Back Clinic Arthropathies Chiropractic and Physical Therapy Team. Charcot’s is degeneration of a weight-bearing joint and arthrogryposis which means, “curving of joints.” this is a general term that describes any disease of the joints. A group of disorders can afflict the joints, such as sacroiliitis, which causes inflammation in the sacroiliac joint. Doctors use arthropathy interchangeably with arthritis, which means “joint inflammation.”The forms that are distinct from arthritis are Neuropathic arthropathy, nerve damage from diabetes, or other nerve conditions resulting in slow damage to joints.
In diabetic people, arthropathy usually affects the foot and ankle. Hypertrophic pulmonary osteoarthropathy is where the bone ends of the ankles, knees, wrists, and elbows start to grow abnormally and painfully. Fingertips start to become rounded, called “clubbing.” This form of arthropathy usually happens to people with lung cancer. And Hemarthrosis is when blood leaks into a joint like the knee. This occurs after injuries or medical procedures and is a problem in people with hemophilia.
Knee pain is a common health issue among athletes and the general population alike. Although symptoms of knee pain can be debilitating and frustrating, knee pain is often a very treatable health issue. The knee is a complex structure made up of three bones: the lower section of the thighbone, the upper region of the shinbone, and the kneecap.
Powerful soft tissues, such as the tendons and ligaments of the knee as well as the cartilage beneath the kneecap and between the bones, hold these structures together in order to stabilize and support the knee. However, a variety of injuries and/or conditions can ultimately lead to knee pain. The purpose of the article below is to evaluate patients with knee pain.
Abstract
Family physicians frequently encounter patients with knee pain. Accurate diagnosis requires a knowledge of knee anatomy, common pain patterns in knee injuries, and features of frequently encountered causes of knee pain, as well as specific physical examination skills. The history should include characteristics of the patient�s pain, mechanical symptoms (locking, popping, giving way), joint effusion (timing, amount, recurrence), and mechanism of injury. The physical examination should include careful inspection of the knee, palpation for point tenderness, assessment of joint effusion, range-of-motion testing, evaluation of ligaments for injury or laxity, and assessment of the menisci. Radiographs should be obtained in patients with isolated patellar tenderness or tenderness at the head of the fibula, inability to bear weight or flex the knee to 90 degrees, or age greater than 55 years. (Am Fam Physician 2003; 68:907-12. Copyright� 2003 American Academy of Family Physicians.)
Introduction
Knee pain accounts for approximately one-third of musculoskeletal problems seen in primary care settings. This complaint is most prevalent in�physically active patients, with as many as 54 percent of athletes having some degree of knee pain each year.1 Knee pain can be a source of significant disability, restricting the ability to work or perform activities of daily living.
The knee is a complex structure (Figure 1),2 and its evaluation can present a challenge to the family physician. The differential diagnosis of knee pain is extensive but can be narrowed with a detailed history, a focused physical examination and, when indicated, the selective use of appropriate imaging and laboratory studies. Part I of this two-part article provides a systematic approach to evaluating the knee, and part II3 discusses the differential diagnosis of knee pain.
History
Pain Characteristics
The patient�s description of knee pain is helpful in focusing the differential diagnosis.4 It is important to clarify the characteristics of the pain, including its onset (rapid or insidious), location (anterior, medial, lateral, or posterior knee), duration, severity, and quality (e.g., dull, sharp, achy). Aggravating and alleviating factors also need to be identified. If knee pain is caused by an acute injury, the physician needs to know whether the patient was able to continue activity or bear weight after the injury or was forced to cease activities immediately.
Mechanical Symptoms
The patient should be asked about mechan- ical symptoms, such as locking, popping, or giving way of the knee. A history of locking episodes suggests a meniscal tear. A sensation of popping at the time of injury suggests liga- mentous injury, probably complete rupture of a ligament (third-degree tear). Episodes of giving way are consistent with some degree of knee instability and may indicate patellar sub- luxation or ligamentous rupture.
Effusion
The timing and amount of joint effusion are important clues to the diagnosis. Rapid onset (within two hours) of a large, tense effusion suggests rupture of the anterior cru- ciate ligament or fracture of the tibial plateau with resultant hemarthrosis, whereas slower onset (24 to 36 hours) of a mild to moderate effusion is consistent with meniscal injury or ligamentous sprain. Recurrent knee effusion after activity is consistent with meniscal injury.
Mechanism of Injury
The patient should be questioned about specific details of the injury. It is important to know if the patient sustained a direct blow to the knee, if the foot was planted at the time of injury, if the patient was decelerating or stopping suddenly, if the patient was landing from a jump, if there was a twisting component to the injury, and if hyperextension occurred.
A direct blow to the knee can cause serious injury. The anterior force applied to the proximal tibia with the knee in flexion (e.g., when the knee hits the dashboard in an automobile accident) can cause injury to the posterior cruciate ligament. The medial collateral ligament is most commonly injured as a result of direct lateral force to the knee (e.g., clipping in football); this force creates a val- gus load on the knee joint and can result in rupture of the medial collateral ligament. Conversely, a medial blow that creates a varus load can injure the lateral collateral ligament.
Noncontact forces also are an important cause of knee injury. Quick stops and sharp cuts or turns create significant deceleration forces that can sprain or rupture the anterior cruciate ligament. Hyperextension can result in injury to the anterior cruciate ligament or posterior cruciate ligament. Sudden twisting or pivoting motions create shear forces that can injure the meniscus. A combination of forces can occur simultaneously, causing injury to multiple structures.
Medical History
A history of knee injury or surgery is important. The patient should be asked about previous attempts to treat knee pain, including the use of medications, supporting devices, and physical therapy. The physician also should ask if the patient has a history of�gout, pseudogout, rheumatoid arthritis, or other degenerative joint diseases.
Knee pain is a common health issue which can be caused by sports injuries, automobile accident injuries, or by an underlying health issue, such as arthritis. The most common symptoms of knee injury include pain and discomfort, swelling, inflammation and stiffness. Because treatment for knee pain varies according to the cause, it’s essential for the individual to receive proper diagnosis for their symptoms. Chiropractic care is a safe and effective, alternative treatment approach which can help treat knee pain, among other health issues.
Dr. Alex Jimenez D.C., C.C.S.T. Insight
Physical Examination
Inspection and Palpation
The physician begins by comparing the painful knee with the asymptomatic knee and inspecting the injured knee for erythema, swelling, bruising, and discoloration. The mus- culature should be symmetric bilaterally. In particular, the vastus medialis obliquus of the quadriceps should be evaluated to determine if it appears normal or shows signs of atrophy.
The knee is then palpated and checked for pain, warmth, and effusion. Point tenderness should be sought, particularly at the patella, tibial tubercle, patellar tendon, quadriceps tendon, anterolateral and anteromedial joint line, medial joint line, and lateral joint line. Moving the patient�s knee through a short arc of motion helps identify the joint lines. Range of motion should be assessed by extending and flexing the knee as far as possible (normal range of motion: extension, zero degrees; flex- ion, 135 degrees).5
Patellofemoral Assessment
An evaluation for effusion should be conducted with the patient supine and the injured knee in extension. The suprapatellar pouch should be milked to determine whether an effusion is present.
Patellofemoral tracking is assessed by observing the patella for smooth motion while the patient contracts the quadriceps muscle. The presence of crepitus should be noted during palpation of the patella.
