturator neuropathy responds well to conservative therapy; however, those with more chronic symptoms have a poor response to conservative therapy.¹⁰² Surgery should be considered in those with pain and weakness that is resistant to conservative therapies and with documented denervation on electrodiagnostic studies. Curative treatment consists of surgical decompression or neurolysis followed by physical therapy and gradual return to play, with most athletes returning to participation within 3 to 6 weeks.^101,102

Meralgia Paresthetica

Meralgia paresthetica is a condition not uncommon to the physiatric practitioner and results in pain, paresthesias, and sensory loss on the lateral thigh (Fig. 29–14). It occurs mostly in males between the ages of 30 and 40 with a reported incidence of 3.4 cases per 10,000 patient years in the general population and 24.7 cases per 10,000 patient years in those with diabetes mellitus.¹⁰³ It is also associated with certain sports and activities such as baseball, gymnastics, soccer, bodybuilding, and strenuous exercise.¹⁰⁵

Meralgia paresthetica is a compressive peripheral mononeuropathy of the lateral femoral cutaneous nerve (LFCN). Symptoms are caused by compression, which most frequently occurs as it exits the pelvis.¹⁰⁴ Risk factors include pregnancy, obesity, seat belts, direct trauma, muscle spasm, scoliosis, iliacus hematoma, tight clothing, surgery, diabetes mellitus, alcoholism, and lead poisoning.¹⁰⁵

Patients typically complain of pain, burning, numbness, paresthesias, or coldness on their lateral or anterolateral thigh, which may range from mild and quickly self-limiting to severe and function limiting. It is typically worse with prolonged standing and walking and alleviated with sitting; however, clinical presentation, including palliative or provocative factors, varies widely between patients.¹⁰⁵ The diagnosis is largely clinical but may be confirmed with electrodiagnostic studies. Although Tinel’s sign over the LFCN as it exits under the inguinal ligament is often used clinically, there are no clinical trials to investigate its diagnostic ability.¹⁰⁵ Temporary nerve block may also be used to confirm the diagnosis.¹⁰⁵ Plain radiography will be unremarkable. Ultrasound may be helpful and may demonstrate swelling with increased echogenicity proximal to the site of compression.¹⁰⁴

There are limited data investigating both nonsurgical and surgical management of meralgia paresthetica. Despite that, conservative therapies, including NSAIDs, avoidance of compression activities (including wearing tight clothing), and physical therapy, should be attempted first. Local injections of lidocaine and corticosteroids have been found to be effective.¹⁰⁵ Limited evidence suggests that manual therapy with active release techniques, mobilization/manipulation of the pelvis, myofascial therapy for the rectus femoris and iliopsoas, transverse friction massage of the inguinal ligament, stretching, pelvic/core stabilization exercises, taping, and acupuncture are safe and effective.¹⁰⁵ LFCN neurolysis and resection are options when conservative measures fail.¹⁰⁵

Compartment Syndrome

Compartment syndrome of the thigh is rare, but when it does occur, it is an orthopedic emergency associated with significant morbidity and mortality. Forty-four percent of patients suffer long-term functional deficits, and mortality is as high as 47%, mainly secondary to polytrauma and infection.¹⁰⁶ Neurologic injury and infection are the most common complications of compartment syndrome.^107,108 Factors associated with worse outcomes include age, polytrauma, femoral fractures, and time to fasciotomy.¹⁰⁸

Compartment syndrome occurs when the osteofascial compartment pressure exceeds capillary perfusion pressure, leading to cellular anoxia, muscle ischemia, and death.¹⁰⁸ The vast majority of cases are trauma related, with 34% related to motor vehicle accidents and 7% from motorcycle accidents and of those, 44% are associated with femoral fractures, 22% of which are open fractures.¹⁰⁸

The diagnosis of compartment syndrome needs to be made swiftly to avoid significant morbidity and mortality. It can often be made by history and physical alone but can be confirmed with measurement of compartment pressure.^108,109 The history and physical may reveal the classic “5 P’s” of pain, paresthesia, pallor, pulselessness, and poikilothermia; however, these are late findings.

