DEGENERATIVE DISEASES OF THE JOINTS AND SPINE COLUMN (OSTEOARTHRITIS, OSTEOCHONDROSIS

DEGENERATIVE DISEASES OF THE JOINTS AND SPINE COLUMN (OSTEOARTHRITIS, OSTEOCHONDROSIS

Practice Essentials

Osteoarthritis is the most common type of joint disease, affecting more than 20 million individuals in the United States alone. It can be thought of as a degenerative disorder arising from the biochemical breakdown of articular (hyaline) cartilage in the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but also the entire joint organ, including the subchondral bone and synovium.

The FDA has approved diclofenac sodium topical solution 2% w/w (Pennsaid 2%, Nuvo Research Inc) for knee pain associated with osteoarthritis. It is dosed twice daily; Pennsaid 1.5% w/w, which has been available in the United States since 2010, is dosed 4 times a day. The drug is contraindicated in patients with a known hypersensitivity and in those who have experienced asthma, urticaria, or allergic-type reactions after taking aspirin or other NSAIDs.^[1]

Symptoms of osteoarthritis include the following:

·                Deep, achy joint pain exacerbated by extensive use – The disease’s primary symptom

·                Reduced range of motion and crepitus – Frequently present

·                Stiffness during rest (gelling) – May develop, with morning joint stiffness usually lasting for less than 30 minutes

Osteoarthritis of the hand

·                Distal interphalangeal (DIP) joints are most often affected

·                Proximal interphalangeal (PIP) joints and the joints at the base of the thumb are also typically involved

·                Heberdeodes, which represent palpable osteophytes in the DIP joints, are more characteristic in women than in men

·                Inflammatory changes are typically absent or at least not pronounced

See Clinical Presentation for more detail.

Osteoarthritis is typically diagnosed on the basis of clinical and radiographic evidence.^{[2, 3, 4, 5, 6]} No specific laboratory abnormalities are associated with osteoarthritis.

Imaging studies

·                Plain radiography – The imaging method of choice because radiographs are cost-effective and can be readily and quickly obtained^{[4, 7]} ; in the load-bearing areas, radiographs can depict joint-space loss, as well as subchondral bony sclerosis and cyst formation

·                Computed tomography (CT) scanning – Rarely used in the diagnosis of primary osteoarthritis; however, it may be used in the diagnosis of malalignment of the patellofemoral joint or of the foot and ankle joints

·                Magnetic resonance imaging (MRI) – Not necessary in most patients with osteoarthritis unless additional pathology amenable to surgical repair is suspected; unlike radiography, MRI can directly visualize articular cartilage and other joint tissues (eg, meniscus, tendon, muscle, or effusion)

·                Ultrasonography – No role in the routine clinical assessment of patients with osteoarthritis; however, it is being investigated as a tool for monitoring cartilage degeneration, and it can be used for guided injections of joints not easily accessed without imaging

·                Bone scanning – May be helpful in the early diagnosis of osteoarthritis of the hand^[8] ; bone scans also can help differentiate osteoarthritis from osteomyelitis and bone metastases

Arthrocentesis

The presence of noninflammatory joint fluid helps distinguish osteoarthritis from other causes of joint pain. Other synovial fluid findings that aid in the differentiation of osteoarthritis from other conditions are negative Gram stains and cultures, as well as the absence of crystals when fluid is viewed under a polarized microscope.

See Workup for more detail.

Nonpharmacologic interventions

The cornerstones of osteoarthritis therapy, nonpharmacologic interventions include the following:

·                Patient education

·                Heat and cold

·                Weight loss^[9]

·                Exercise

·                Physical therapy

·                Occupational therapy

·                Unloading in certain joints (eg, knee and hip)

Pharmacologic therapy

For hand osteoarthritis, the American College of Rheumatology (ACR) conditionally recommends using one or more of the following:

·                Topical capsaicin

·                Topical nonsteroidal anti-inflammatory drugs (NSAIDs) – Including trolamine salicylate

·                Oral NSAIDs

·                Tramadol

For knee osteoarthritis, the ACR conditionally recommends using one of the following:

·                Acetaminophen

·                Oral NSAIDs

·                Topical NSAIDs

·                Tramadol

·                Intra-articular corticosteroid injections

For hip osteoarthritis, the ACR conditionally recommends using 1 or more of the following for initial management:

·                Acetaminophen

·                Oral NSAIDs

·                Tramadol

·                Intra-articular corticosteroid injections

Surgery

A referral to an orthopedic surgeon may be necessary if the osteoarthritis fails to respond to a medical management plan. Surgical procedures for osteoarthritis include the following:

·                Arthroscopy

·                Osteotomy

·                Arthroplasty – Particularly with knee or hip osteoarthritis

·                Fusion

See Treatment and Medication for more detail.