The quadriceps angle (Q angle) is determined by drawing one line from the anterior superior iliac spine through the center of the patella and a second line from the center of the patella through the tibial tuberosity (Figure 2).6 A Q angle greater than 15 degrees is a predisposing factor for patellar subluxation (i.e., if the Q angle is increased, forceful contraction of the quadriceps muscle can cause the patella to sublux laterally).
A patellar apprehension test is then performed. With fingers placed at the medial aspect of the patella, the physician attempts to sublux the patella laterally. If this maneuver reproduces the patient�s pain or a giving-way sensation, patellar subluxation is the likely cause of the patient�s symptoms.7 Both the superior and inferior patellar facets should be palpated, with the patella subluxed first medially and then laterally.
Cruciate Ligaments
Anterior Cruciate Ligament. For the anterior drawer test, the patient assumes a supine position with the injured knee flexed to 90 degrees. The physician fixes the patient�s foot in slight external rotation (by sitting on the foot) and then places thumbs at the tibial tubercle and fingers at the posterior calf. With the patient�s hamstring muscles relaxed, the physician pulls anteriorly and assesses anterior displacement of the tibia (anterior drawer sign).
The Lachman test is another means of assessing the integrity of the anterior cruciate ligament (Figure 3).7 The test is performed with the patient in a supine position and the injured knee flexed to 30 degrees. The physician stabilizes the distal femur with one hand, grasps the proximal tibia in the other hand, and then attempts to sublux the tibia anteriorly. Lack of a clear end point indicates a positive Lachman test.
Posterior Cruciate Ligament. For the posterior drawer test, the patient assumes a supine position with knees flexed to 90 degrees. While standing at the side of the examination table, the physician looks for posterior displacement of the tibia (posterior sag sign).7,8 Next, the physician fixes the patient�s foot in neutral rotation (by sitting on the foot), positions thumbs at the tibial tubercle, and places fingers at the posterior calf. The physician then pushes posteriorly and assesses for posterior displacement of the tibia.
Collateral Ligaments
Medial Collateral Ligament. The valgus stress test is performed with the patient�s leg slightly abducted. The physician places one hand at the lateral aspect of the knee joint and the other hand at the medial aspect of the distal tibia. Next, valgus stress is applied to the knee at both zero degrees (full extension) and 30 degrees of flexion (Figure 4)7. With the knee at zero degrees (i.e., in full extension), the posterior cruciate ligament and the articulation of the femoral condyles with the tibial plateau should stabilize the knee; with the knee at 30 degrees of flexion, application of valgus stress assesses the laxity or integrity of the medial collateral ligament.
Lateral Collateral Ligament. To perform the varus stress test, the physician places one hand at the medial aspect of the patient�s knee and the other hand at the lateral aspect of the distal fibula. Next, varus stress is applied to the knee, first at full extension (i.e., zero degrees), then with the knee flexed to 30 degrees (Figure 4).7 A firm end point indicates that the collateral ligament is intact, whereas a soft or absent end point indicates complete rupture (third-degree tear) of the ligament.
Menisci
Patients with injury to the menisci usually demonstrate tenderness at the joint line. The McMurray test is performed with the patient lying supine9 (Figure 5). The test has been described variously in the literature, but the author suggests the following technique.
The physician grasps the patient�s heel with one hand and the knee with the other hand. The physician�s thumb is at the lateral joint line, and fingers are at the medial joint line. The physician then flexes the patient�s knee maximally. To test the lateral meniscus, the tibia is rotated internally, and the knee is extended from maximal flexion to about 90 degrees; added compression to the lateral meniscus can be produced by applying valgus stress across the knee joint while the knee is�being extended. To test the medial meniscus, the tibia is rotated externally, and the knee is extended from maximal flexion to about 90 degrees; added compression to the medial meniscus can be produced by placing varus stress across the knee joint while the knee is degrees of flexion. A positive test produces a thud or a click, or causes pain in a reproducible portion of the range of motion.
Because most patients with knee pain have soft tissue injuries, plain-film radiographs generally are not indicated. The Ottawa knee rules are a useful guide for ordering radiographs of the knee10,11.
If radiographs are required, three views are usually sufficient: anteroposterior view, lateral view, and Merchant�s view (for the patellofemoral joint).7,12 Teenage patients who report chronic knee pain and recurrent knee effusion require a notch or tunnel view (posteroanterior view with the knee flexed to 40 to 50 degrees). This view is necessary to detect radiolucencies of the femoral condyles (most�commonly the medial femoral condyle), which indicate the presence of osteochondritis dissecans.13
Radiographs should be closely inspected for signs of fracture, particularly involving the patella, tibial plateau, tibial spines, proximal fibula, and femoral condyles. If osteoarthritis is suspected, standing weight-bearing radiographs should be obtained.
Laboratory Studies
The presence of warmth, exquisite tenderness, painful effusion, and marked pain with even slight range of motion of the knee joint is consistent with septic arthritis or acute inflammatory arthropathy. In addition to obtaining a complete blood count with differential and an erythrocyte sedimentation rate (ESR), arthro- centesis should be performed. The joint fluid should be sent to a laboratory for a cell count with differential, glucose and protein measure- ments, bacterial culture and sensitivity, and polarized light microscopy for crystals.
Because a tense, painful, swollen knee may present an unclear clinical picture, arthrocentesis may be required to differentiate simple effusion from hemarthrosis or occult osteochondral fracture.4 A simple joint effusion produces clear, straw-colored transudative fluid, as in a knee sprain or chronic meniscal injury. Hemarthrosis is caused by a tear of the anterior cruciate ligament, a fracture or, less commonly, an acute tear of the outer portion of the meniscus. An osteochondral fracture causes hemarthrosis, with fat globules noted in the aspirate.
Rheumatoid arthritis may involve the knee joint. Hence, serum ESR and rheumatoid factor testing are indicated in selected patients.
The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.
In conclusion, knee pain is a common health issue which occurs due to a variety of injuries and/or conditions, such as sports injuries, automobile accidents, and arthritis, among other problems. Treatment of knee pain depends largely on the source of the symptoms. Therefore, it is essential for the individual to seek immediate medical attention to receive a diagnosis.
Chiropractic care is an alternative treatment option which focuses on the treatment of a variety of injuries and/or conditions associated with the musculoskeletal and nervous system. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Relieving Knee Pain without Surgery
Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
1. Rosenblatt RA, Cherkin DC, Schneeweiss R, Hart LG. The content of ambulatory medical care in the United States. An interspecialty comparison. N Engl J Med 1983;309:892-7.
2. Tandeter HB, Shvartzman P, Stevens MA. Acute knee injuries: use of decision rules for selective radiograph ordering. Am Fam Physician 1999;60: 2599-608.
3. Calmbach WL, Hutchens M. Evaluation of patients presenting with knee pain: part II. Differential diag- nosis. Am Fam Physician 2003;68:917-22
4. Bergfeld J, Ireland ML, Wojtys EM, Glaser V. Pin- pointing the cause of acute knee pain. Patient Care 1997;31(18):100-7.
6. Juhn MS. Patellofemoral pain syndrome: a review and guidelines for treatment. Am Fam Physician 1999;60:2012-22.
7. Smith BW, Green GA. Acute knee injuries: part I. History and physical examination. Am Fam Physi- cian 1995;51:615-21.
8. Walsh WM. Knee injuries. In: Mellion MB, Walsh WM, Shelton GL, eds. The team physician�s hand- book. 2d ed. St. Louis: Mosby, 1997:554-78.
