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좀 긴 논문이지만 요것도 재미있넹

- 스포츠 의학 통계에 의하면 Overuse injuries는 acute injury의 두배

- 대부분의 손상이 달리기 손상 상황. 비율을 보면  lower leg (20%), ankle (15%), and foot (15%) 

-  It is important to realize that, in theory, this sub-clinical tissue damage can accumulate for some time before the person experiences pain and becomes symptomatic. 

- Common overuse injuries of the lower leg, ankle, and foot include tendinopathies, stress fractures, chronic exertional compartment syndrome, and shin splints.

panic bird...

Overuse injuries: tendinopathies, stress fractures, compartment syndrome, and shin splints

Overuse injuries. tendinopathy, stress fracture, compartmen.pdf

Approximately 50% of all sports injuries are secondary to overuse [1]. The frequency of overuse injuries eval‎uated in primary care sports medicine clinics is even greater, reportedly up to twice the frequency of acute injuries [2]. The majority of injuries eval‎uated in running injury clinics are related to overuse [3,4], and approximately half of these involve the lower leg (20%), ankle (15%), and foot (15%) [5,6]. Overuse injuries result from repetitive microtrauma that leads to local tissue damage in the form of cellular and extracellular degeneration, and are most likely to occur when an athlete changes the mode, intensity, or duration of training a phenomenon described as the ‘‘principle of transition’’ [7,8]. 

Physical training uses prescribed periods of intense activity to induce the desired goal of ‘‘super-compensation’’

or performance improvement. A mismatch between overload and recovery can lead to breakdown on a cellular, extracellular, or systemic level, however. At the cellular level, repetitive overload on tissues that fail to adapt to new

or increased demands can lead to tissue breakdown and overuse injury. It is important to realize that, in theory, this sub-clinical tissue damage can accumulate for some time before the person experiences pain and becomes symptomatic. On the systemic level, rapid increases in training load without adequate recovery may cause a global ‘‘overtraining syndrome.’’ Strong predictors of overuse musculoskeletal injury include a previous history of injury as well as walking or running more than 20 miles per week [9]. 

Both intrinsic and extrinsic factors contribute to overuse injuries. Intrinsic factors are biomechanical abnormalities unique to a particular athlete and include such features as mal-alignments, muscle imbalance, inflexibility, weakness, and instability. High arches, for example, have been demonstrated to predispose to a greater risk of musculoskeletal overuse injury than low arches (‘‘flat feet’’) in military recruits [10]. 

Extrinsic (avoidable) factors that commonly contribute to overload include poor technique, improper equipment, and improper changes in the duration or frequency of activity. These improper changes in activity duration/frequency or ‘‘training errors’’ are the most common causes of overuse injuries in recreational athletes. Vulnerability to extrinsic overload varies with the intrinsic risk factors of an individual athlete [7].

Sports-acquired deficiencies, categorized as an extrinsic risk factor, actually represent the product of biomechanical abnormalities and training errors. Because sports activity can overload an athlete’s musculoskeletal system in predictable

ways, athletic repetition without proper conditioning can propagate muscular imbalance and flexibility deficits. Injuries are often related to biomechanical abnormalities removed from the specific site of injury, underscoring the importance of eval‎uation of the entire kinetic chain [11]. Common overuse injuries of the lower leg, ankle, and foot include tendinopathies, stress fractures, chronic exertional compartment syndrome, and shin splints.

 Tendinopathies

Tendinopathies of the foot and ankle are relatively common and encompass a

wide spectrum of maladies ranging from tendinitis (acute inflammation of the

tendon) to tendinosis (chronic degeneration) to tenosynovitis (inflammation of

tendon sheath) to partial and complete ruptures. Each one of these disorders is

distinct, although they may be seen in combination. Four tendons in the foot and

ankle—the Achilles, posterior tibialis, peroneal brevis, and peroneal longus

tendons—are most often involved. In contrast to acute traumatic tendinous

injury, sport-related injuries most often involve repetitive submaximal loading

of the tissues, resulting in repetitive microtrauma. An understanding of the

anatomical pathophysiologic basis of these maladies is critical to their diagnosis

and management.