This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it may occur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.

Background

Osteoarthritis is the most common type of joint disease, affecting more than 20 million individuals in the United States alone (see Epidemiology). It represents a heterogeneous group of conditions resulting in common histopathologic and radiologic changes. It can be thought of as a degenerative disorder arising from biochemical breakdown of articular (hyaline) cartilage in the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but also the entire joint organ, including the subchondral bone and synovium.

Osteoarthritis predominantly involves the weight-bearing joints, including the knees, hips, cervical and lumbosacral spine, and feet. Other commonly affected joints include the distal interphalangeal (DIP), proximal interphalangeal (PIP), and carpometacarpal (CMC) joints. This article primarily focuses on osteoarthritis of the hand, knee, and hip joints (see Pathophysiology). For more information on arthritis in other joints, see Glenohumeral Arthritis and Wrist Arthritis.

Although osteoarthritis was previously thought to be caused largely by excessive wear and tear, increasing evidence points to the contributions of abnormal mechanics and inflammation. Therefore, the term degenerative joint disease is no longer appropriate in referring to osteoarthritis. (See Pathophysiology.)

Historically, osteoarthritis has been divided into primary and secondary forms, though this division is somewhat artificial. Secondary osteoarthritis is conceptually easier to understand: It refers to disease of the synovial joints that results from some predisposing condition that has adversely altered the joint tissues (eg, trauma to articular cartilage or subchondral bone). Secondary osteoarthritis can occur in relatively young individuals (see Etiology).^{[10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20]}

The definition of primary osteoarthritis is more nebulous. Although this form of osteoarthritis is related to the aging process and typically occurs in older individuals, it is, in the broadest sense of the term, an idiopathic phenomenon, occurring in previously intact joints and having no apparent initiating factor.

Some clinicians limit the term primary osteoarthritis to the joints of the hands (specifically, the DIP and PIP joints and the joints at the base of the thumb). Others include the knees, hips, and spine (apophyseal articulations) as well.

As underlying causes of osteoarthritis are discovered, the term primary, or idiopathic, osteoarthritis may become obsolete. For instance, many investigators believe that most cases of primary osteoarthritis of the hip may, in fact, be due to subtle or even unrecognizable congenital or developmental defects.

No specific laboratory abnormalities are associated with osteoarthritis. Rather, it is typically diagnosed on the basis of clinical findings, with or without radiographic studies (see Workup).

The goals of osteoarthritis treatment include pain alleviation and improvement of functional status. Nonpharmacologic interventions are the cornerstones of osteoarthritis therapy and include the following:

·                Patient education

·                Application of heat and cold

·                Weight loss

·                Exercise

·                Physical therapy

·                Occupational therapy

·                Joint unloading, in certain joints (eg, knee and hip)

Intra-articular pharmacologic therapy includes corticosteroid injection and viscosupplementation, which may provide pain relief and have an anti-inflammatory effect on the affected joint. (See Treatment.) Oral pharmacologic therapy begins with acetaminophen for mild or moderate pain without apparent inflammation.

If the clinical response to acetaminophen is not satisfactory or the clinical presentation is inflammatory, consider nonsteroidal anti-inflammatory drugs (NSAIDs). (See Medication.) If all other modalities are ineffective and osteotomy is not viable, or if a patient cannot perform his or her daily activities despite maximal therapy, arthroplasty is indicated.

The high prevalence of osteoarthritis entails significant costs to society. Direct costs include clinician visits, medications, and surgical intervention. Indirect costs include such items as time lost from work.

Costs associated with osteoarthritis can be particularly significant for elderly persons, who face potential loss of independence and who may need help with daily living activities. As the populations of developed nations age over the coming decades, the need for better understanding of osteoarthritis and for improved therapeutic alternatives will continue to grow. (See Epidemiology.)