9. McMurray TP. The semilunar cartilage. Br J Surg 1942;29:407-14.
10. Stiell IG, Wells GA, Hoag RH, Sivilotti ML, Cacciotti TF, Verbeek PR, et al. Implementation of the Ottawa knee rule for the use of radiography in acute knee injuries. JAMA 1997;278:2075-9.
11. Stiell IG, Greenberg GH, Wells GA, McKnight RD, Cwinn AA, Caciotti T, et al. Derivation of a decision rule for the use of radiography in acute knee injuries. Ann Emerg Med 1995;26:405-13.
12. Sartoris DJ, Resnick D. Plain film radiography: rou- tine and specialized techniques and projections. In: Resnick D, ed. Diagnosis of bone and joint disor- ders. 3d ed. Philadelphia: Saunders:1-40.
13. Schenck RC Jr, Goodnight JM. Osteochondritis dis- secans. J Bone Joint Surg [Am] 1996;78:439-56.
Ischemic Osteonecrosis (More accurate term) aka avascular necrosis AVN: this term describes subarticular (subchondral) bone death
Intramedullary bone infarct: depicts osteonecrosis within the medullary cavity of the bone (above x-ray image)
Causes: m/c: trauma, systemic corticosteroids, diabetes, vasculitis in SLE. The list is long. Other vital causes: Sickle cell disease, Gaucher disease, alcohol, caisson disease, SCFE, LCP, etc.
Pathology: ischemia and bone infarct with resultant devitalized center surrounded by ischemia and edema with normal bone on the outer periphery (MRI double line sign)
Sub-articular necrotic bone eventually collapses and fragments leading to progressive bone and cartilage destruction and rapidly progressing DJD
Early Dx often missed but crucial to prevent severe DJD
M/C Sites
Hips, shoulders, talus, scaphoid bone. Many peripheral idiopathic AVN sites are known by their eponyms (e.g., Kienbock aka AVN of the lunate bone, Preisier aka scaphoid AVN)
Radiography is insensitive to early AVN and may only present as subtle osteopenia
Some of the early appreciable rad features are increased patchy bone sclerosis followed by sub-articular bone collapse or “crescent sign” signifying stage-3 on Ficat classification (above)
Earliest detection and early intervention can be achieved by MRI (most sensitive modality)
If MRI contraindicated or unavailable, 2nd most sensitive modality is radionuclide bone scan (scintigraphy)
X-ray and CT scanning are of equal value
Coronal MRI Slice
Fluid sensitive, sensitive coronal MRI slice revealing bill ischemic osteonecrosis of the femoral head
MRI findings: l
Tc99-MMDP Radionuclide Bone
Bone scan reveals a central area of photopenia (cold spot) d/t necrotic fragment surrounded by increased osteoblastic activity as increased uptake of Tc-99 MDP in the right hip
The patient is a 30-year-old female with breast cancer and chemotherapy treatment who suddenly presented with right hip pain
Radiographic Progression of AVN
Later stages present with articular collapse, subarticular cysts, increased patchy sclerosis and complete flattening of the femoral head with resultant severe DJD. Rx: THA
Management
Early imaging Dx with MRI or bone scintigraphy is essential
Referral to the Orthopedic surgeon
Core decompression (above) can be used to revascularize the affected bone during earlier stages but produces mixed results
Delayed changes of AVN: THA as IN severe DJD cases
B/L THA
B/L THA in the patient with ischemic osteonecrosis of the right and later left hip
When B/L hip AVN is present, typically consider systemic causes (corticosteroids, diabetes)
Inflammatory Arthritis Affecting the Hip
Consider common systemic inflammatory condition such as RA and AS/EnA
Hip RA may develop in 30% of patients with RA
Key features to DDx inflammatory arthritis vs. DJD is symmetrical/uniform aka concentric joint loss often leading to axial migration and Protrusion Acetabule in advanced cases
Key element between RA vs. AS: the presence of RA bone erosion w/o productive bone changes or enthesitis in AS d/t inflammatory subperiosteal bone proliferation, whiskering/fluffy periostitis (collar-type enthesitis circumferentially affecting head-neck junction)
Dx: Hx, PE, labs: CRP, RH, anti-CCP Ab (RA)
CRP, HLA-B27, RF- (AS)
Septic Arthritis
Gonococcal infections, iatrogenic causes, I.V. drug use, and some others
Routes:�hematogenous, adjacent spread, direct inoculation (e.g., iatrogenic)
Clinically: pain and reduced ROM presented as monoarthritis, generalized signs/symptoms. CBC, ESR, CRP changes. ARthrocentesis and culture are crucial
M/C pathogen Staph. Aureus & Neisseria Gonorrhea
1st step: radiography, often unrewarding in the early stage. Later (4-10 days) indistinctness of the white cortical line at the femoral articular epiphysis, loss of joint space, effusion as a widening of the medial joint area (Waldenstrom sign)
MRI – best at early DX: T1, T2, STIR, T1+C may help with early. Early I.V. antibiotics crucial to prevent rapid joint destruction
Slipped Capital Femoral Epiphysis (SCFE)
Important to diagnose but easily missed potentially leading to Ischemic Osteonecrosis of the femoral head aka AVN
Presents typically in overweight children (more often boys), age over eight years. Greater incidence in African-American boys
1st step: radiography, especially look for a widened physeal growth plate (so-called pre-slip). Later, slip and disturbed Klein’s line (above image). MRI – best modality for early Dx and early intervention
The frog lateral view often demonstrates the medial slip better than the AP view
Clinically Limping Child or Adolescent
M>F (10-18 years). African-Americans are at greater risk. 20% of cases of SCFE are B/L. Complications: AVN >>DJD
Radiography:�AP pelvis, spot, and frog leg may reveal slippage as Klein line failed to cross through the lateral aspect of the femoral head
Additional features: physis may appear widened
MRI w/o gad, is required for the earliest Dx and prevention of complications (AVN)
Normal and Abnormal Klein Line
Consistent with SCFE. The physis is also widened. Dx: SCFE
Urgent referral to the Pediatric Orthopedic surgeon
Subtle Changes in Left Hip
Note suspected subtle changes in the left hip that may require MR examination to confirm the Dx
Delay in care may result in major complications
Perthes’ Disease
aka Legg-Calves-Perthes Disease (LCP)
Refers to Osteochondritis of the femoral head with osteonecrosis likely d/t disturbed vascularization of the femoral head
Presents typically in children (more often boys) aged under eight years as atraumatic “limping child.” 15% may have B/L Perthe’s
Imaging steps: 1st step x-radiography, followed by MRI especially in stage 1 (early) w/o x-ray abnormalities
Unspecific signs: joint effusion with Waldenstrome sign+ (>2-mm increase in medial joint space compared to the opposite side). Past approach: Fluoroscopic Arthrography (replaced by MRI)
Pathologic-Radiologic Correlation: in well-established cases, the femoral head characteristically becomes sclerotic, flattened and fragmented due to avascular necrosis (AVN). Later on, an occasional Coxa Magna changes may develop (>10% femoral head enlargement)
Management: symptoms control, bracing. Boys at younger ate show better prognosis d/t more immaturity and better chances of bone/cartilage repair mechanisms. In advanced cases, operative care: osteotomy, hip arthroplasty in adulthood if advanced DJD develops
Common Neoplasms & Other Conditions Affecting Hip/Pelvis
M/C hip & pelvis neoplasms in adults: bone metastasis ( above far left), 2nd m/c Multiple Myeloma (M/C primary bone malignancy in adults). Tips: remember Red Marrow distribution. Less frequent: Chondrosarcoma
Paget’s disease of bone (above-bottom left image) is m/c detected in the pelvis and Femurs
Children and young adults ‘limping child’ benign neoplasms: Fibrous Dysplasia (above middle image), Solitary Bone Cyst (21%), Osteoid Osteoma, Chondroblastoma. Malignant pediatric neoplasms: m/c Ewing Sarcoma (above middle right and bottom images) vs. Osteosarcoma. >2y.o-consider Neuroblastoma
Imaging: 1st step: radiography followed by MRI are most appropriate.