The management of compartment syndrome is emergent fasciotomy to relieve intracompartmental pressure. While the surgical approach may depend on the compartments and muscles involved, it has been recommended by some to release all compartments.¹⁰⁹ After fasciotomy, interval closure is performed until the edges can be approximated, typically at a minimum of 1 week, and may occasionally require split-thickness skin grafts.¹⁰⁸

Knee pain and related symptoms may derive from damage to one or more of the bony and soft tissue structures that stabilize and cushion the knee joint (including the ligaments, muscles, tendons, and menisci) or from infection to the knee joint or surrounding structures (Fig. 29–15). One must determine the etiology and acuity of the patient’s presenting symptoms. Accurate and timely diagnosis increases the likelihood of fully restoring normal and pain-free use of the affected knee.

Fracture

Patellar and tibial plateau fractures each account for 1% of all skeletal fractures. Distal femoral condyle fractures account for 4% of all femur fractures. Fractures of the knee can result in neurovascular compromise or compartment syndrome, with resultant risk of limb loss.¹¹⁰

Soft tissue infection or osteomyelitis can occur with open fractures. Other complications include nonunion, delayed union, osteoarthritis, avascular necrosis, fat embolism, and thrombophlebitis.

Patellar Fracture

As mentioned, patellar fractures account for approximately 1% of all skeletal injuries. They become problematic if the extensor mechanism of the knee is nonfunctional, articular congruity is lost, or stiffness of the knee joint ensues. To avoid these problem the practitioner must achieve anatomic restoration of the joint and must allow early motion.

The subcutaneous location of the patella makes it prone to injury. Fractures occur as a result of a compressive force (as occurs with a direct blow), a sudden tensile force (as occurs with hyperflexion of the knee), or a combination of these. Various fracture patterns result, depending on the mechanism of injury. The most common patterns are often described as stellate or transverse; less common patterns include vertical, marginal, and osteochondral (Fig. 29–16).

A direct blow to the patella most often results in a stellate fracture. The compressive forces applied to the patella result in a comminuted pattern. The energy of the blow is absorbed by the fracture and may cause damage to the articular cartilage of both the patella and the femoral condyles; thus, free osteochondral lesions must be excluded. About 65% of these fractures do not involve the extensor retinaculum. If the extensor mechanism has not been disrupted, the fracture may be treated nonoperatively.

Another mechanism of injury to the patella is a tensile force, as is sustained with hyperflexion of the knee with an eccentric contraction of the quadriceps. Approximately 35% of these are nondisplaced fractures with an intact retinaculum. This type of fracture can be treated with a nonoperative modality.

The prognosis depends primarily on the quality of articular restoration.¹¹¹ Any intra-articular incongruities lead to posttraumatic arthritis. To a certain extent, the prognosis also depends on the amount of chondral damage sustained at the time of injury. If arthrofibrosis develops, it may require manipulation with the patient under anesthesia or arthroscopic release of adhesions.

Treatment consists of immobilization if the fracture is not displaced and the extensor mechanism is intact for 4 to 6 weeks with WBAT in the cast during ambulation. This is later changed to a removable brace once radiographic evidence indicates union and clinical signs of healing are present. A hinged knee brace is used during ambulation.

A program emphasizing range of motion and strengthening is then implemented. Once the patient is able to perform a straight-leg raise without extensor lag and has greater than 90 degrees of knee flexion, brace use may be discontinued.

For displaced patellar fractures, surgical treatment is warranted to maximize the potential for successful outcomes.

Tibial Plateau Fracture

More than 50% of patients who sustain a tibial plateau fracture are aged 50 years or older. The increased frequency of tibial plateau fractures in older females is due to the increased prevalence of osteoporosis in these individuals. Tibial plateau fractures in younger patients are commonly the result of high-energy injuries.

Most tibial plateau fractures are easy to identify on standard anteroposterior (AP) and lateral projections of the knee. Lateral views should not be considered adequate if a rotational component obscures the visualization of the femoral condyles as a single unit.

Oblique projections should be added if a nondisplaced tibial plateau fracture is suspected but not seen on the standard projections.

By acquiring thin axial slices through the knee and reconstructing the image data in the sagittal and coronal planes, CT provides more detailed information that can help determine the best surgical approach based on the fracture planes seen on the computer images (Fig. 29–17).

MRI is acknowledged as a reliable and accurate tool for assessing meniscal, collateral, and cruciate ligamentous injury,¹¹² as well as for identifying occult fractures of the tibial plateau.