Histopathology

The debate over the nomenclature of chronic tendon injury highlights some of

the unresolved issues in the histopathology, etiology, and management of tendinopathies

of the foot and ankle. Although the pathological label ‘‘tendinosis’’ has

been in use for more than 25 years to describe collagen degeneration in tendinopathy

[12], many clinicians still use the term ‘‘tendinitis’’ to describe painful

chronic overuse injury, implying that the fundamental problem is inflammatory

[13]. Maffulli, Khan, and Puddu advocate the use of the term tendinopathy as a

generic descriptor of clinical conditions such as pain, swelling, and impaired

performance in and around tendons arising from overuse, with the labels tendinosis

and tendinitis most appropriately applied after histopathological examination [14].   This nomenclature separates chronic degeneration of tendons from acute and

mainly inflammatory processes, with implications for treatment and management.

Tendinosis has been described as a failure of cell matrix adaptation to trauma

because of an imbalance between matrix degeneration and synthesis [8] . The

classic pathology is a loss of the normal collagenous architecture and replacement

with an amorphous mucinous material that lacks the parallel, longitudinal architecture

of normal tendon [15,16] . Histological examination reveals intratendinous

collagen degeneration with fiber disorientation and thinning, hypercellularity,

scattered vascular ingrowth, increases in the amount of ground substance and the

proteoglycan concentration of ground substance, and a decrease in the ratio of

Type I to Type III collagen [15,17,18] . Any inflammatory response or the presence

of inflammatory cells is notably lacking in tissue samples of tendinopathy,

differentiating tendinosis, or chronic overuse pathology from acute injury and

tendinitis. Astrom and Rausing describe the major lesion in chronic Achilles

tendinopathy as ‘‘a degenerative process characterized by a curious absence of

inflammatory cells and a poor healing response’’ [18] . Similar histopathological

findings in posterior tibial tendon dysfunction of a degenerative tendinosis with

mucinous degeneration, fibroblast hypercellularity and neovascularization [19] ,

and higher proportions of collagen Type III at the expense of collagen Type I [20]

 support the notion of a common disease process in overuse tendon injury, leading

ultimately to tendon degeneration and an insufficient repair response.

Functionally, whereas the healing response to an acute tendon injury involves an

organized triphasic response of inflammation, proliferation, and maturation, the

response to an overuse injury involves an inadequate, incomplete, and disorganized

repair mechanism resulting in a substantially defective ‘‘repaired’’ tendon lacking

in extracellular tissue organization, with decreased resistive strength and more

vulnerability to further injury. Although the exact role of overuse in the pathogenesis

of chronic tendon injuries and disorders is not completely understood, it is

speculated that fatigued tendon loses its basal reparative ability with intensive

repetitive activity, often eccentric in nature, leading to cumulative microtrauma that

further weakens the collagen cross-linking and noncollagenous matrix and disturbs

the micro- and macrovasculature of the tendon [21] . Ensuing local tissue hypoxia

and impaired nutrition and energy metabolism likely play an important role in the

sequence of events leading to tendon degeneration [13,21] . Leadbetter has called

this the ‘‘tendinosis cycle’’ [8] . One of the first animal models of tendinopathy,

developed by Soslowsky et al [22,23] , has shown persistent microscopic changes

of tendinosis in rat rotator-cuff supraspinatus tendon after exposure to multiple

factors, including impingement and overuse [23] . Neither impingement alone nor

overuse alone produced the same degree of changes, implying a multifactorial

etiology for the pathologic effects of overuse on rotator cuff tendon.

Current thinking supports the belief that a spontaneous tendon rupture is a

typical end-state manifestation of degenerative processes in the tendon tissue [21] ,

with partial macroscopic tears as a stage in the continuum of tendon degeneration

[14] . Analysis of surgical specimens of Achilles tendons reveals that, although

ruptured and tendinopathic tendons are histologically significantly more degen erated than control tendons, the general pattern of degeneration seen is common to

the ruptured and tendinopathic tendons, suggesting the possibility of a common, as

yet unidentified, pathological mechanism acting on both tendon populations [24] .