Anatomy

Joints can be classified in either functional or structural terms. A functional classification, based on movement, would categorize joints as follows:

·                Synarthroses (immovable)

·                Amphiarthroses (slightly moveable)

·                Diarthroses (freely moveable)

A structural classification would categorize joints as follows:

·                Synovial

·                Fibrous

·                Cartilaginous

Normal synovial joints allow a significant amount of motion along their extremely smooth articular surface. These joints are composed of the following:

·                Articular cartilage

·                Subchondral bone

·                Synovial membrane

·                Synovial fluid

·                Joint capsule

The normal articular surface of synovial joints consists of articular cartilage (composed of chondrocytes) surrounded by an extracellular matrix that includes various macromolecules, most importantly proteoglycans and collagen. The cartilage facilitates joint function and protects the underlying subchondral bone by distributing large loads, maintaining low contact stresses, and reducing friction at the joint.

Synovial fluid is formed through a serum ultrafiltration process by cells that form the synovial membrane (synoviocytes). Synovial cells also manufacture hyaluronic acid (HA, also known as hyaluronate), a glycosaminoglycan that is the major noncellular component of synovial fluid. Synovial fluid supplies nutrients to the avascular articular cartilage; it also provides the viscosity needed to absorb shock from slow movements, as well as the elasticity required to absorb shock from rapid movements.

Pathophysiology

Primary and secondary osteoarthritis are not separable on a pathologic basis, though bilateral symmetry is often seen in cases of primary osteoarthritis, particularly when the hands are affected.^{[2, 21]} Traditionally, osteoarthritis was thought to affect primarily the articular cartilage of synovial joints; however, pathophysiologic changes are also known to occur in the synovial fluid, as well as in the underlying (subchondral) bone, the overlying joint capsule, and other joint tissues (see Workup).^{[22, 23, 24, 25]}

Although osteoarthritis has been classified as a noninflammatory arthritis, increasing evidence has shown that inflammation occurs as cytokines and metalloproteinases are released into the joint. These agents are involved in the excessive matrix degradation that characterizes cartilage degeneration in osteoarthritis.^[26] Therefore, it is no longer appropriate to use the term degenerative joint disease when referring to osteoarthritis.

In early osteoarthritis, swelling of the cartilage usually occurs, because of the increased synthesis of proteoglycans; this reflects an effort by the chondrocytes to repair cartilage damage. This stage may last for years or decades and is characterized by hypertrophic repair of the articular cartilage.

As osteoarthritis progresses, however, the level of proteoglycans eventually drops very low, causing the cartilage to soften and lose elasticity and thereby further compromising joint surface integrity. Microscopically, flaking and fibrillations (vertical clefts) develop along the normally smooth articular cartilage on the surface of an osteoarthritic joint. Over time, the loss of cartilage results in loss of joint space.

In major weight-bearing joints of persons with osteoarthritis, a greater loss of joint space occurs at those areas experiencing the highest loads. This effect contrasts with that of inflammatory arthritides, in which uniform joint-space narrowing is the rule.

In the osteoarthritic knee, for example, the greatest loss of joint space is commonly seen in the medial femorotibial compartment, though the lateral femorotibial compartment and patellofemoral compartment may also be affected. Collapse of the medial or lateral compartments may result in varus or valgus deformities, respectively.

Erosion of the damaged cartilage in an osteoarthritic joint progresses until the underlying bone is exposed. Bone denuded of its protective cartilage continues to articulate with the opposing surface. Eventually, the increasing stresses exceed the biomechanical yield strength of the bone. The subchondral bone responds with vascular invasion and increased cellularity, becoming thickened and dense (a process known as eburnation) at areas of pressure.^[27]

The traumatized subchondral bone may also undergo cystic degeneration, which is attributable either to osseous necrosis secondary to chronic impaction or to the intrusion of synovial fluid. Osteoarthritic cysts are also referred to as subchondral cysts, pseudocysts, or geodes (the preferred European term) and may range from 2 to 20 mm in diameter. Osteoarthritic cysts in the acetabulum (see the image below) are termed Egger cysts.

This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it may occur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.

At areas along the articular margin, vascularization of subchondral marrow, osseous metaplasia of synovial connective tissue, and ossifying cartilaginous protrusions lead to irregular outgrowth of new bone (osteophytes). Fragmentation of these osteophytes or of the articular cartilage itself results in the presence of intra-articular loose bodies (joint mice).