If Mets are suspected: Tc99 bone scintigraphy is most sensitive
Multiple Myeloma
Multiple Myeloma in a 75-y.o male (AP pelvis view)
Chondrosarcoma in a 60-y.o male (axial and coronal reconstructed CT+C slices in the bone window)
Macroscopic & Microscopic Appearance of Normal vs. Damaged Articular Hyaline Cartilage by DJD
Hip Osteoarthritis (OA) aka Osteoarthrosis
Symptomatic and potentially disabling DJD
Progressive damage and loss of the articular cartilage causing denudation and eburnation of articular bone
Cystic changes, osteophytes, and gradual joint destruction
Develops d/t repeated joint loading and microtrauma
Obesity, metabolic/genetic factors
Secondary Causes: trauma, FAI syndrome, osteonecrosis, pyrophosphate crystal deposition, previous inflammatory arthritis, Slipped Capital Femoral Epiphysis, Leg-Calves-Perthes disease in children, etc.
Hip OA, 2nd m/c after knee OA. Women>men
88-100 symptomatic cases per 100000
Radiography is the Modality of Choice for the Dx and Grading of DJD
Special imaging is not required unless other complicating factors exist
The acetabular-femoral joint is divided into superior, axial and medial compartments/spaces
Normal joint space at the superior compartment should be 3-4-mm on the AP hip/pelvis view
Understanding the pattern of hip joint narrowing/migration helps with the DDx of DJD vs. Inflammatory arthritis
In DJD, m/c hip narrowing is superior-lateral (non-uniform) vs. inflammatory axial (uniform)
AP Hip Radiograph Demonstrates DJD
With a non-uniform loss of joint space (superior migration), large subcortical cysts and subchondral sclerosis
Radiographic features:
Like with any DJD changes: radiography will reveal L.O.S.S.
L: loss of joint space (non-uniform or asymmetrical)
O: osteophytes aka bony proliferation/spurs
S: Subchondral sclerosis/thickening
S: Subcortical aka subchondral cysts “geodes.”
Hip migration is m/c superior resulting in a “tilt deformity.”
Radiographic Presentation of Hip OA May Vary Depending On Severity
Mild OA: mild reduction of joint space often w/o marked osteophytes and cystic changes
During further changes, collar osteophytes may affect femoral head-neck junction with more significant joint space loss and subchondral bone sclerosis (eburnation)
Cyst formation will often occur along the acetabular and femoral head subarticular/subchondral bone “geodes” and usually filled with joint fluid and some intra-articular gas
Subchondral cysts may occasionally be very large and DDx from neoplasms or infection or other pathology
Coronal Reconstructed CT Slices in Bone Window
Note moderate joint narrowing that appears non-uniform
Sub-chondral cysts formation (geodes) are noted along the acetabular and femoral head subchondral bone
Other features include collar osteophytes along head-neck junction
Dx: DJD of moderate intensity
Referral to the Orthopedic surgeon will be helpful for this patient
AP Pelvis (below the first image), AP Hip Spot (below the second image) CT Coronal Slice
Note multiple subchondral cysts, severe non-uniform joint narrowing (superior-lateral) and subchondral sclerosis with osteophytes
Advanced hip arthrosis
Severe DJD, Left Hip
When reading radiological reports pay particular attention to the grading of hip OA
Most severe (advanced) OA cases require total hip arthroplasty (THA)
Refer your patients to the Orthopedic surgeon for a consultation
Most mild cases are a good candidate for conservative care
Hip Arthroplasty aka Hip Replacement
Can be total or hemiarthroplasty
THA can be metal on metal, metal on polyethylene and ceramic on ceramic
A hybrid acetabular component with polyethylene and metal backing is also used (above right image)
THA can be cemented (above right image) and non-cemented (above-left image)
Non-cemented arthroplasty is used on younger patients utilizing porous metallic parts allowing good fusion and bone ingrowth into the prosthesis
Failed THA May Develop
Most develop within the first year and require revision
Femoral stem may fracture (above left)
Postsurgical infection (above right)
Fracture adjacent to the prosthesis (stress riser)
Particle disease
Femoroacetabular Impingement Syndrome
(FAI): abnormality of normal morphology of the hip leading to eventual� cartilage damage and premature DJD
Clinically:�hip/groin pain aggravated by sitting (e.g., hip flexed & externally rotated). Activity related pain on axial loading esp. with hip flexion (e.g., walking uphill)
Pincer-type�acetabulum: > in middle age women potentially� many causes
CAM-type deformity:�> in men in 20-50 m/c 30s
Mixed type (pincer-CAM) is most frequent
Up until the 90s, FAI was not well-recognized
FAI Syndrome
CAM-type FAI syndrome
Radiography can be a reliable Dx tool
X-radiography findings:�osseous bump on the lateral aspect of femoral head-neck junction. Pistol-grip deformity. Loss of normal head sphericity. Associated features: os acetabule, synovial herniation pit (Pit’s pit). Evidence of DJD in advanced cases
MRI and MR arthrography (most accurate Dx of labral tear) can aid the diagnosis of labral tear and other changes of FAI
Referral to the Orthopedic surgeon is necessary to prevent DJD progression and repair labral abnormalities. Late Dx may lead to irreversible changes of DJD
AP Pelvis: B/L CAM-type FAI syndrome
Pincer-Type FAI with Acetabula Over-Coverage
Key radiographic signs: “Cross-over sign” and abnormal center-edge and Alfa-angle evaluation methods
Dx of FAI
Center-edge angle (above the first image) and Alfa-angle (above the second image)
B/L CAM-type FAI with os acetabule�(above right image)
MR Arthrography
Labral tear and CAM-type FAI syndrome on axial (above left) and coronal T2 W (above right) MR arthrography
Note acetabula labral tear. Referral to an orthopedic surgeon is required. For more information:
Ankylosing Spondylitis is a type of arthritis that typically begins during adolescence or in a person�s early twenties and occurs more often in men than in women. However, once experiences onset, they are affected for the rest of their lives. It is estimated that between 0.2% and 0.5% of individuals in the United States suffers from ankylosing spondylitis. �It can cause significant pain, discomfort, and immobility. While there is no cure for the condition, the symptoms can be treated, bringing some degree of comfort and mobility.
What is Ankylosing Spondylitis?
Ankylosing Spondylitis, or AS, is a type of arthritis that causes inflammation in the spine. While the vertebrae are primarily involved, it can also affect other joints as well, including the hips, shoulders, heels, ribs, and the small joints of the feet and hands.
In some cases, the heart, lungs, and even eyes can be involved. If left untreated, the condition can progress, causing chronic pain that can be severe as the spinal inflammation increases. More advanced cases can cause the spine to grow new bone formations so that it is immobile, or fixed, sometimes resulting in kyphosis, which is a bowed or forward-stooped posture.