Laboratory and molecular analyses of tendinopathy have begun to reveal

strategies that may guide future clinical management of overuse tendon injury. It

has been hypothesized in the past that tendon degeneration may be preceded by

acute and then chronic phases of inflammatory ‘‘tendinitis’’ [12,25,26] . Although

no inflammatory infiltration has been observed in multiple studies of biopsy

specimens of tendinopathic tendons, recent in-vitro work demonstrates that a

‘‘molecular inflammation cascade’’ mediated by IL-1 beta in human tendon cells

can induce connective tissue cell expression‎ of cytokines that further induces

known matrix destructive enzymes such as matrix metalloproteinases (MMP-1 and

MMP-3) [27] . Clinically, the activity of metalloproteinases in tendon destruction

and degeneration is the target of the use of injectable aprotinin, a metalloproteinase

inhibitor, in the setting of patellar and Achilles tendinopathy as an alternative to

corticosteroid therapy [28,29] . Apoptosis, mediated by overuse-induced, stressactivated

protein kinases, may also play a role in tendon degeneration and

weakening, presenting another set of molecular targets for future therapies aimed

at preventing or treating tendinopathy more effectively [16,30,31] .

Achilles tendon disorders

 Commonly and inappropriately generalized as ‘‘Achilles tendinitis’’ by many

clinicians, posterior heel pain in the setting of an overuse injury of the foot and

ankle actually encompasses a spectrum of distinct and often coexistent pathological

disorders with both inflammatory and degenerative etiologies [32] . The classification

system set forth by Puddu et al separates degenerative conditions of the

tendon itself (tendinosis with or without partial rupture) from inflammation of the

paratenon (paratenonitis), inflammation of the tendon substance at its insertion

(insertional tendonitis), and inflammation of the commonly afflicted bursa anterior

to the insertion of the Achilles tendon on the calcaneus (retrocalcaneal bursitis)

from complete tears caused by acute injury [12] .

Puddu reserves a mixed category for paratenonitis with tendinosis including

degeneration, partial tears, and calcification within the tendon [12] , and Maffulli

et al agree that clinically observed tendinopathy should include both of the

histopathological entities peritendonitis and tendinosis [14] . According to Paavola

et al, this suggestion has a sound basis because the clinical rationale to differentiate

the histopathologic entities of Achilles peritendinitis and tendinosis is an uncertain

one and there have been no randomized controlled studies comparing the outcomes

of treatment or the natural history of these two conditions [25] . In clinical studies,

the most common diagnosis of Achilles disorders was tendinopathy (55%–66%),

followed by insertional problems (retrocalcaneal bursitis and insertional tendinopathy)

(20%–25%) [25,33–36] .

Achilles tendon disorders occur most often in athletes, and most often in those

involved in running sports. An annual incidence of Achilles tendon disorders of 7%  to 9% in top-level runners has been reported [6,37] . Kvist reviewed cases of

455 athletes with Achilles tendon disorders [33] . Eighty-nine percent of the athletes

studied were men, with 53% involved in running sports and 11% involved in

soccer. The rest of the patients were involved in other sports in which running was

an important training means [13,33] . Interestingly, malalignment of the lower

extremity was found in 60% of the athletes with Achilles tendon disorders

[25,33,36] .

Many intrinsic and extrinsic etiologic factors have been proposed to account for

the development of Achilles tendon disorders. Common intrinsic etiologies

invoked include various alignment and biomechanical faults, including hyperpronation

of the foot, limited mobility of subtalar joints and limited range of motion

of the ankle joint, leg-length discrepancy, varus deformity of the forefoot and

increased hindfoot inversion, decreased ankle dorsiflexion with the knee in extension,

poor vascularity, genetic makeup, and gender, age, endocrine, or metabolic

factors [33,34,38–40] . Changes in training pattern, poor technique, monotonous,

asymmetric, and specialized training, previous injuries, footwear, and environmental