Along with joint damage, osteoarthritis may also lead to pathophysiologic changes in associated ligaments and the neuromuscular apparatus. For example, lateral collateral ligament complex abnormalities are common in knee osteoarthritis.

Pain, the main presenting symptom of osteoarthritis, is presumed to arise from a combination of mechanisms, including the following:

·                Osteophytic periosteal elevation

·                Vascular congestion of subchondral bone, leading to increased intraosseous pressure

·                Synovitis with activation of synovial membrane nociceptors

·                Fatigue in muscles that cross the joint

·                Overall joint contracture

·                Joint effusion and stretching of the joint capsule

·                Torn menisci

·                Inflammation of periarticular bursae

·                Periarticular muscle spasm

·                Psychological factors

·                Crepitus (a rough or crunchy sensation)

·                Central pain sensitization

When the spine is involved in osteoarthritis, especially the lumbar spine, the associated changes are very commonly seen from L3 through L5. Symptoms include pain, stiffness, and occasional radicular pain from spinal stenosis. Foraminal narrowing is caused by facet arthritic changes that result in compression of the nerve roots. Acquired spondylolisthesis is a common complication of arthritis of the lumbar spine.

Etiology

The daily stresses applied to the joints, especially the weight-bearing joints (eg, ankle, knee, and hip), play an important role in the development of osteoarthritis. Most investigators believe that degenerative alterations in osteoarthritis primarily begin in the articular cartilage, as a result of either excessive loading of a healthy joint or relatively normal loading of a previously disturbed joint. External forces accelerate the catabolic effects of the chondrocytes and further disrupt the cartilaginous matrix.^{[28, 29, 30, 31]}

Risk factors for osteoarthritis include the following^{[32, 33, 34, 35]} :

·                Age

·                Obesity^{[36, 37, 38]}

·                Trauma

·                Genetics (significant family history)

·                Reduced levels of sex hormones

·                Muscle weakness^[39]

·                Repetitive use (ie, jobs requiring heavy labor and bending)^[40]

·                Infection

·                Crystal deposition

·                Acromegaly

·                Previous inflammatory arthritis (eg, burnt-out rheumatoid arthritis)

·                Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, and Wilson disease)

·                Hemoglobinopathies (eg, sickle cell disease and thalassemia)

·                Neuropathic disorders leading to a Charcot joint (eg, syringomyelia, tabes dorsalis, and diabetes)

·                Underlying morphologic risk factors (eg, congenital hip dislocation and slipped femoral capital epiphysis)

·                Disorders of bone (eg, Paget disease and avascular necrosis)

·                Previous surgical procedures (eg, meniscectomy)

With advancing age come reductions in cartilage volume, proteoglycan content, cartilage vascularization, and cartilage perfusion. These changes may result in certain characteristic radiologic features, including a narrowed joint space and marginal osteophytes. However, biochemical and pathophysiologic findings support the notion that age alone is an insufficient cause of osteoarthritis.

Obesity increases the mechanical stress in a weight-bearing joint. It has been strongly linked to osteoarthritis of the knees and, to a lesser extent, of the hips. A study that evaluated the associations between body mass index (BMI) over 14 years and knee pain at year 15 in 594 women found that a higher BMI at year 1 and a significant increase in BMI over 15 years were predictors of bilateral knee pain at year 15.^[38] The association between BMI increase and knee pain was independent of radiographic changes.

In addition to its mechanical effects, obesity may be an inflammatory risk factor for osteoarthritis. Obesity is associated with increased levels (both systemic and intra-articular) of adipokines (cytokines derived from adipose tissue), which may promote chronic, low-grade inflammation in joints.^[41]

Trauma or surgery (including surgical repair of traumatic injury) involving the articular cartilage, ligaments, or menisci can lead to abnormal biomechanics in the joints and accelerate osteoarthritis. Although repairs of ligament and meniscal injuries usually restore joint function, osteoarthritis has been observed 5-15 years afterward in 50-60% of patients.^[42]

Insults to the joints may occur even in the absence of obvious trauma. Microtrauma may also cause damage, especially in individuals whose occupation or lifestyle involves frequent squatting, stair-climbing, or kneeling.

