Heterotopic Ossification

March 27, 2004

Hi Everyone,

I am contemplating hip resurfacing to my right hip. However I have

been warned about the increased possibility of developing heterotopic

ossification (HO) as a post-operative complication. Has anyone out

there developed this complicationo. If so I would appreciate hearing

about your experience. Also does anyone know of any data looking at

the incidence of HO following hip resurfacing?

Thanks,

Mark M

March 27, 2004

See this: http://www.emedicine.com/pmr/topic112.htm

Background: In 1918, Dejerine and Ceillier first described heterotopic

ossification (HO) in paraplegic patients injured in World War I, referring to

the process as paraosteoarthropathy. HO has been defined as the formation of

mature lamellar bone in soft tissues. The process involves true osteoblastic

activity and bone formation. HO has been reported in cases of brain injury,

spinal cord injury (SCI), stroke, poliomyelitis, myelodysplasia, tabes dorsalis,

carbon monoxide poisoning, spinal cord tumors, syringomyelia, tetanus, and

multiple sclerosis (MS). This condition also has been reported after burns and

total hip replacement.

Several terms have been used to describe the condition, including heterotopic

ossification, ectopic ossification, and myositis ossificans. HO usually involves

the large joints of the body (eg, hips, elbows, shoulders, knees). Excessive

bone formation may result in significant disability by severely limiting the

range of motion (ROM) of these joints (see Picture 1).

The following 3 categories of HO have been described:

Myositis ossificans progressiva is a rare metabolic bone disease in children

with progressive metamorphosis of skeletal muscle to bone and is characterized

by an autosomal dominant pattern of genetic transmission.

Myositis ossificans circumscripta without trauma is a localized soft tissue

ossification after neurologic injury or burns. This process also is referred to

as neurogenic HO.

Traumatic myositis ossificans occurs from direct injury to the muscles.

Fibrous, cartilaginous, and osseous tissues near bone are affected. The muscle

may not be involved.

Pathophysiology: The specific cause and pathophysiology of HO remain unclear. HO

may be due to an interaction between local factors (eg, the pool of available

calcium in adjacent skeleton, soft-tissue edema, vascular stasis tissue hypoxia,

mesenchymal cells with osteoblastic activity) and an unknown systemic factor or

factors. The basic defect in HO is the inappropriate differentiation of

fibroblasts to bone-forming cells. Early edema of connective tissue proceeds to

tissue with foci of calcification and then to maturation of calcification and

ossification.

Frequency:

In the US: Reported incidence of HO varies. In cases of severe trauma or

insult to the central nervous system (CNS), 10-20% of patients develop HO, and

the condition has been observed in 20% of patients with severe brain injury. The

incidence is higher in patients who undergo open reduction and internal fixation

of a fracture. With an elbow fracture, dislocation, or fracture-dislocation, the

incidence of traumatic HO at the elbow approaches 90%. Traumatic HO of the elbow

occurs in 20% of forearm fractures. Fifty-five percent of patients with hip

fractures develop HO. The incidence increases to 83% if open reduction and

internal fixation are performed. The incidence is similar in the upper and lower

extremities.

An association has been cited between spasticity and HO. The incidence is higher

in a spastic extremity; 84% of patients with HO had spasticity, and 54% of

patients with HO had no spasticity. HO is seen in the elbow in 4% of patients

with traumatic brain injury (TBI); however, if fracture or dislocation is

associated with brain injury, the incidence of HO rises to 89%.

Internationally: Studies from Europe and Japan have shown the incidence of HO

from 11-76%, depending on the population studied and the method of detection.

Mortality/Morbidity: Only 10-20% of all HO patients have functionally

significant deficits.

Race: HO occurs without correlation to race.

Sex: The development of HO is independent of the patient's sex.

Age: Increased incidence of HO was found associated with age greater than 30

years. The incidence in children appears to be lower than in adults (8-22.5%).

CLINICAL Section 3 of 11 Author Information Introduction Clinical

Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures

Bibliography

History: The earliest sign of HO often is decreased joint ROM. Other findings

include swelling, erythema, heat, pain with ROM testing, and contracture

formation, but the condition may be occult. Fever also may be present. Patients

can experience pain, increased spasticity, vascular and nerve compression, and

lymphedema.