factors such as training on hard, slippery, or slanting surfaces have been

cited by many authors as extrinsic factors which may predispose the athlete to

tendinopathy. Training errors have been reported to be involved in 60% to 80% of

runners who have tendon overuse injuries [25] . Training errors cited include

running a distance that is too long, running at an intensity that is too high,

increasing distance too greatly or intensity too rapidly, and performing too much

uphill or downhill work [25,34,40,41] . Training errors, alignment, biomechanics,

and extrinsic factors such as footwear and training surfaces can create microtrauma

resulting from nonuniform stress within the Achilles tendon from different

individual force contributions of the gastrocnemius and soleus, producing abnormal

load concentrations within the tendon and frictional forces between the fibrils,

and leading to localized fiber damage [13,42] . In this manner, excessive motion of

the hindfoot in the frontal plane, especially a heel strike with excessive compensatory

pronation, is thought to cause a ‘‘whipping action’’ on the Achilles tendon

and predispose it to tendinopathy [13,43] .

A complete discussion of the etiological factors of Achilles tendon disorders

must include the caveat that the exact pathogenesis of Achilles tendinopathy and

other disorders remains largely unknown [25] . In addition to the epidemiological

studies showing Achilles tendon disorders in athletes, other studies have shown a

significant incidence of Achilles tendinopathy in nonathletes and middle aged men

with sedentary lifestyles [18,44] . In the absence of a true inflammatory reaction in

chronic Achilles tendinopathy, the etiology of pain, the most limiting factor and

usual chief complaint of patients with Achilles tendon disorders, is not well

understood [45,46] . Puddu et al have shown that long-standing degeneration of

the tendon can occur without clinical symptoms or pain, and yet tendinopathy can

become symptomatic with the introduction of heavy training [12] .

History and physical examination play a key role in the diagnosis of Achilles

tendon injury. The onset of pain, its duration, and aggravating factors should be

documented. A classic history involves an insidious and gradual increase in pain  located 2 cm to 6 cm proximal to the insertion of the tendon and felt after exercise

within days of a change in activity levels or training techniques. Rest often relieves

symptoms, but return to activity reactivates the pain, generally within a few training

sessions. In patients with advanced tendinopathy, pain may occur during exercise,

and when severe, may interfere with the activities of daily living. Runners typically

experience pain at the beginning and at the end of a training session, with a period

of diminished discomfort in between.

Clinical examination should start by the exposure of both legs from above the

knees, and the patient should be examined standing and prone. Careful inspection

should reveal malalignment, deformity, areas of swelling, obvious asymmetry in

the size of the tendon, localized thickening, erythema, and any previous scars.

Palpation should document contours of the tendons, tenderness, thickening,

palpable tendon nodules or defects, crepitation, and warmth. Biomechanics of

the foot, ankle, and leg during walking and running, including slow motion

analysis, should be eval‎uated in athletes. All patients should be examined for

evidence of ankle instability [25] . The ‘‘painful arc’’ sign may help to distinguish

between lesions of the tendon and paratendon [47] . Whereas peritendinitis is

characterized by crepitus, exquisite tenderness, and swelling that does not move

with tendon action, chronic Achilles tendinopathy is notable for absence of

crepitation and swelling, with focal tender nodules that move as the ankle is

dorsiflexed and plantar flexed [47] . The VISA-A scale is a subjective, quantitative

scale of symptoms and dysfunction in the Achilles tendon and may be a useful tool

to assess and follow symptomatology over time [48] .

Both ultrasound and magnetic resonance imaging (MRI) play a role in the

diagnosis of Achilles tendon disorders. Ultrasonography provides an inexpensive,

sensitive analysis of the pathology of the Achilles tendon, with data regarding

tendon width, water content within the tendon and peritendon, and collagen

integrity. Abnormal tendons may have increased tendon diameter, focal hypoechoic

intratendinous areas (areas of increased water content which at surgery have

been shown to be degenerated tissue), localized tendon swelling and thickening,

collagen discontinuity, and tendon sheath swelling or calcifications [25] . In the

acute phase, ultrasound examination may reveal fluid surrounding the tendon. In

the chronic phase, thickening of the hypoechoic paratenon may be seen, although

ultrasonography has not been shown to reliably differentiate focal tendinosis from

partial rupture [49] . Abnormalities detected by ultrasonography in an asymptomatic

Achilles tendon can accurately presage the development of Achilles tendinopathy

[50] .

