By Dr Ann Noble ZachariahMD Resident

Department of Physical Medicine and Rehabilitation

DefinitionHO is the formation of lamellar bone within the soft tissue surrounding the joint Can occur in skin, subcutaneous tissue , skeletal muscles and fibrous tissue surrounding the bone. First described by Patin in 1692 – while working with children with myositis ossifican progressiva In 1918, Dejerine & Ceillier detailed the anatomical, clinical, and histological features of HO

Site of HOOnly the joints below the Neurological level

of Injury will develop HOThe most common sites are - Hip - Knee - Shoulders Other sites also include spine, elbow, wrist.

Incidence of HOFollowing lower extremity amputee→ about

7%Following traumatic brain injuries→ 11%

(ranges reported from 10-20%)Following spinal cord injuries→ 20% (ranges

reported from 20-40%)Following THR→ 53% (ranges reported from

0.6-90%)Following TKR→ 15% (ranges reported from

1-42%)

Risk Factors

- Older age (children and adolescents have a lower incidence) -Neurological complete lesions - Male gender - Spasticity - DVT - Pressure sores - Fractures

Etiology Exact etiopathophysiology is unknownBone morphogenic protein ( released in TBI )

plays a key role Damage to the sympathetic tracts in the

spinal cord - promote HO by increasing the local vascularity and blood perfusion around the joint.

When passive ROM is delayed more than 1 week after injury.

Forced ROM of contracted limb may cause micro trauma and bleeding, leading to HO

Pathophysiology

Classification of HO

HO in Hip HO in Knee

Clinical featuresClinical signs and symptoms usually appear

with 3 – 12 weeks Symptoms include - Pain - Malaise - Low grade fever - Warmth of the joint - Increase in spasticity the initial inflammatory phase of HO may

mimic other pathologies such as cellulitis, thrombophlebitis, osteomyelitis, or a tumorous process

Associated Comorbidities Traumatic Brain InjuryTraumatic Spinal Cord injuryAnkylosing spondylitisRhuematoid arthritisHypertrophic osteoarthitisDiffuse idiopathic skeletal hyperostosisPaget's disease

Differential Diagnosis Tumours – Osteosarcoma, Osteochrondroma Infections- Osteomyelitis Inflammation – Cellulitis Circulatory complications – Deep Vein

Thrombosis , Thromphoblebitis

Investigations Alkaline Phosphatase is frequently used in early detection of HO. It has high sensitivity, low specificity.Serum ALP levels can be dependent on renal and hepatic function, so they are not always useful.An elevation of serum creatinine phosphokinase(CPK) may be a more reliable predictor of HO Elevated levels of nonspecific markers of inflammation such as C-reactive protein (CRP) and the erythrocyte sedimentation rate (ESR) can be useful CRP is a more reliable predictor of disease activity, with normalization of the CRP correlating with resolution of the inflammatory phase of HO

Prostoglandin E2: - monitior PGE2 excretion in 24-hour urinalysis - PGE2 felt to be reliable bone marker for early

detection and determining treatment efficacy  - A sudden increase is an indication for bone

scintigraphy

Urinary excretion of hydroxyproline and collagen metabolites correlates with alkaline phosphatase levels and can also serve as indirect markers for the presence of HO.

Radiological ImagingThree Phase bone scintigraphy

both diagnostic and therapeutic follow-up purposes most sensitive imaging modality for early detection Phases 1 and 2 are indicative of hyperaemia and blood pooling (precursors to process of HO) Usually positive after 2-4 weeks Serial bone scans used to monitor metabolic activity of HO to determine optimal timing for surgical resection and to predict postoperative occurrence

Bone Scan showing Heterotrophic Ossification of Right Hip

Radiography, MRI, CT Scan:all have low specificity in early stage of disease process better for detection in later stages when ossification is

more pronouncedMRI and CT are valuable pre-operative tools to

determine relationship to blood vessels and peripheral nerve structures 

HO demonstrable on radiographs 4-6 weeks post-injury MRI better than radiograph at detecting HO in early

phasesPlain film radiographs are most commonly used due to

their simplicity and low cost.Typical radiologic presentation of HO is circumfrential

ossification with a lucent center

CT scan showing heterotrophic ossification of proximal femur

Ultrasonography:earlier detection than conventional

radiographlocal signs of inflammation in SCI patients

are suggestive of HOhigh sensitivity and specificity for early

detection of HO 1-week post-THR.