Muscle dysfunction compromises the body’s neuromuscular protective mechanisms, leading to increased joint motion and ultimately resulting in osteoarthritis. This effect underscores the need for continued muscle toning exercises as a means of preventing muscle dysfunction.

Valgus malalignment at the knee has been shown to increase the incidence and risk of radiographic progression of knee osteoarthritis involving the lateral compartment.^[43]

A hereditary component, particularly in osteoarthritis presentations involving multiple joints, has long been recognized.^{[44, 45, 46]} Several genes have been directly associated with osteoarthritis,^[47] and many more have been determined to be associated with contributing factors, such as excessive inflammation and obesity.

Genes in the BMP (bone morphogenetic protein) and WNT (wingless-type) signaling cascades have been implicated in osteoarthritis. Two genes in particular,GDF5 (growth and differentiation factor 5) and FRZB (frizzled related protein) have been identified in the articular cartilage in animal studies and share a strong correlation with osteoarthritis.^{[48, 49, 50, 51]}

Genome-wide association studies (GWAS) have identified an association between osteoarthritis of large joints and the MCF2L gene. This gene is key ieurotrophin-mediated regulation of peripheral nervous system cell motility.^[52]

Genetic factors are also important in certain heritable developmental defects and skeletal anomalies that can cause congenital misalignment of joints. These may result in damage to cartilage and the structure of the joint.

Currently, clinical genetic testing is not offered to patients who have osteoarthritis unless they also have other anomalies that could be associated with a genetic condition. In the future, testing may allow individualization of therapeutics.

Epidemiology

Osteoarthritis affects more than 20 million individuals in the United States, though statistical figures are influenced by how the condition is defined—that is, by self-report, by radiographic or symptomatic criteria, or by a combination of these.^[53]On the basis of the radiographic criteria for osteoarthritis, more 50% of adults older than 65 years are affected by the disease.

Internationally, osteoarthritis is the most common articular disease. Estimates of its frequency vary across different populations.

Primary osteoarthritis is a common disorder of the elderly, and patients are often asymptomatic. Approximately 80-90% of individuals older than 65 years have evidence of radiographic primary osteoarthritis.^[54]

Symptoms typically do not become noticeable until after the age of 50 years. The prevalence of the disease increases dramatically among persons older than 50 years, likely because of age-related alterations in collagen and proteoglycans that decrease the tensile strength of the joint cartilage and because of a diminished nutrient supply to the cartilage.^[54]

In individuals older than 55 years, the prevalence of osteoarthritis is higher among women than among men.^[54] Women are especially susceptible to osteoarthritis in the DIP joints of the fingers. Women also have osteoarthritis of the knee joints more frequently than men do, with a female-to-male incidence ratio of 1.7:1. Women are also more prone to erosive osteoarthritis, with a female-to-male ratio of about 12:1.

Interethnic differences in the prevalence of osteoarthritis have been noted.^[55] The disorder is more prevalent in Native Americans than in the general population. Disease of the hip is seen less frequently in Chinese patients from Hong Kong than in age-matched white populations. Symptomatic knee osteoarthritis is extremely common in China.^[56]

In persons older than 65 years, osteoarthritis is more common in whites than in blacks. Knee osteoarthritis appears to be more common in black women than in other groups. Jordan et al found that in comparison with whites, African American men and women had a slightly higher prevalence of radiographic and symptomatic knee osteoarthritis but a significantly higher prevalence of severe radiographic knee osteoarthritis.^[57]

Prognosis

The prognosis in patients with osteoarthritis depends on the joints involved and on the severity of the condition. No proven disease- or structure-modifying drugs for osteoarthritis are currently known; consequently, pharmacologic treatment is directed at symptom relief.

A systematic review found the following clinical features to be associated with more rapid progression of knee osteoarthritis^[58] :

·                Older age

·                Higher BMI

·                Varus deformity

·                Multiple involved joints

Patients with osteoarthritis who have undergone joint replacement have a good prognosis, with success rates for hip and knee arthroplasty generally exceeding 90%. However, a joint prosthesis may have to be revised 10-15 years after its placement, depending on the patient’s activity level. Younger and more active patients are more likely to require revisions, whereas the majority of older patients will not. (See Treatment.)