Physical: Ectopic bone usually forms around major joints (eg, the elbows,

shoulders, hips, knees) following brain injury, as well as over long-bone

fractures. The proximal interphalangeal joints of the hand, the wrist, and the

spine also may be affected. Local pain and a palpable mass may be noted in the

periarticular region, usually presenting 1-3 months after the injury, but the

onset of HO also has been reported at 1-7 months after severe brain injury.

HO can mimic thrombophlebitis, with pain, swelling, erythema, and induration of

the affected area. If HO affects a joint, a decrease in ROM often is observed.

Major long-term disability from untreated HO can include limited ROM or even

joint ankylosis.

In patients with a history of fractures, spasticity, and low-level

responsiveness, the detection of restricted motion should trigger suggestion of

HO. Excessive bone formation may result in significant disability by severely

limiting the ROM of a joint.

Causes: Patients with brain injuries are at greater risk for developing HO if

they have significant spasticity or increased muscle tone in the involved

extremity, duration of unconsciousness longer than 2 weeks, long-bone or

associated fractures, and decreased ROM. Therefore, the risk of development of

HO in a patient with brain injury increases as the severity of injury, length of

immobilization, and duration of coma increase. DIFFERENTIALS Section 4 of 11

Author Information Introduction Clinical Differentials Workup Treatment

Medication Follow-up Miscellaneous Pictures Bibliography

Related Articles

Continuing Education CME available for this topic. Click here to take this CME.

Patient Education Click here for patient education.

WORKUP Section 5 of 11 Author Information Introduction Clinical

Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures

Bibliography

Lab Studies:

Progressive loss of joint mobility and markers of increased osteoblastic

activity, such as an elevated fractionated alkaline phosphatase level, warrant a

comprehensive musculoskeletal examination with a 3-phase bone scan and

radiographs to confirm the presence, distribution, and extent of HO.

The diagnosis of HO following brain injury typically is made by the clinical

examination and by assessing for elevations in alkaline phosphatase. Early

increases in alkaline phosphatase may be difficult to interpret because the

level rises with other causes such as fractures or hepatotoxicity. The level of

alkaline phosphatase has been reported to parallel the activity of ossification.

When ossification stopped, the levels returned to normal. Alkaline phosphatase

fractionation studies reportedly can distinguish among different reasons for

electrical levels.

Osteocalcin, another marker of osteoblastic activity, does not appear to be

useful in the early detection of HO or in assessing its maturity. The

erythrocyte sedimentation rate (ESR) is too nonspecific to be of much help in

the diagnosis of HO, but an elevated level associated with other clinical

features suggests the need for further evaluation.

Imaging Studies:

Radiographs may not show abnormalities during the acute phase of erythema and

swelling. Later radiographs (1-2 weeks after onset) often show only soft tissue

swelling. Radiographs show immature ossification and then the appearance of

mature bone. HO may take 8-14 months to reach maturity. Plain radiographs may

not show evidence of HO until 4-5 weeks after injury. HO is located most

commonly inferior and medial to the humeral head on anteroposterior radiography.

Excision also may be undertaken to improve passive shoulder functions. CT scans

of the shoulder (cross-sections) and 3-dimensional reconstruction assist with

preoperative planning. Radiographic assessment of joints with HO may be limited

severely by difficulties with positioning the patient for the necessary view.

Other Tests:

Many clinicians rely on early detection of HO using triple-phase bone scan

technology. Triple-phase technetium 99 bone scanning detects early increases in

vascularity and is a reliable indicator in making a diagnosis. The first and

second phases of the triple-phase bone scan show increased uptake. Areas

demonstrating increased blood flow and soft tissue concentration of the tracer

on early imaging (blood flow phase) correlate with sites of subsequent HO

development. The optimal timing of the imaging for accurate assessment of the

presence of ectopic bone has not been established, but 3 weeks or more following

the injury should be sufficient for early detection.

Procedures:

Various authors who reviewed the association of the human leukocyte antigen

(HLA) system and HO have suggested a genetic predisposition to an associated

systemic factor; thus, an antigenic marker should be available to mark

susceptible patients. Others found no evidence of any association between the

HLA system and HO. An association between HLA-B 18 and patients with neurologic

disorders has been described, as well as an association with patients who

develop HO; however, 75% of patients with HO lack this marker.