What Causes Ankylosing Spondylitis?
While genetics is believed to be a key player in the development of Ankylosing Spondylitis, the exact cause has not yet been determined. The majority of people who have AS also carry a specific gene that has been linked to the condition.
This gene produces HLA-B27, a protein or genetic marker, that more than 95% of Caucasians with ankylosing spondylitis have. However, some people don�t have this protein who develop AS and many people do carry this marker yet never develop the condition.
Researchers theorize that there may be other genes that may be involved, as well as environmental factors that trigger the gene activation, such as a bacterial infection, causing people who are susceptible to AS to activate it. Scientists have identified more than 60 genes that are believed to be associated with AS with only about 30% that are linked to HLA-B27 regarding overall risk. Other genes that have been identified as key to AS include IL-23, IL-17, IL-12, and ERAP.
It is also believed that AS can be triggered when the intestinal defenses break down, allowing certain bacteria into the bloodstream. This can, in turn, cause an immune response.
How is Ankylosing Spondylitis Treated?
AS cannot be cured, but the symptoms can be treated to relieve stiffness and pain as well as delay or prevent spinal deformity and other complications. The damage that it does to the joints is irreversible, so it is best if treatment is started before that occurs. There are several ways that AS is treated:
Medication � Nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin (Indocin) and naproxen (Naprosyn) are commonly used to treat the symptoms of AS. They can be useful in relieving pain, inflammation, and stiffness but may cause some side effects, including gastrointestinal bleeding. This makes long-term use impractical and even unsafe. If NSAIDs do not help, other medications may be prescribed, including:
Golimumab (Simponi; Simponi Aria)
Certolizumab pegol (Cimzia)
Adalimumab (Humira)
Etanercept (Enbrel)
Infliximab (Remicade)
Physical therapy – PT is often recommended to help with flexibility, strength, and pain relief. It can help with posture and prevent some of the more debilitating symptoms.
Surgery � Most people with AS do not require surgery, but it may be recommended if there is severe joint damage or pain. In some cases, it can cause significant damage to hip joints, and they will need to be replaced.
Chiropractic � Many patients with AS have with outstanding results with chiropractic treatment. It is non-invasive and does not have the unpleasant side effects that many medications have.
Chiropractic Treatment for Ankylosing Spondylitis
Chiropractors strongly recommend chiropractic treatment for the non-acute inflammatory stage of AS. Once the condition has progressed to acute joint disease, there is a very high risk of injury or damage to the connective tissue. Adjustments and exercise are used to relieve symptoms, but some of the traditional spinal manipulation treatments are not performed.
A chiropractor will also make recommendations to the patient regarding lifestyle changes that can help with symptoms, such as stopping smoking. Tobacco use can increase inflammation and damage connective tissue. They may also advise increasing their intake of omega three fatty acids in their diet. Regular chiropractic care can help patients manage symptoms and prevent disease progression, improving their quality of life.
Ossification of Posterior Longitudinal Ligament (OPLL). Less frequent than DISH.
Greater clinical importance d/t spinal canal stenosis and cervical myelopathy
Asian patients are at higher risk
Both OPLL & DISH may co-exist and increase the risk of Fx
Imaging: x-rad: linear radioopacity consistent with OPLL
Imaging modality of choice: CT scanning w/o contrast
MRI may help� to evaluate myelopathy
Care: surgical with laminoplasty (above right image) that has been pioneered and advanced in the Far East
M/C Inflammatory Arthritis In Spine
Rheumatoid spondylitis (Rheumatoid arthritis) d/t inflammatory synovial proliferation pannus rich in lymphocytes, macrophages, and plasma cells
C/S RA may affect 70-90% of patients
Variable severity from mild to destructive disabling arthropathy
RA IN C/S m/c affects C1-C2 due to an abundance of rich synovial tissue
Typically infrequent in the thoracic/lumbar region
Sub-axial C/spine may be affected later due to facets, erosions, ligament laxity and instability showing “Stepladder” appearance
Clinically: HA, neck pain, myelopathy, etc. inc. Risk of Fx/subluxation. Any spinal manipulation HVLT ARE STRICTLY CONTRAINDICATED.
Rx: DMARD, anti-TNF-alfa, operative for subluxations, etc.
Rheumatoid Spondylitis C1-C2. Perform X-radiography initially with flexed-extended views. Note Dens erosion, C1-2 subluxation (2.5 mm) that changes on mobility
RA spondylitis: an erosion of the odontoid with the destruction of C1-C2 ligaments and instability
M:F 4:1, age: 20-40 m/c. Clinic LBP/stiffness, reduced rib expansion <2 cm is > specific than HLA-B27, progressive kyphosis, risk of Fx’s.
Imaging steps: 1st step-x-rays to id. Sacroiliitis/spondylitis.�MRI & CT may help if x-rays are unrewarding.
Labs: HLA-B27, CRP/ESR, RF-
Dx: clinical+labs+imaging.
Rx: NSAID, DMARD, anti-TNF factor therapy
Key Imaging Dx: always presents initially as b/l symmetrical sacroiliitis that will progress to complete ankylosis. Spondylitis presents with continuous ascending discovertebral osteitis (i.e., marginal syndesmophytes, Romanus lesion, Anderson lesion), facets and all spinal ligament inflammation and fusion with a late feature of “bamboo spine, trolley track, dagger sign,” all indicating complete spinal ossification/fusion. Increasing risk of Fx’s.
Key Dx of Sacroiliitis
Blurring, cortical indistinctness/irregularity with adjacent reactive subchondral sclerosis initially identified primarily on the iliac side of� SIJs.
Normal SIJ should maintain a well defined white cortical line. Dimension 2-4 mm. May look incongruous d/t 3D anatomy masked by 2D x-rays.
Key Imaging Dx In Spine
Marginal syndesmophytes and inflammation at the annulus-disc (above arrows) at the earliest dx; by MRI as marrow signal changes on T1 and fluid sensitive imaging (above top images).
These represent enthesitis-inflammation that will ossify into bamboo spine.