Patient Education

Educate patients on the natural history of and management options for osteoarthritis, emphasizing the benefits of exercise and weight loss. Explain the differences between osteoarthritis and more rapidly progressive arthritides, such as rheumatoid arthritis.

Several Arthritis Foundation studies have demonstrated that education in osteoarthritis benefits the patient. Through education, patients can learn and implement strategies for reducing pain and improving joint function. Emphasize the need for physician follow-up visits.

For patient education information, see the Arthritis Center, as well asOsteoarthritis.

Spondylolisthesis, Spondylolysis, and Spondylosis 

Background

Spondylolisthesis refers to the forward slippage of one vertebral body with respect to the one beneath it. This most commonly occurs at the lumbosacral junction with L5 slipping over S1, but it can occur at higher levels as well. It is classified based on etiology into 5 types: congenital or dysplastic, isthmic, degenerative, traumatic, and pathologic.^[1] Many cases can be managed conservatively. However, in persons with incapacitating symptoms, radiculopathy, neurogenic claudication, postural or gait abnormality resistant to nonoperative measures, and significant slip progression, surgery is indicated. The goal of surgery is to stabilize the spinal segment and decompress the neural elements if needed.^{[2, 3, 4, 5, 6, 7, 8]}

See the images below.

Spondylolisthesis, spondylolysis, and spondylosis. Isthmic spondylolisthesis (type IIa) with grade 2 slippage of L5 over S1 and spondylolysis (lytic pars defect) is depicted posteriorly.Spondylolisthesis, spondylolysis, and spondylosis. Although interbody devices afford immediate stability to the anterior column, their use as stand-alone devices has been associated with pseudoarthrosis. Thus, concomitant posterior fixation is often used to augment their stability.

Spondylolisthesis Imaging

Spondylolysis Imaging

Lumbar Spondylosis

Diagnosis and Management of Cervical Spondylosis

Lumbosacral Spondylolysis

History of the Procedure

In 1854, Killian coined the term spondylolisthesis to describe the gradual slippage of the L5 vertebra due to gravity and posture. In 1858, Lambi demonstrated the neural arch defect (absence or elongation of pars interarticularis) in isthmic spondylolisthesis. Albee and Hibbs separately published their initial work on spinal fusion. Their methods were applied quickly to cases involving trauma, tumors, and, later, scoliosis. In the latter half of the 20th century, spinal fusion was used increasingly to treat degenerative disorders of the spine, including degenerative spondylolisthesis and degenerative scoliosis.

Problem

Spondylolisthesis is the forward slippage of one vertebra on another. This may or may not be associated with gross instability of the spine. Some individuals remain asymptomatic even with high-grade slips, but most complain of some discomfort. It may cause any degree of symptoms, from minimal symptoms of occasional low back pain to incapacitating mechanical pain, radiculopathy from nerve root compression, and neurogenic claudication.

Epidemiology

The incidence of isthmic type (see Etiology for definition) of spondylolisthesis is believed to be approximately 5% based on autopsy studies.

Degenerative spondylolisthesis is observed more frequently as the population ages and occurs most frequently at the L4-L5 level. Up to 5.8% of men and 9.1% of women are believed to have this type of listhesis.

Etiology

The etiology of spondylolisthesis is multifactorial. A congenital predisposition exists in types 1 and 2, and posture, gravity, rotational forces, and high concentration of stress loading all play parts in the development of the slip.

The following scheme of spondylolisthesis types, based on etiology, is adapted from Wiltse et al^[1] :

·                Type 1: The dysplastic (congenital) type represents a defect in the upper sacrum or arch of L5. A high rate of associated spina bifida occulta and a high rate of nerve root involvement exist (see Pathophysiology).

·                Type 2: The isthmic (early in life) type results from a defect in pars interarticularis, which permits forward slippage of the superior vertebra, usually L5. The following 3 subcategories are recognized:

o           Lytic (ie, spondylolysis) or stress fracture of the pars

o           Elongated yet intact pars

o           Acutely fractured pars

·                Type 3: The degenerative (late in life) type is an acquired condition resulting from chronic disc degeneration and facet incompetence, leading to long-standing segmental instability and gradual slippage, usually at L4-5. Spondylosis is a general term reserved for acquired age-related degenerative changes of the spine (ie, discopathy or facet arthropathy) that can lead to this type of spondylolisthesis.