Histologic Findings: Histologic examination demonstrates that tissue developed

through HO is composed of true osseous tissue, rather than of calcified soft

tissue. Heterotopic bone is metabolically active and exhibits approximately

triple the normal rate of bone formation and double the normal number of

osteoclasts. TREATMENT Section 6 of 11 Author Information Introduction

Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous

Pictures Bibliography

Rehabilitation Program:

Physical Therapy: The treatment of HO often is quite challenging and, in many

cases, unsatisfactory. Therefore, emphasis should be placed on the importance of

understanding the natural history of HO in developing treatment strategies. Most

cases of HO occur within 3 months after SCI. Most roentgenographic evaluation

occurs during a 6-month period, and progress of HO is related to the severity of

injury. In patients with severe injuries, roentgenographic progression subsided

by 6 months, and serum alkaline phosphatase and bone scan activity became normal

or significantly decreased. Patients with more severe deficits had larger

amounts of bone formation that progressed for more than 1 year, and elevated

alkaline phosphatase levels and increased bone scan activity were observed for

up to 2 years and, in some cases, longer.

The role of physical therapy in patients with HO is controversial. The major

goal of treatment is to maintain ROM and thereby preserve function; however,

opinions differ regarding ROM exercises for patients with HO.

Several authors have reviewed the literature that compares opposing

philosophies. One theory is that an aggressive regimen of passive ROM exercises

may predispose the patient to the development of HO because of microtrauma or

local hemorrhage. Several authors suggest that passive stretching and ROM

exercises are contraindicated after HO is suggested, but they recommend active

exercise within the pain-free range. Other authors stress the importance of ROM

exercises to maintain joint mobility and to prevent or retard fibrous ankylosis.

They found no evidence for increased HO or decreased ROM with passive ROM

exercises.

Forceful manipulation of joints with preexisting HO under anesthesia helps to

maintain useful joint ROM and to prevent ankylosis. Sixty-four percent of

affected joints maintained or gained ROM with rehabilitation after manipulation.

Some required repeated manipulations; none had a detectable increase in HO. The

literature generally supports the common use of active and gentle passive ROM

exercises to maintain available joint motion and to avoid progressive

contractures. If ankylosis seems inevitable despite exercises, it is best for

the patient if it occurs in the most functional position.

Medical Issues/Complications: The patient presents to the acute rehabilitation

hospital with an undoubted mixture of deforming spasticity and contracture 3

months after a severe head injury. As is often the case, such deformities had

additional time to develop because of the time needed to handle prolonged

complications in acute care (eg, craniotomy facial bone surgeries,

cholecystitis, pneumonia, other infections). In addition, the low level of

responsiveness during much of the hospital course often casts doubt in the mind

of acute care personnel about the patient's suitability for rehabilitation.

Aggressive measures to prevent deformities may be given a lesser priority,

especially if staff members are dealing with complications that have a greater

medical priority. The resulting deformities may be quite advanced by the time

the patient reaches acute rehabilitation, and intervention becomes more

difficult.

Surgical Intervention: Surgery for removal of ectopic bone should be undertaken

only for clear functional goals, such as improved standing posture or ambulation

or independent dressing and feeding. In general, surgery is not undertaken

earlier than 18 months after injury.

Excision should be considered for patients in whom shoulder motion is limited

severely by extensive heterotopic bone, especially if dynamic electromyography

(EMG) studies reveal volitional capacity for the various shoulder muscles.

Excision also may be undertaken to improve passive shoulder functions.

If HO restricts elbow motion, HO is excised surgically at maturation. Maturation

of HO is determined by the radiographic appearance of a defined cortex and by a

normal level of serum alkaline phosphatase. Additional prognostic indicators for

successful HO excision are good cognitive recovery (Rancho scale level VI or

greater) and selective motor control in the extremity. Time since onset of brain

injury alone is not an accurate prognosticator.

lf joint deformity from HO results in significant functional limitations, such

as difficulty with hygiene, sitting, or ambulation, surgical resection of HO may

be indicated. Surgery also may be appropriate if an underlying bone mass

contributes to repeated pressure sores. Various recommendations have been made

for the timing of surgery. Surgery is contraindicated in patients with clinical,

laboratory, or radiographic evidence of active ossification. Waiting for the

maturation of heterotopic bone before operating may take 1-2 years. Heterotopic

bone should be excised when it significantly restricts joint ROM and limits

function and rehabilitation. Other authors believe the process is stabilized

after 6-8 months and that surgery is of benefit after that time, although the

authors do not state whether radiation treatments were given.