Lig ossification: trolley track/dagger sign
AS in extraspinal joints: root joints, hips, and shoulders
Symphysis pubis
Less frequent in peripheral joints (hands/feet)
All seronegatives may present with heel pain d/t enthesitis
Complication: Above Carrot-stick/chaulk-stick Fx
PsA & ReA (formerly Reiter’s) present with b/l sacroiliitis that virtually identical to AS
In the spine PsA & ReA DDx from AS by the formation of non-marginal syndesmophytes aka bulky paravertebral ossifications (indicate vertebral enthesitis)
For a clinical discussion of Spondyloarthropathies refer to:
Spondylosis aka Degenerative disease of the spine represents an evolution of changes affecting most mobile spinal segments beginning with:
Intervertebral disc (IVD) dehydration (desiccation) and degeneration aka Degenerative Disc Disease (DDD) with an abnormal increase in mechanical stress and degeneration of posterior elements affecting 4-mobile synovial articulations ( true osteoarthritis)
2-Facets in the L/S & 2-Facets & 2-Uncovertebral joints in the C/S
Imaging plays a significant role in the diagnosis, grading, and evaluation of neurological complications (e.g., spondylotic myelopathy/radiculopathy)
X-radiography with AP, Lateral & Oblique spinal views provides Dx and classification of Spondylosis
MR imaging may help to evaluate the degree of neurological changes associated with degenerative spinal canal and neural foraminal stenosis
Spinal motion segment:
2-adjacent vertebrae
IVD (fibrocartilage)
2-facets (synovial)
Pathology: loss of disc height increases mechanical stress on mobile elements
Ligamentum flavum “hypertrophy” or thickening due to buckling
Loss of normal lordosis with or w/o reversal or kyphosis
Vertebral canal & neural foraminal stenosis
Neutral lateral cervical radiograph: note mild to moderate disc narrowing and spondylophyte formation at C5-6 & C6-C7 (most common levels affected by cervical spondylosis). Straightening or flattening with mild reversal of cervical lordosis. Some mild facet proliferation is noted at the above levels
On radiographs: evaluate for disc height (mild, moderate or severe) loss
End-plate sclerosis & spondylophytes; mild, moderate or severe
Facet and uncinate irregularity, hypertrophy/degeneration; mild, moderate or severe
Key Dx: correlate with a clinical presentation: neck/back pain with or w/o neurological disturbance ( myelopathy vs. radiculopathy or both)
Uncinate processes undergo degeneration/proliferation resulting in uncovertebral arthrosis
Early findings present with mild bone proliferation along the cortical margin (white and black arrows) if compared to normal uncinate (orange arrow)
Later, more extensive bone proliferation extending into and narrowing vertebral canal and neural osseous foramina (IVF’s) may be noted. The latter may contribute to spinal/IVF stenosis and potential neurological changes
Posterior oblique views may help further
AP lower cervical (a) and posterior oblique (b) views
Note mild uncinated process proliferation with neural foraminal narrowing (arrows)
Typically if less than a third of IVF becomes narrowed, patients may present w/o significant neurological signs
Lumbar spondylosis is evaluated with AP and lateral views with additional AP L5-S1 spot view to examine lumbosacral junction
Typical features include disc height loss/degeneration
Intra-discal gas (vacuum) phenomenon (blue arrow) along with spondylophytes
Degenerative spondylolisthesis and/or retrolisthesis (green arrow) may follow disc and facet degeneration and can be graded by the Meyerding classification
In most cases, degenerative spondylolisthesis rarely progresses beyond Grade 2
Lumbar facet degeneration seen as bone proliferation/sclerosis and IVF narrowing
MR imaging w/o gad C is an effective modality to evaluate clinical signs of spondylosis & associated neurological complications with pre-surgical evaluation
Case: 50-y.o Fe with neck pain. Case b-45-y.o.M (top a b images). MRI reveals: loss of disc hydration or desiccation, spondylophytes and disc herniation w/o neurological changes
(Bottom images) Left: preoperative and right postoperative MRI slices of the patient presented with clinical signs of cervical spondylotic myelopathy. Note disc herniation, ligam flavum hypertrophy and canal stenosis (left)
Sagittal MRI slice of lumbar DDD manifested with disc desiccation and posterior herniation effacing thecal sac
Correlating sagittal and axial slices will be more informative to evaluate canal stenosis and potential degree of neurological involvement (above-bottom images)
Use the following resources to learn more on MRI evaluation and diagnosis of Degenerative Disc Disease:
Many types of arthritis can affect the structure and function of the muscles, bones and/or joints, causing symptoms such as, pain, stiffness and swelling. While arthritis can commonly affect the hands, wrists, elbows, hips, knees and feet, it can also affect the facet joints found along the length of the spine. One of the most well-known types of arthritis, known as rheumatoid arthritis or RA, is a chronic inflammatory disease of the joints which occurs when the human body’s own immune system attacks the synovium, the thin membrane that lines the joints. According to the article below, imaging the spine in arthritis is fundamental towards its proper treatment.
Abstract
Spinal involvement is frequent in rheumatoid arthritis (RA) and seronegative spondyloarthritides (SpA), and its diagnosis is important. Thus, MRI and CT are increasingly used, although radiography is the recommended initial examination. The purpose of this review is to present the typical radiographic features of spinal changes in RA and SpA in addition to the advantages of MRI and CT, respectively. RA changes are usually located in the cervical spine and can result in serious joint instability. Subluxation is diagnosed by radiography, but supplementary MRI and/or CT is always indicated to visualize the spinal cord and canal in patients with vertical subluxation, neck pain and/or neurological symptoms. SpA may involve all parts of the spine. Ankylosing spondylitis is the most frequent form of SpA and has rather characteristic radiographic features. In early stages, it is characterized by vertebral squaring and condensation of vertebral corners, in later stages by slim ossifications between vertebral bodies, vertebral fusion, arthritis/ankylosis of apophyseal joints and ligamentous ossification causing spinal stiffness. The imaging features of the other forms of SpA can vary, but voluminous paravertebral ossifications often occur in psoriatic SpA. MRI can detect signs of active inflammation as well as chronic structural changes; CT is valuable for detecting a�fracture.
The spine can be involved in most inflammatory disorders encompassing rheumatoid arthritis (RA), seronegative spondyloarthritides (SpA), juvenile arthritides and less frequent disorders such as, arthro-osteitis and SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome.
During the last decade, the diagnostic use of magnetic resonance imaging (MRI) and computed tomography (CT) has increased considerably, although radiography is still the recommended initial examination. It is therefore important to know the characteristic radiographic findings in arthritides in addition to the advantages of supplementary MRI and CT. This review will focus on the different imaging features and be concentrated on the most frequent inflammatory spinal changes seen in RA and SpA, respectively. These two entities display somewhat different imaging features, which are important to recognize.
Rheumatoid arthritis is an autoimmune disease which causes the human body’s own immune system to attack and often destroy the lining of the joints. Although it commonly affects the small joints of the hands and feet, rheumatoid arthritis, or RA, can affect any joint in the human body. The neck, or cervical spine, can be affected more often than the lower back if rheumatoid arthritis affects the joints in the spine.�
Dr. Alex Jimenez D.C., C.C.S.T.
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Rheumatoid Arthritis
Involvement in RA is usually located in the cervical spine where erosive changes are predominantly seen in the atlanto-axial region. Inflamed and thickened synovium (pannus) can occur around the odontoid process (dens) and cause bone erosion and destruction of surrounding ligaments, most seriously if the posterior transverse ligament is involved. Laxity or rupture of the transverse ligament causes instability with a potential risk of spinal cord injury. Cervical RA involvement is a progressive, serious condition with reduced lifetime expectancy [1], and its diagnosis is therefore important [2, 3].
Radiography of the cervical spine is mandatory in RA patients with neck pain [3]. It should always include a�lateral view in a flexed position compared with a neutral position in addition to special views of the dens area to detect any lesions and/or instability (Fig. 1). A supplementary lateral view during extension can be useful to assess reducibility of atlanto-axial subluxation possibly limited by pannus tissue between the anterior arc of the atlas and dens.
Anterior atlanto-axial subluxation is the most frequent form of RA instability in the occipito-atlanto-axial region, but lateral, rotatory and vertical subluxation can also occur. The definition of the different forms of instability by radiography is as follows [3].
Anterior atlanto-axial subluxation. Distance between the posterior aspect of the anterior arc of the atlas and the anterior aspect of the dens exceeding 3 mm in a neutral position and/or during flexion (Fig. 1). It may cause stenosis of the atlanto-axial canal presenting as a posterior atlanto-dental interval<14 mm (Fig. 1).
Lateral and rotatory atlanto-axial subluxation.�Displacement of the lateral masses of the atlas more than 2 mm in relation to that of the axis and asymmetry of the lateral masses relative to the dens, respectively (Fig. 2). Rotatory�and lateral subluxation is diagnosed on open-mouth anterior-posterior (AP) radiographs. Anterior subluxation often coexists because of the close anatomical relation between the atlas and the axis.