Nonoperative indications for treatment of tibial plateau fracture include nondisplaced stable split fractures; minimally displaced or depressed fractures; submeniscal rim fractures; and fractures in elderly, low-demand, or osteoporotic patients.

Segond Fracture

Avulsion fracture of the lateral capsule off the lateral tibial plateau, immediately beyond the surface, is often associated with an anterior cruciate ligament (ACL) injury. Segond fracture is typically the result of abnormal varus, or “bowing,” stress to the knee, combined with internal rotation of the tibia. Reverse Segond fracture, as its name suggests, is caused by abnormal valgus, or “knock-knee,” stress and external rotation.

Segond fracture is characterized by a small avulsion,¹¹³ or “chip,” fragment of characteristic size that is best seen on plain x-ray in the anteroposterior plane. The chip of bone may be very difficult to see on the plain x-ray exam, and may be better seen on computerized tomography. MRI may be useful for visualization of the associated bone marrow edema of the underlying tibial plateau.

Stress Fracture

Stress fractures are caused by repetitive and submaximal loading of the bone; this eventually becomes fatigued and leads to a true fracture. The typical presentation is a complaint of increasing pain in the lower extremity during exercise or activity. The patient’s history usually reveals a recent increase in either training volume or intensity.

The treatment of most knee stress fractures is relatively straightforward and includes decreased activity and immobilization.

The women most at risk for stress fractures were those who restricted their food intake and those who had dysmenorrhea. Stress fractures may not show up on radiographs for the first 2 to 4 weeks after injury. The first radiographic finding may be a localized periosteal reaction or an endosteal cortical thickening. The low sensitivity of radiography for stress fractures makes bone scanning, MRI, and CT the preferred tests for diagnosis.

Dislocation

Knee dislocations are uncommon. A knee dislocation is defined as complete displacement of the tibia with respect to the femur, with disruption of three or more of the stabilizing ligaments.^114,115 Small avulsion fractures from the ligaments and capsular insertions may be present (Fig. 29–18).

Multiple ligament injuries are required for knee dislocation. Generally, both cruciate and one or both collateral ligaments are injured. It is important to evaluate the competence of each ligament and to consider the possibility of a knee dislocation in knees with three or more ligaments torn.

Standard anteroposterior (AP) and lateral radiographs can be obtained to detect a knee dislocation.¹¹⁶ After reduction, repeat AP and lateral radiographs are obtained to confirm reduction. Oblique views after reduction may delineate small avulsion or rim fractures and osteochondral fractures.¹¹⁷

For ligament injuries of the knee, MRI can be used to assess the extent and location of ligament disruption, meniscal tears, and subtle injuries to the bone, as well as to determine which tears are repairable.^117,118

Emergency vascular surgery is indicated for limbs that are dysvascular after reduction. Nonsurgical management is recommended in patients who have low functional demands or cannot cooperate with postoperative rehabilitation, such as those with significant closed head injuries. Bracing would be appropriate with monitoring of skin integrity and hygiene.

Rehabilitation of this injury is to maintain ROM, emphasizing extension.⁵² If tolerated, gentle active and active-assisted flexion is performed in the prone position for 2 months to minimize posterior tibial sag. Strengthening begins with isometric hamstring and quadriceps co-contraction and progresses to isotonic exercises.

Patellar dislocations are common, particularly in adolescent females and athletes. Patients usually present with an inability to extend an obviously deformed knee. A sizable effusion may also be seen. This injury may be due to direct trauma to the patella or to a valgus stress combined with flexion and external rotation. The most common type of patellar dislocation is lateral direction, although horizontal, vertical, and intercondylar types may occur.

Management of patellar dislocation can be done by reduction either on the lateral or medial aspect. When reduction is complete, apply a knee immobilizer so that the knee is in full extension. Arrange a follow-up appointment for the patient with an orthopedic surgeon. Some patients with complete dislocation may require surgery to prevent recurrence.

Soft Tissue Injuries

Tendonitis is an inflammatory condition characterized by pain at tendinous insertions into bone. The term tendinosis refers to the histopathologic finding of tendon degeneration. Most pain from tendon conditions is not actually inflammatory in nature; thus, tendinopathy may be a better term than tendonitis.