Magnetic resonance imaging provides extensive information on the internal

morphology of the tendon and the surrounding structures and is used often for

eval‎uation before surgical intervention [32] . MRI can also help characterize

retrocalcaneal bursitis and insertional tendinitis. In patients with chronic tendinopathy,

MRI often reveals tendon thickening and increased signal within the

Achilles tendon. Areas of mucoid degeneration are shown onMRI as a zone of high

signal intensity on T1- and T2-weighted images. Two caveats on MRI interpretation

in Achilles tendon disorders include the unreliability of MRI to demonstrate  changes of paratenonitis [51]  and the temptation of the clinician to mistake areas of

increased signal on MRI for pathologic, clinically significant foci rather than

asymptomatic areas of degeneration [32] .

The goals of treatment in Achilles tendinopathy are threefold: (1) to minimize

the pain, (2) to prevent further degeneration, and (3) to allow return to baseline

activity. In athletes, an additional demand is that the recovery time should be as

short as possible [25] . Initial conservative management aims to relieve symptoms

and correct factors causing load imbalance and repetitive strain on the tendon and

surrounding structures. This includes a combination of strategies aimed at

controlling inflammation and correcting training errors, limb malalignment,

decreased flexibility, and muscle weakness, and the use of appropriate equipment

during sports [25,52] . The role of anti-inflammatory therapy such as oral nonsteroidal

anti-inflammatory drugs (NSAIDS) or steroid pain relievers to control

inflammation remains controversial. Although no inflammatory infiltrate has been

documented in histological analyses of tendinopathic samples, anti-inflammatory

medication does help to diminish pain and facilitate rehabilitation in cases of

chronic tendinopathy and most certainly has a place in the management of

retrocalcaneal bursitis and insertional tendinitis [17,53] . Cryotherapy has also

been shown to be useful to help control inflammation and facilitate therapy in

tendinopathy [54] . Occasionally, complete rest or cessation of the training that

caused the symptoms may be required for a short time to settle severe symptoms.

Because the repair and remodeling of collagen fibers are stimulated by loading of

the tendon, only very short courses of complete rest should be prescribed. Heparin

may be injected to prevent fibrin exudate in the paratenon region [17] . Recently,

Ohberg and Alfredson have described successful ultrasound-guided injection of

polidocanol, a sclerosing agent, to decrease the neovascularization and symptomotology

of chronic midportion Achilles tendinosis [55] .

Appropriate and progressive exercises using eccentric exercise programs

targeting specific muscle hypertrophy, speed, strength, and endurance requirements

represent the gold standard for Achilles tendon rehabilitation and appear to

be effective in most athletes [56] . Mafi et al have shown prospectively that a

program of eccentric calf muscle training was superior to concentric training in

Achilles tendinosis [57] . Correction of biomechanical imperfections is clinically

important, even if their effects on tendonitis are unclear. Interventions improving

flexibility of the ankle joint, flexibility of calf muscles, amount or speed of foot

pronation, and foot and ankle mechanics (with orthotics) have been implicated in

ameliorating symptoms of tendinopathies.

Operative treatment is recommended for patients who do not respond adequately

to a 3- to 6-month trial of appropriate conservative treatment. To date, no

prospective randomized controlled studies comparing operative and conservative

treatment of Achilles tendinopathy have been published [25] . Surgery for overuse

tendinopathies usually involves excision of fibrotic adhesions and degenerated

nodules, or decompression of the tendon by longitudinal tenotomies. Reconstructive

procedures may be necessary if large nodules and lesions are excised. Some

authors have used open or percutaneous multiple longitudinal incisions of the  tendon [58] . In most studies, satisfactory results in 75% to 100% of the patients

have been reported after operative intervention of Achilles tendinopathy [25] .