Posterior atlanto-axial subluxation. The anterior arc of the atlas moves over the odontoid process. This is rarely seen, but may coexist with fracture of the dens.
Vertical atlanto-axial subluxation is also referred to as atlanto-axial impaction, basilar invagination or cranial�setting, and is defined as migration of the odontoid tip proximal to McRae�s line corresponding to the occipital foramen. This line can be difficult to define on radiographs, and vertical subluxation has therefore also been defined by several other methods. Migration of the tip of the odontoid process >4.5 mm above McGregor�s line (between the postero-superior aspect of the hard palate and the most caudal point of the occipital curve) indicates vertical subluxation (Fig. 3).
The occurrence of dens erosion can, however, make this measurement difficult to obtain. The Redlund-Johnell method is therefore based on the minimum distance between McGregor�s line and the midpoint of the inferior margin of the body of the axis on a lateral radiograph in a neutral position (Fig. 3) [4]. Visualisation of the palate may not always be obtained. Methods without dens and/or the palate as landmarks have therefore been introduced [4]. The method described by Clark et al. (described in [4]) includes assessment of the location of the atlas by dividing the axis into three equal portions on a lateral radiograph. Location of the anterior arc of the atlas in level with the middle or caudal third of the axis indicates vertical subluxation (Fig. 3). Ranawat et al. have proposed using the distance between the centre of the second cervical pedicle and the�transverse axis of the atlas at the odontoid process (Fig. 3) [4]. To obtain the diagnosis of vertical subluxation a combination of the Redlund-Johnell, Clark and Ranawat methods has been recommended (described in [4]). If any of these methods suggests vertical subluxation MRI should be performed to visualize the spinal cord (Fig. 4). Using this combination of methods vertical subluxation will be missed in only 6% of patients [4]. It is mandatory to diagnose vertical subluxation; this can be fatal because of the proximity of the dens to the medulla oblongata and the proximal portion of the spinal cord. Risk of cord compression/injury occurs, especially in patients with flexion instability accompanied by erosive changes in the atlanto- axial and/or atlanto-occipital joints, causing the vertical subluxation with protrusion of the dens into the occipital foramen (Figs. 4, 5).
Subaxial RA changes also occur in the form of arthritis of the apophyseal and/or uncovertebral joints, appearing as narrowing and superficial erosions by radiography. It can cause instability in the C2-Th1 region, which is mainly seen in patients with severe chronic peripheral arthritis. Anterior subluxation is far more frequent than posterior subluxation. It is defined as at least 3 mm forward slippage of a vertebra�relative to the underlying vertebra by radiography including a flexion view (Fig. 6). Changes are particularly characteristic at the C3�4 and C4�5 level, but multiple levels may be involved, producing a typical �stepladder� appearance on lateral radiographs. The condition is serious if the subaxial sagittal spinal canal diameter is <14 mm, implying a possibility of spinal cord compression [2]. The instability may progress over time, especially if the C1�C2 region is stabilized surgically (Fig. 6) [5].
Discitis-like changes and spinous process erosion may also be detected by radiography in RA, but are relatively rare, whereas concomitant degenerative changes occur occasionally (Fig. 1).
Cross-sectional imaging in the form of CT and MRI eliminates overprojecting structures and can improve the detection of RA changes. Osseous changes (erosions, etc.) can be clearly delineated by CT [6]. Additionally, MRI visualizes soft tissue structures (pannus; spinal cord, etc.), signs of disease activity and sequelae of inflammation in the form of fibrous pannus. These advantages of CT and MRI in patients with atlanto-axial involvement are illustrated in Figs. 7 and 8, including the possibility of detecting signs of arthritis by MRI before the occurrence of erosive changes (Fig. 8) [3].
A diagnostic strategy according to Younes et al. [3] is recommended (Fig. 9). This includes an indication for radiography in all RA patients with disease duration >2 years as cervical involvement may occur in over 70% of patients and has been reported to be asymptomatic in 17% of RA patients. It is recommended to monitor patients with manifest peripheral erosions accompanied by RF (rheumatoid factor) and antiCCP (antibodies to cyclic citrullinated peptide) positivity every second year and�patients with few peripheral erosions and RF negativity at 5-year intervals. MRI is indicated in patients with neurological deficit, radiographic instability, vertical subluxation and subaxial stenosis [2, 3]. Visualisation of the spinal cord is especially important to detect cord injury or risk of injury. MRI should therefore always be performed in RA patients with neck pain and/or neurological symptoms [3, 7].
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Seronegative Spondyloarthritides
According to European classification criteria [8, 9], SpA is divided into: (1) ankylosing spondylitis (AS), (2) psoriatic arthritis, (3) reactive arthritis, (4) arthritis associated with inflammatory bowel disorders (enteropathic arthritis) and (5) undifferentiated SpA. Inflammatory changes at the sacroiliac joints always occur in AS and are part of most other forms of SpA. Spinal changes are also a feature of SpA, especially in the late stages of AS.
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Ankylosing Spondylitis
Ankylosing spondylitis is the most frequent and usually the most disabling form of SpA. It has a genetic predisposition in the form of a frequent association with the human leukocyte antigen (HLA) B27 [10]. AS often starts in early adulthood and has a chronic progressive course. It is therefore important to diagnose this disorder. According to the modified New York Criteria [11], the diagnosis of definite AS requires the following: manifest sacroiliitis by radiography (grade ?2 bilateral or unilateral grade 3�4 sacroiliitis; Fig. 10) and at least one of the following clinical criteria: (1) low back pain and stiffness for more than 3 months improving with activity, (2) limited movement of the lumbar spine and (3) reduced chest expansion. These criteria are still used in the diagnosis of AS despite the increasing use of MRI to detect the disease early. It is therefore important to know both the characteristic radiographic features and the MR features of AS.
Early radiographic spinal changes encompass erosion of vertebral corners (Romanus lesions) causing vertebral squaring and eliciting reactive sclerosis appearing as condensation of vertebral corners (shiny corners; Fig. 10). These changes are caused by inflammation at the insertion of the annulus fibrosus (enthesitis) at vertebral corners provoking reactive bone formation [12]. Later on slim ossifications appear in the annulus fibrosus (syndesmo- phytes) (Fig. 11) [13]. With disease progression the spine gradually fuses because of syndesmophytes crossing the intervertebral spaces in addition to fusion of apophyseal joints, resulting in complete spinal fusion (bamboo spine;�Fig. 12). In advanced disease the supra- and interspinous ligaments may ossify and be visible on frontal radiographs as a slim ossified streak (Fig. 12). The occurrence of a single central radiodense streak has, the �dagger sign�. When the ligamentous ossification occurs together with ossification of apophyseal joint capsules, there are three vertical radiodense lines on frontal radiography (trolley-track sign).
Erosive changes within intervertebral spaces (Andersson lesions) have been detected by radiography in approximately 5% of patients with AS [14], but more frequently by MRI (Fig. 11) [15].
Persistent movement at single intervertebral spaces may occur in an otherwise ankylosed spine, sometimes caused by non-diagnosed fractures. This can result in pseudo- arthrosis-like changes with the formation of surrounding reactive osteophytes due to excessive mechanical load at single movable intervertebral spaces [14]. The diagnosis of such changes may require a CT examination to obtain adequate visualization (Fig. 13).