In general, surgery should be delayed for 18 months after brain injury. Patients

with good neurologic recovery, with good motor control, normal or slightly

elevated levels of alkaline phosphatase, and a mature lesion may be candidates

for surgery before the 18 months. In more severely compromised patients, surgery

should be delayed longer than 18 months if motor control is still improving and

laboratory test values still indicate abnormalities. With such patients, the

major indication for surgery is limb positioning. Once HO has matured, at 12-18

months or more after injury, it can be removed surgically or partially resected

if clinically indicated. Post excision low-dose radiation or the use of EHDP can

prevent its recurrence.

Consultations:

Physiatrists - To plan the best rehabilitative approach

Neurologists - To rule out other neurologic impairments

Orthopedics surgeons - If any surgical treatment is necessary

Other Treatment (injection, manipulation, etc.): Forceful joint manipulation

appeared to enhance formation of HO, and it has been postulated that the force

generated by muscle spasticity may promote its development.

MEDICATION Section 7 of 11 Author Information Introduction Clinical

Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures

Bibliography

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Nonsteroidal anti-inflammatory drugs (NSAIDs) -- Have analgesic,

anti-inflammatory, and antipyretic activities. Their mechanism of action is not

known, but they may inhibit cyclo-oxygenase activity and prostaglandin

synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene

synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil

aggregation, and various cell-membrane functions. Drug Name

Indomethacin (Indocin, Indochron ER) -- An indoleacetic acid derivative and

NSAID, indomethacin is related structurally and pharmacologically to sulindac.

Theoretically, indomethacin decreases inflammation associated with HO and quiets

the spastic muscles driven by pain. The effect is thought to be due to

inhibition of the synthesis of prostaglandin. Indomethacin is known to be highly

potent in preventing HO after total hip replacement, due to one of the most

potent inhibitors of the cyclo-oxygenase enzyme, which catalyzes the formation

of prostaglandin precursors (endoperoxides) from arachidonic acid. Adult Dose25

mg PO tid for 3 mo after surgery Pediatric Dose1 mg/kg PO tid for 3 mo after

surgery ContraindicationsDocumented hypersensitivity; complete or partial

syndrome of nasal polyps, angioedema, or bronchospastic reactivity to aspirin or

other NSAIDs InteractionsRisks of bleeding increase with concomitant NSAIDs,

anticoagulant or heparin therapy, or alcohol ingestion; decreases

anti-hypertensive effects of alpha-adrenergic blocking agents; serum levels of

indomethacin are decreased slightly by concomitant aspirin and increased by

concomitant probenecid; renal elimination decreased and serum levels and toxic

effects of methotrexate and lithium increased by concomitant administration; GI

absorption delayed by food and milk; antihypertensive effects of thiazide

diuretics antagonized by indomethacin; antagonizes prostaglandin-mediated

natriuretic effects of loop diuretics PregnancyB - Usually safe but benefits

must outweigh the risks. PrecautionsCategory D in third trimester of pregnancy;

acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis,

and renal papillary necrosis may occur; increases risk of acute renal failure in

patients with preexisting renal disease or compromised renal perfusion;

reversible leukopenia may occur; discontinue if there is persistent leukopenia,

granulocytopenia, or thrombocytopenia

Drug Category: Bisphosphonate derivative -- Analogs of pyrophosphate and act by

binding to hydroxyapatite in bone-matrix, thereby inhibiting the dissolution of

crystals. Prevent osteoclast attachment to the bone matrix and osteoclast

recruitment and viability. Drug Name

Etidronate disodium (EHDP, Didronel) -- The role of etidronate disodium in

preventing HO has been studied extensively. The literature to date does not

support efficacy adequately in patients with brain injuries. EHDP is a

bisphosphonate that reportedly retards formation, growth, and dissolution of

hydroxyapatite crystals; therefore, it is thought to limit ectopic soft tissue

calcification by preventing conversion of calcium phosphate compounds in

hydroxyapatite crystals. EHDP often is used to retard HO once it is discovered;

thought to be more effective if given prophylactically or in the earlier stages

of formation. EHDP does not dissolve established calcification. An active HO

process is often painful and treatment with agents such as EHDP is often

effective in reducing the inflammatory aspects of the HO process and quieting

the spastic muscles driven by pain. Therefore, EHDP is the mainstay of drug

treatment by reducing the incidence and severity of ectopic bone formation with

minimal side effects. Effective prophylactic treatment should be

initiated as soon as possible.