Generally, long-standing tendinopathies are associated with poorer surgical outcomes

[51,58] . Recently, an overall complication rate of 11% was documented in a

series of 432 consecutive patients [59] .

Although much is known about Achilles tendon disorders, and much more is

known about Achilles tendinopathies than about other tendinopathies of the foot

and ankle, ample opportunity exists for better controlled studies to examine

operative and conservative treatment regimens, postoperative rehabilitation protocols,

and long-term follow-up of clinical interventions. In addition, further study

of the etiologies of Achilles tendon disorders, the causative factors in the pain of

chronic tendon injury, and the factors contributing to the histopathology of

tendinopathy could help identify therapeutic targets for molecular medicine.

Posterior tibial tendon dysfunction

 Posterior tibial tendon dysfunction (PTTD) is a common cause of painful

acquired flatfoot deformity in adults and is associated with substantial functional

problems resulting in significant morbidity. These patients typically have a loss of

hindfoot inversion, inability to negotiate uneven ground, climb, and descend stairs

[60] . As acquired flatfoot syndrome advances, progressive collapse of the medial

longitudinal arch, hindfoot valgus, and forefoot abduction abnormalities are noted

[19] . Shoe fitting is difficult. Pain and instability in the hindfoot have significant

impact on daily routines [60] .

Johnson and Strom [61]  have described three distinct stages of posterior tibial

tendon dysfunction. In Stage I, the patient has pain and swelling along the course of

the tendon. Because the length of the tendon is normal, the patient is able to perform

single heel raise. The flatfoot deformity is minimal, the alignment of the hindfootforefoot

complex is normal and the subtalar joint remains flexible [19,62] . In

Stage II, the patient is unable to performa single heel raise because of attenuation or

disruption of the posterior tibial tendon. The tendon is enlarged and elongated and

functionally incompetent. The foot has adopted a pes planovalgus position with

collapse of the medial longitudinal arch, hindfoot valgus and subtalar joint

eversion, and forefoot abduction through the talonavicular joint. The subtalar joint

remains flexible, and the hallmark of this stage is that with the ankle in equinus, the

talonavicular joint can be reduced [19,62] . Stage III disease presents with the

patient unable to performa single heel raise and a more severe flatfoot deformity. In

Stage III disease, the pes planovalgus deformity is fixed and the laterally subluxed

navicular cannot be reduced [19,62] .

The histopathology of PTTD reveals a degenerative intratendinous process

similar to that seen in Achilles tendinopathy. Mosier et al studied 15 normal

cadaveric tendons and 15 surgical specimens from patients with Stage II

PTTD [63] . Four types of histopathology were present in the disease samples:

(1) increased mucin content, (2) hypercellularity, (3) neovascularization, and

(4) chondroid metaplasia. Disruption of the normal array of collagen bundles  represented a degenerative tendinosis with a nonspecific reparative response to

tissue injury [63] .

Both ultrasound and magnetic resonance imaging can play a role in the

diagnosis of PTTD. According to Perry et al, ultrasonography can positively

identify peritendinitis and tendonitis. Tendon interruption, or inhomogeneity of

tendon by MRI assessment, however, remains more sensitive than either clinical

or ultrasound eval‎uation to eval‎uate for partial tears. In their study comparing

clinical findings with those of magnetic resonance imaging and ultrasonography

in 31 subjects, tendon dysfunction, as measured by heel raise, was not correlated

with inhomogeneity by MRI [60] . They concluded that partial tears

without painful sequelae may be missed by the clinician when doing tests to

eval‎uate tendon function and resistance testing in an attempt to assess pain or

dysfunction. Ultrasound to assess pain or dysfunction also may miss patients with

partial tears. If ligamentous structures remain intact, they noted that there may be

little change in the medial arch until the posterior tibial tendon finally tears, that

pain on clinical palpation or resistance testing usually means inflammation is

present, and that in these cases, the structure most likely to be affected is the

tendon sheath [60] .