·                Type 4: The traumatic (any age) type results from fracture of any part of the neural arch or pars that leads to listhesis.

·                Type 5: The pathologic type results from a generalized bone disease, such as Paget disease or osteogenesis imperfecta.

Pathophysiology

Spondylolisthesis can be graded based on the amount of vertebral subluxation in the sagittal plane, as adapted from Meyerding (1932):

·                Grade 1 – Less than 25% of vertebral diameter

·                Grade 2 – 25-50%

·                Grade 3 – 50-75%

·                Grade 4 – 75-100%

·                Spondyloptosis – Greater than 100%

The dysplastic type occurs from a neural arch defect in the upper sacrum or L5. In this type, 94% of cases are associated with spina bifida occulta. A high rate of nerve root compression at the S1 foramen exists, although the slip may be minimal (ie, grade 1).

The pars interarticularis, or isthmus, is the bone between the lamina, pedicle, articular facets, and the transverse process. This portion of the vertebra can resist significant forces during normal motion. The pars may be congenitally defective (eg, in spondylolytic subtype of isthmic spondylolisthesis) or undergo repeated stress under hyperflexion and rotation, resulting in microfractures. If a fibrous nonunion forms from ongoing insult, elongation of the pars and progressive listhesis results. This occurs in the second and third subtypes of type 2 (isthmic) spondylolisthesis. These typically present in the teenage or early adulthood years and are most common at L5-S1.

A unilateral pars defect (spondylolysis) may not demonstrate any degree of slippage; thus, a patient may have spondylolysis without spondylolisthesis. The reverse is also true as in the degenerative-type slips described below.

Biomechanical factors are significant in the development of spondylolysis leading to spondylolisthesis. Gravitational and postural forces cause the greatest stress at the pars interarticularis. Both lumbar lordosis and rotational forces are also believed to play a role in the development of lytic pars defects and the fatigue of the pars in the young. An association exists between high levels of activity during childhood and the development of pars defects. Genetic factors also play a role.

In the degenerative type, intersegmental instability is present as a result of degenerative disc disease and facet arthropathy. These processes are collectively known as spondylosis (ie, acquired age-related degeneration). The slip occurs from progressive spondylosis within this 3-joint motion complex. This typically occurs at L4-5, and elderly females are most commonly affected. The L5 nerve root is usually compressed from lateral recess stenosis as a result of facet and/or ligamentous hypertrophy.

In the traumatic type, any part (usually not pars) of the neural arch can be fractured, leading to the unstable vertebral subluxation.

Pathologic spondylolisthesis results from generalized bone disease, which causes abnormal mineralization, remodeling, and attenuation of the posterior elements leading to the slip.

Presentation

The clinical presentation differs, depending on the type of slip and the age of the patient.

During the early years of life, the presentation is one of mild low back pain that occasionally radiates into the buttocks and posterior thighs, especially during high levels of activity. The symptoms rarely correlate with the degree of slip, although they are attributable to segmental instability. Neurologic signs often correlate with the degree of slippage and involve motor, sensory, and reflex changes corresponding to nerve root impingement (usually S1). Progression of listhesis in these young adults usually occurs in the setting of bilateral pars defects and can be associated with the following physical findings:

·                Palpable step-off in higher-grade slips

·                Restricted spinal motion

·                Hamstring tightness

·                Inability to flex hips with fully extended knees

·                Hyperlordosis of the lumbar and thoracolumbar regions

·                Hyperkyphosis at lumbosacral junction (as the center of gravity shifts to compensate for slip progression)

·                Trunk shortening when a complete slip is present (spondyloptosis)

·                Gait difficulty (worse with high-grade slips)

The patient with degenerative spondylolisthesis is typically older and presents with back pain, radiculopathy, neurogenic claudication, or a combination of these symptoms. The slip is most common at L4-5 and less common at L3-4. The radicular symptoms often result from lateral recess stenosis from facet and ligamentous hypertrophy and/or disc herniation. The L5 nerve root is affected most commonly and causes weakness of the extensor hallucis longus. Concomitant central stenosis and neurogenic claudication may or may not exist.

The cause of claudication symptoms during ambulation is multifactorial. The pain is relieved when the patient flexes the spine by sitting or by leaning on shopping carts. Flexion increases canal size by stretching the protruding ligamentum flavum, reduction of the overriding laminae and facets, and enlargement of the foramina. This relieves the pressure on the exiting nerve roots and, thus, decreases the pain.