Optimal drug dose and length of treatment have not been established adequately

in TBI. Adult DoseNot established; 20 mg/kg/d PO for 3 mo, followed by 10

mg/kg/d PO for 3-6 mo for a total of 6-9 mo suggested Pediatric DoseNot

established ContraindicationsDocumented hypersensitivity, hypocalcemia, and

renal impairment InteractionsCoadministration with calcium containing products

and other multivalent cations decrease absorption PregnancyB - Usually safe but

benefits must outweigh the risks. PrecautionsBecause effect on normal bone

healing is questionable, EHDP caution in long-bone fractures; GI side effects

(eg, diarrhea, nausea) are infrequent and can be minimized by dividing total

daily dose FOLLOW-UP Section 8 of 11 Author Information Introduction

Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous

Pictures Bibliography

Further Inpatient Care:

If, at discharge from acute care, the residual impairments are of such

severity that the patient remains dependent, options include either an acute or

subacute rehabilitation program. The typical candidate for a TBI acute

rehabilitation unit is the patient who is able to follow a one-step command

consistently, but often is confused, disoriented, and restless, if not overtly

agitated; many have a combination of physical limitations or medical

complications. The ideal goal of this phase of rehabilitation is to assist the

patient from the late stages of unconsciousness through the clearing of

posttraumatic amnesia, resolution of agitation, and at least minimal

independence in activities of daily living (ADL). For both patient and family,

the most salient goal of the acute rehabilitation phase is to regain optimal

independence in ADL. To remain in this rehabilitation environment, the patient

must be able to tolerate and benefit from a minimum of 3 hours of therapy, 5

days per week.

Subacute rehabilitation programs are largely based in nursing homes. Such

programs do not require that the patient tolerate 8 hours of therapy per day.

Consequently, subacute rehabilitation programs are most appropriate for patients

who remain in the coma stages, respond to simple commands inconsistently, or

show a low rate of progress. The typical length of stay is considerably longer

than the present national average of approximately 30 days in acute

rehabilitation. Largely because of staffing and overhead, subacute

rehabilitation offers health care providers a less expensive form of specialized

intervention. Although data support the importance of early rehabilitation

interventions to outcome, virtually no data compare the outcomes of acute versus

subacute intervention.

Further Outpatient Care:

After documenting the extent of impairment and estimating functional outcome,

the physiatrist should determine the most appropriate rehabilitation

interventions. Early rehabilitation is initiated while the patient remains on

the trauma or neurosurgical service units. Rehabilitation options after this

early stage are predicated on the nature of residual impairments. In the

unlikely event that a patient with severe TBI recovers sufficiently during acute

care to permit rehabilitation management on an outpatient basis, individual

outpatient services or a day treatment program may be recommended. Day treatment

rehabilitation typically offers integrated programs of physical therapy,

occupational therapy, speech therapy, cognitive remediation, and psychological

services up to 8 hours per day, 5 days a week.

Transfer:

After inpatient rehabilitation, a number of postacute management strategies

are available once the patient is ready to be transferred from inpatient

rehabilitation. If the patient can be given effective treatment at home, then

rehabilitation options include individual in-home or outpatient therapy or

comprehensive day treatment services. If the patient in an acute rehabilitation

setting fails to achieve basic functional independence in a timely fashion,

transfer to a subacute rehabilitation program may be warranted. In the event

that behavioral problems such as agitation preclude discharge to the home, more

specialized inpatient behavioral treatment programs are indicated. Another level

in the continuum of rehabilitation includes transitional living programs, which

typically are residential community-based alternatives for patients with

primarily cognitive and neurobehavioral deficits.

Deterrence/Prevention:

Various recommendations have been made to prevent recurrence of HO. Low-dose

radiation is thought to be effective in the immediate postoperative phase.

Low-dose radiation also has been used to prevent HO. The recommended dose is

2000 rads over 12 days for extensive lesions and 1000 rads over 5-7 days for

small lesions of HO. Radiation is thought to prevent conversion of mesenchymal

cells to bone precursor cells. As a result, concerns about neoplasia limit its

application in younger patient groups.

Complications:

Once developed, HO may cause complications through pressure on surrounding

anatomic structures. Peripheral nerve compression and vascular compression with

subsequent thrombophlebitis and lymphedema may result from HO. As a result,

serial evaluation of deep tendon reflexes is recommended to track peripheral

nerve function. The most common complication is decreased ROM, which in rare

cases may progress to joint ankylosis.

Prognosis:

Patients who have higher functional abilities and exhibit normal alkaline

phosphatase levels are less likely to experience recurrence of HO.