Medical ManagementThe two types of medications shown to have both prophylactic and treatment benefits are as follows:

Non-steroidal anti-inflammatory drugs: NSAIDSIndomethacin -inhibition of the differentiation of mesenchymal cells into osteogenic cells. - inhibition of post-traumatic bone remodelling by suppression of prostaglandin-mediated response Dose – 25 mg TID Bisphosphonates: - inhibition of calcium phosphate precipitation - slowing of hydroxyapatite crystal aggregation -inhibition of the transformation of calcium phosphate to hydroxyapatite

Treatment with bisphosphonates - decrease the rate of new bone formation in patients with HO; however, it has no effect on bone which has already been deposited. -Disodium etidronate inhibits osteoclastic activity and conversion of calcium phosphate to hydroxyapatite. - Although IV administration of etidronate reportedly led to quicker resolution of edema with less rebound formation after the medication was discontinued, it is no longer available. - Current recommendation is for oral administration of etidronate 20 mg/kg/d for 6 months if the CPK level is elevated at the time of diagnosis or 20 mg/kg/d for 3 months, followed by 10 mg/kg/d for an additional 3 months if the initial CPK level is normal

RadiotherapyThe use of radiotherapy as a prophylactic

treatment comes mainly from the literature concerning total hip arthroplasty.

Radiating pluripotential mesenchymal cells may effectively prevent the development of HO. 

A dose of 700-800 cGy of local radiation in the first four post-operative days has shown to prevent HO formation in patients who are at high risk.

Surgical managementThe two main goals of sugical intervention

are to alter the position of the affected joint or improve its range of motion (ROM).

Clinicians must determine if the lesion has reached maturation before surgical excision to decrease the risk of intraoperative complications such as hemorrhage, and the reoccurance of the ectopic lesion.

The use of bone scans to determine metabolic activity of the lesion and serum ALP levels are common aids in this decision making process.

Criteria for surgical removal of HOThe criteria are as follows:significantly limited ROM of involved joint (should have < 50oROM); for most patients, progression to joint ankylosis is the most serious complication of heterotopic ossification.Absence of local fever, swelling, erythema, or other clinical findings of acute heterotopic ossification.Normal serum alkaline phosphate levels.Return of bone scan findings to normal or near normal; if serial quantitative bone scans are obtained, there should be a sharply decreasing trend followed by a steady state for 2-3 months.

Rehabilitation MeasuresPhysical therapy along with pharmacotherapy

has been shown to benefit patients suffering from heterotopic ossification.

Pre-operative PT can be used to help preserve the structures around the lesion.

ROM exercises (PROM, AAROM, AROM) and strengthening will help prevent muscle atrophy and preserve joint motion.

Therapy which is too aggressive can aggrevate the condition and lead to inflammation, erythema, hemorrhage, and increased pain.

Post-operative rehabilitation has also shown benefit patients with recent surgical resection of heterotopic ossification. 

The post-op management of HO is similar to pre-op treatment but much more emphasis is placed on edema control, scar management, and infection prevention. 

Phases of RehabPhase I (Week 1) Goals

Prevent infectionProtect and decrease stress on surgical siteDecrease painControl and decrease edemaROM to 80% of affected jointMaintain ROM of joint proximal and distal to

surgical site

Phase II ( 2 – 8 weeks ) Goals Reduce painManage edemaEncourage limited ADL performancesPromote scar mobility and proper remodelingPromote full ROM of affected jointEncourage quality muscle contractions

Phase III (9-24 weeks)GoalsSelf-manage painPrevent flare-up with functional activitiesImprove strengthImprove ROM (if still limited)Return to previous levels of activity