Indications

The goal of surgery is to stabilize the segment with listhesis and decompress any of the neural elements under pressure. Restoration of normal sagittal alignment must also be achieved. When evaluating a patient, many factors, such as age, degree of slip, and risk of slip progression, must be considered. Thus, each patient’s treatment algorithm should be individualized to achieve optimal outcome.

The indications for spinal fusion clearly differ in the pediatric and adult populations. For the younger population, the following factors are known to correlate with higher risk of slip progression:

·                Younger age (< 15 y)

·                High-grade listhesis (>30%)

·                Female sex

·                Ligamentous laxity

·                Type 1 (dysplastic) slip

·                Lumbosacral hypermobility

However, many young patients are treated with immobilization or activity modification alone, with a significant success rate. In the absence of high-grade slips, minimal symptomatology, and lack of slip progression, fusion is generally not indicated in this population.

Before surgery is considered for adult patients presenting with degenerative spondylolisthesis, minimal neurologic signs, or mechanical back pain alone, conservative measures should be exhausted, and a thorough evaluation of social and psychological factors should be undertaken.

Indications for surgical intervention (fusion) are as follows:

·                Neurologic signs – Radiculopathy (unresponsive to conservative measures), myelopathy, neurogenic claudication

·                Any high-grade slip (>50%)

·                Type 1 and type 2 slips, with evidence of instability, progression of listhesis, or lack of response to conservative measures

·                Traumatic spondylolisthesis

·                Iatrogenic spondylolisthesis

·                Type 3 (degenerative) listhesis with gross instability and incapacitating pain

·                Postural deformity and gait abnormality

Relevant Anatomy

In persons with congenital-type spondylolisthesis, dysplastic articular facets predispose the spinal segment to listhesis due to their inability to resist anterior shear stress. The pars may be intact, or it may undergo microfractures. Thus, it may not be the initiator of listhesis in dysplastic types. The risk of slip progression is high.

The pars interarticularis, or isthmus, resists significant forces during normal motion. The pars may be congenitally defective (isthmic spondylolisthesis is spondylolysis) or undergo repeated stress under hyperflexion and rotation resulting in microfractures. Lumbar lordosis, gravity, posture, high-intensity activities (eg, gymnastics), and genetic factors all play a role in the slip development. If a fibrous nonunion forms from ongoing insult, elongation of the pars and progressive listhesis results; this is observed in another subtype of type 2 (isthmic) spondylolisthesis. In persons with spondylolysis, 30-50% are believed to progress to spondylolisthesis. The most common location is at L5-S1.

Degenerative spondylolisthesis results from intersegmental instability. The pathophysiology of disc degeneration and facet arthropathy has been investigated extensively; however, the nature and etiology of pain generation in the absence of canal or lateral recess stenosis is still debated. Degeneration of the annulus fibrosis results in radial tears through which a posteriorly migrated nucleus pulposus can herniate. Degeneration of the disc may also lead to changes affecting the stability of the spinal motion segment, thus affecting the articular facets. Disc desiccation places greater stress on the facets, which are then subjected to shear forces. The subluxation occurs as a result of progressive facet incompetence. This type most commonly occurs at L4-5 and L3-4.

Contraindications

Surgery is contraindicated if the patient is in poor medical health and if the operative risk is not outweighed by the potential benefits.

Anticoagulation with warfarin, or antiplatelet therapy, can make the risk of hemorrhage much higher than routinely expected. Antiplatelet therapy should be discontinued 3-5 days prior to the procedure. Coumadin should be stopped 5-7 days prior to the procedure, and a prothrombin time result within reference range should be achieved before surgery.

Smoking significantly decreases the chance for a successful fusion. Some surgeons prefer that a patient commit to smoking cessation up to one month before the surgical procedure.

Correction of the listhesis is associated with risk of neurologic injury, both transient and permanent. Some surgeons prefer to fuse the spine in place rather than to reduce the subluxation. In persons with higher-grade spondylolisthesis, use of interbody grafts is associated with a high rate of complications. However, the use of these devices adds to the stability of the spinal segment, helps with the reduction of the deformity, and helps achieve sagittal balance, thus ensuring better outcome.