Patient Education:

At 3 months after injury, families often have high hopes for recovery,

especially if certain milestone signs have recently appeared. The patient

recently may have begun to speak and follow some voluntary commands. Family

members are elated to see these signs, which give them hope for future recovery

and possible avoidance of many other problems. Moreover, because speech seems to

be returning spontaneously, the family could hope for spontaneous remission of

deformities.

Expectations tend to color the family's perception and understanding of the

limits of recovery, the nature of the various pathologies, and the effects and

side effects of medical intervention. For example, spasticity of a muscle may

give way to voluntary activity as neurologic recovery unfolds during the first

9-18 months after head injury. Families, therefore, may think that contracture

of the same spastic muscle also disappears when voluntary movement recovers.

Aggressive interventions for contracture in the spastic state, therefore, may

not make sense to the family. Education of the family clearly is needed, but

what they need to know may well depend on drawing out their beliefs, hopes, and

expectations. The educational campaign is designed to promote compliance with

clinical goals.

MISCELLANEOUS Section 9 of 11 Author Information Introduction Clinical

Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures

Bibliography

Medical/Legal Pitfalls:

Surgery for HO is challenging because the ossified mass is highly vascular;

postoperative bleeding, hematoma, and infection are common complications. Trauma

to nerves also may occur. Preoperative CT scans may guide the surgeon and lower

the rate of complications. Active ROM exercises may be initiated 2-3 days after

surgery. More active exercises may begin about 10-14 days after pain and

swelling have subsided. Patients with more severe cognitive and motor deficits

may require several months of postoperative physical therapy to maintain ROM. If

HO recurs, it becomes evident within 3 months after surgery.

Special Concerns:

Indications for treatment of increased muscle tone

Interference with active movement

Contracture formation or progression in a posturing limb

Interference with appropriate positioning or hygiene

Self-inflicted trauma during muscle spasms

Excessive pain with ROM exercises or during muscle spasms

Excessive therapy time devoted to contracture prevention rather than

functional activities

Prevention of HO

mattosma mattosma@...> wrote:

Hi Everyone,

I am contemplating hip resurfacing to my right hip. However I have

been warned about the increased possibility of developing heterotopic

ossification (HO) as a post-operative complication. Has anyone out

there developed this complicationo. If so I would appreciate hearing

about your experience. Also does anyone know of any data looking at

the incidence of HO following hip resurfacing?

Thanks,

Mark M

April 1, 2004

Hi Mark,

I developed severe (Booker Stage IV) H.O. after right hip resurfacing

Feb. 03. I was just unlucky - " young " (44) white male - highest risk

group for HO. I had the standard prophylaxis - 25mg indomethacin,

3X, for a week. It's quoted around 95% effective in preventing

H.O., and of the 5 % who form it, only a few of those develop growth

which actually inhibits movement.

I had less than 60 degree hip flexion by several weeks post-op - the

bone growth happens pretty quickly. Couldn't put shoes or socks on,

couldn't reach the handlebars of a bicycle.

However, I must stress H.O. is a VERY LOW risk - I was only the 2nd

of over 650 hip resurfacings by my surgeon requiring surgical

excision of the H.O.

There is a theory that resurfacing is perhaps more susceptible to

H.O. formation than standard hip replacements - more bone dust

generated during the surgery (femoral head shaping) which " may "

contribute to H.O. - just a theory.

if your family has any history of it, or you are in a risk group, you

could be susceptible - talk w/your surgeon. I believe there's a test

for susceptibility, but it's not a high-confidence test - i.e., not a

firm indicator.

Anyway, it can be fixed - I'm an example. I went back this past

October - my resurfacing device was dislocated, and the bone cut

out. Also, I had the most effective (and expensive) prophylaxis this

time - pre-op low dose 700 rad local radiation - 99% efficacy. I now

have at least 115 degrees flexion and feel great.

yes - it was a drag to have to go thru another surgery/recovery, but

at least it could be fixed and the implant wasn't affected.

Feel free to email me directly with questions.

Andy

> Hi Everyone,

> I am contemplating hip resurfacing to my right hip. However I have

> been warned about the increased possibility of developing

heterotopic

> ossification (HO) as a post-operative complication. Has anyone out

> there developed this complicationo. If so I would appreciate

hearing

> about your experience. Also does anyone know of any data looking

at

> the incidence of HO following hip resurfacing?

> Thanks,

> Mark M

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