One of the life-threatening complications of AS is spinal fracture. Non-fatal fractures have been reported to occur in up to 6% of AS patients, especially in patients with long disease duration [16]. Fractures may occur after minor trauma because of the spinal stiffness and frequently accompanying osteoporosis. Fractures often occur at intervertebral spaces, but usually involve the ankylosed posterior structures and are thereby unstable (Fig. 14). Obvious fractures can visualize by radiography, but fractures may be obscured. It is therefore mandatory to supplement a negative radiography with CT if fracture is suspected (in the case of trauma history or a change in spinal symptoms). The occurrence of cervico-thoracic fractures may cause spinal cord injury and be lethal even following minor trauma [17].
Cross-sectional CT or MR imaging can be advantageous in the diagnosis of AS changes. CT providing a clear delineation of osseous structures is the preferred technique for visualizing pseudo-arthrosis and detecting fractures (Figs. 13, 14). CT is superior to MRI in detecting minor osseous lesions such as erosion and ankylosis of the apophyseal, costo-vertebral and costo-transversal joints (Fig. 15). MRI can visualize signs of active inflammation in the form of bone marrow and soft tissue oedema and/or contrast enhancement. It has therefore gained a central role in the evaluation of disease activity [15]. MRI can, however, also detect sequelae of inflammation consisting of fatty deposition in the bone marrow and chronic structural changes such as erosion and fusion of vertebral bodies [15].
Characteristic MR findings early in the disease are activity changes mainly consisting of oedema at vertebral corners and/or costo-vertebral joints (Fig. 16) [13]. The inflammatory changes at vertebral corners are characteristic of AS. Based on the occurrence of severe or multiple (?3) lesions in young patients, AS changes can be distinguished from degenerative changes with a high reliability [18].
During the disease course signs of activity can also occur at syndesmophytes, apophyseal joints and interspinous ligaments (Fig. 16). Detection of inflammation at apophyseal joints by MRI, however, demands pronounced involvement�histopathologically [19]. The inflammation at vertebral corners is the most valid feature and has been observed related to the development of syndesmophytes by radiography [12], establishing a link between signs of disease activity and chronic structural changes.
Chronic AS changes detectable by MRI mainly consist of fatty marrow deposition at vertebral corners (Fig. 17), erosion (Fig. 11) and vertebral fusion in advanced disease (Fig. 12). Fatty marrow deposition seems to be an a sign of chronicity being significantly correlated with radiographic changes, in particular, vertebral squaring [15]. Erosions are more frequently detected by MRI than by radiography (Fig. 11) [15] and can present with signs of active inflammation and/or surrounding fatty marrow deposition compatible with sequels of osseous inflammation. Syndesmophytes, however, may not always be visible by MRI because they may be difficult to distinguish from fibrous tissue unless there is concomitant active inflammation or fatty deposition (Figs. 11, 16) [15, 20].
The possibility of visualizing disease activity by MRI has increased its use to monitor AS, especially during anti-TNF (anti-tumour necrosis factor) therapy [21, 22]. Several studies have shown that MR changes are frequent in the thoracic spine (Fig. 16) [15, 23]. It is therefore important to examine the entire spine using sagittal STIR or T2 fat-saturated (FS) and T1-weighted sequences. Supplementary axial slices can be necessary for visualising involvement of apophyseal, costo-vertebral and costo-transversal joints (Fig. 16) [24, 25]. Post-contrast T1FS sequences can sometimes be advantageous as they provide better anatomical delineation [26]. Additionally, dynamic contrast-enhanced MRI may be superior to static MRI in monitoring disease activity during anti-TNF therapy [27]. Whole-body MRI gives the possibility of detecting involvement in other areas without losing important information about spinal and sacroiliac joint involvement [28, 29].
Other Forms of SpA
Radiographic changes in reactive and psoriatic arthritis are often characterized by voluminous non-marginal syndesmophytes (parasyndesmophytes) or coalescing ossification of the paravertebral ligaments in addition to asymmetrical sacroiliitis (Fig. 18) [30].
Reactive arthritis is self-limiting in most patients. However, in patients with chronic reactive arthritis and HLA B27 the axial changes may progress to changes somewhat similar to those seen in AS and can then be regarded as AS elicited by infection [10].
Axial psoriatic arthritis (PsA) occurs in approximately 50% of patients with peripheral PsA [31]. It differs radiographically from AS by the voluminous paravertebral ossifications and the occurrence of spinal changes without concomitant sacroiliitis in 10% of patients [32]. Axial PsA may be clinically silent [33], and involvement of the cervical spine is frequent (atlanto-axial or apophyseal joint changes). The cervical recognize may include atlanto-axial instability as seen in RA (Fig. 19), but the pathogenesis and thereby imaging findings are different. In PsA radiography and CT usually visualize new bone formation in the region of the dens. This is elicited by osseous inflammation (osteitis) and/or inflammation at ligament/ tendon attachments (enthesitis) detectable by MRI (Fig. 19). Osteitis is often a feature of spinal PsA and can occur together with paravertebral ossification/para- syndesmophytes and erosion of vertebral plates (Fig. 20). , and illustrated MR findings in PsA are based on personal observations and seem to reflect the radiographic changes encompassing a mixture of osteitis, enthesitis and erosion. Unfortunately, there is a lack of�systematic description of spinal changes in PsA by MRI. Some of the patients described under the term SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome may have PsA. SAPHO is a collective term often used for inflammatory disorders primarily presenting with osseous hyperostosis and sclerosis, and they are frequently associated with skin disorders. The most commonly affected site in SAPHO is the anterior chest followed by the spine [34]. The PsA changes shown in Fig. 20 are characterized by hyperostosis and sclerosis, both main features of SAPHO. However, this patient did not have anterior chest involvement.
In patients with enteropathic arthritis associated with Crohn�s disease or ulcerative colitis, the spine is often osteoporotic with various accompanying SpA features by radiography, mostly AS-like changes. However, by MRI there may be more pronounced inflammation in the posterior ligaments than seen in the other forms of SpA (Fig. 21).
Rheumatoid arthritis of the spine can cause neck pain, back pain, and/or radiating pain in the upper and lower extremities. In severe cases, RA can also lead to the degeneration of the spine, resulting in the compression or impingement of the spinal cord and/or the spinal nerve roots. As a chiropractor, we offer diagnostic imaging to help determine a patient’s health issue, in order to develop the best treatment program.
Dr. Alex Jimenez D.C., C.C.S.T.
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Conclusion
Radiography is still valuable in the diagnosis of spinal inflammatory disorders. It is necessary for visualizing instability and is superior to MRI for detecting syndesmophytes. However, MRI and CT can detect signs of spinal involvement before they can be visualized by radiography. MRI adds information about potential involvement of the spinal cord and nervous roots in addition to signs of disease activity and chronic changes such as fibrous pannus in RA and fatty marrow deposition, erosion and vertebral fusion in SpA. MRI is�therefore widely used to monitor inflammatory spinal diseases, especially during anti-TNF therapy.
Computed tomography is particularly valuable in the detection of fracture and minor osseous lesions as well as in the evaluation of pseudo-arthrosis. In conclusion, rheumatoid arthritis most commonly affects the structure and function of your hands, wrists, elbows, hips, knees, ankles and feet, however, people with this chronic inflammatory disease can experience back pain. Imaging the spine�in arthritis is fundamental to determine treatment. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Acute Back Pain
Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
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