Treatment of PTTD depends on many factors. During the time that the foot

remains flexible, treatment is possible with a corrective orthosis such as the

University of California Biomechanics Laboratory brace, molded ankle-foot

orthosis, articulated molded ankle-foot orthosis, or Marzano brace [60] . The goal

of nonoperative treatment in flexible flatfoot deformities is to control the

progressive valgus of the calcaneus [62] . If a rigid deformity of the foot develops,

then the orthosis should be accommodative to bony deformity and help prevent

progression of the deformity. If nonoperative or conservative treatment fails,

surgery is indicated because the progression of dysfunction may be rapid and

disabling. When conservative treatment fails in the early stages of posterior tibial

dysfunction, soft-tissue surgical procedures such as tenosynovectomy and tendon

debridement may halt the progression of disease. Once flatfoot deformity develops,

surgical procedures involving osteotomies and arthrodesis are necessary

[60,62] .

Many etiological factors have been proposed for PTTD including trauma,

anatomic, mechanical, and ischemic processes [19] . None has been specifically

proven to be a causative agent. Hypotheses on the association between pre-existing

pes planus and PTTD suggest that the chronic stress placed on the posterior tibial

tendon because of the flexible planovalgus foot and a tight heel cord could lead to

an overuse injury, resulting in repetitive microtrauma and degeneration with time

[19,64] . Further studies will be needed to more specifically identify risk factors and

therapeutic targets in PTTD.

Peroneal tendinopathies

 Peroneal tendon injuries are less common, and perhaps less commonly

diagnosed, than corresponding injuries in the Achilles and posterior tibial tendons.  Accordingly, there are fewer studies in the current literature on peroneal injury and

peroneal tendinopathy.

Case reports and case series document ruptures of the peroneus longus and peroneus

brevis tendons in athletes and acute and chronic subluxation of peroneal tendon

amenable to surgical correction [65–69] . In one series, Alanen et al reported on

38 operated cases of peroneal tendon injuries [70] . Eighty-two per cent of patients

were competitive athletes. Of the 38 cases, there were 11 partial and 3 total ruptures

of the peroneal brevis tendon, 2 partial and 2 total ruptures of the peroneus longus

tendon, 9 cases of subluxation, 5 cases of chronic tendinitis, and 1 ganglion [70] .

Peroneal injury including tendinopathy and partial tears of both the peroneus

longus and brevis tendons has been linked to persistent lateral ankle pain and

chronic lateral ankle instability [70–72] . Di Giovanni et al report on 61 patients

who underwent a primary ankle ligament reconstruction for chronic instability

[73] . Associated injuries found at surgery included 77% of patients with peroneal

tenosynovitis, 54% with attenuated peroneal retinaculum, and 25% with peroneus

brevis tear [73] . Based on their experiences, both Di Giovanni et al and Alanen et al

suggest that peroneal tendon injuries may be an often overlooked cause of

persistent lateral ankle pain and chronic ankle instability in settings of overuse

and after acute trauma.

In cases of primary peroneus longus tendinopathy without antecedent acute

trauma, the specific anatomy of the peroneus longus tendon as it courses through

three fibro-osseus tunnels and changes directions in the hindfoot is thought to play

a role in the evolution of the disease process [74] . Brandes and Smith found that

there was an association, although not a statistically significant one, between

location and type of injury in peroneal tendinopathy [74] . Complete ruptures of the

peroneus longus were all found at the cuboid notch, whereas 89% of the partial

tears involved the region of the lateral calcaneal process. Eighty-two percent of

patients presenting with peroneal tendinopathy had a cavo-varus hindfoot position

with arch height in the ninetieth percentile for the general population [74] . Thirtythree

percent of cases had associated peroneus brevis involvement [74] . Sammarco

also found associated peroneus brevis pathology in 9 of 14 cases of acute and

chronic peroneus longus tears [69] .

Our understanding of the mechanisms involved in peroneal tendon injury, the

histopathology of peroneal tendinopathy preceding partial and acute rupture, and

the specific biomechanics and extrinsic factors contributing to development of

disease is in its earliest stages. As more research is done on the etiology and

evolution of tendinopathies of the foot and ankle, we hope that more will come to

be known about accurate diagnosis, initial treatment, and prevention.