20: Rheumatologic and Connective Tissue Disorders

Chapter 20

Rheumatologic and Connective Tissue Disorders

Rheumatologic (or rheumatoid) disease is much more than “arthritis” and encompasses a large group of disorders of the rheumatic diseases that affect bones, joints, and muscles.< ?xml:namespace prefix = "mbp" />1 Arthritis is a nonspecific term that means “inflammation of the joints.” Often arthritis is used interchangeably with rheumatism or rheumatoid arthritis to denote aches, pains, and stiffness in the joints and muscles, but these terms are not synonymous. More than 100 rheumatologic (or rheumatoid) diseases affect various parts of the body. Some of the more common types include rheumatoid arthritis (RA), osteoarthritis (OA), systemic lupus erythematosus (SLE), juvenile rheumatoid arthritis (jRA), scleroderma (SD), Sjögren syndrome (SS), gout, ankylosing spondylitis, Lyme disease, giant cell arteritis (or temporal arteritis), fibromyalgia syndrome (FMS), and psoriatic rheumatoid arthritis (pRA).1

Rheumatologic (or rheumatoid) diseases have significant personal and economic impact. According to the Arthritis Foundation, more than 40 million Americans suffer from various forms of arthritis, and more than 8 million of them are disabled. In terms of its overall economic impact, arthritis costs the American economy more than $20 billion annually, and nearly 30 million workdays are lost per year.1

Categories of Musculoskeletal Diseases

Musculoskeletal diseases can be classified into nine categories, defined by the predominantly affected tissues, such as joint, synovium, cartilage, or connective tissues (Table 20-1). At each point in the evaluation (history, physical examination, and laboratory testing), it is important to ask what tissues are involved. Recognition of the pattern of predominant tissue involvement can direct attention toward the disease primarily associated with that tissue. Before consideration of clinical approaches to the evaluation of patients with musculoskeletal problems, it is useful to first review the anatomy and pathophysiology of the affected structures.1

TABLE 20-1 Classification of Musculoskeletal Diseases

image

Anatomy

The structures that are commonly involved in rheumatoid diseases include the joint, the joint cavity, synovial fluid, and periarticular structures. The lining membrane, known as the synovium, consists of a thin layer of macrophages (type A cells) and fibroblasts (type B cells) with a sublining of rich, vascular, loose connective tissue. Hyaline cartilage overlies the bony end plates and provides a cushion to joint motion. The cartilage has high water content and obtains its nutrition solely from the synovial fluid, which is derived from the synovium primarily as an ultrafiltrate of plasma. The synovium also secretes specialized molecules into the synovial fluid, such as hyaluronic acid. An intact bony end plate is required to support the cartilage. The joint capsule and ligaments provide further support and blend with the periosteum. Periarticular anatomy is equally important and includes the tendons, bursae, and muscles associated with each joint.1

Pathophysiology

The cause of musculoskeletal problems is usually inflammatory, metabolic, degenerative, tumor, or some combination thereof. Synovial inflammatory disorders, such as rheumatoid arthritis, begin in the synovium and secondarily damage the cartilage, joint capsule, and bone. Inflammation at entheses, the insertion sites of tendons or ligaments on bone, is characteristic of the spondyloarthropathies, such as ankylosing spondylitis. Crystal deposition disorders, such as gout or pseudogout, may also cause articular inflammation. Infections primarily involve the joint cavity (septic arthritis) or bone (osteomyelitis). The noninflammatory, degenerative disease osteoarthritis begins in the cartilage and leads to cartilage loss, subchondral new bone formation, and marginal bony overgrowth. Cartilage loss also may occur secondarily to synovial inflammation or trauma.1 Osteonecrosis of bone may be associated with secondary cartilage damage after collapse of the bony end plate. Inflammatory diseases of the muscle usually manifest with painless proximal weakness. Periarticular inflammation may involve tendons or bursae, and these structures are common causes of pain and stiffness, often misinterpreted as arising from the joint itself. Finally, the common clinical problem of fibromyalgia (widespread muscle pain) is characterized by soft tissue pain with local tenderness in specific points but without abnormal blood studies.1

Although the rheumatologic diseases comprise a group of more than 100 important diseases, this chapter is limited to a discussion of eight: rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis (PsA), systemic lupus erythematosus (SLE), Lyme disease, fibromyalgia (FMS), temporal arteritis, and Sjögren syndrome (SS), which are among the most common forms encountered, are more dentally related conditions, and can serve as models for the dental management of other forms. Several important items regarding the dental management of patients with rheumatologic and connective tissue disorders, including effects on the temporomandibular joint (TMJ), salivary glands, and oral mucosal tissues, organ and system involvement, and drug therapy, are discussed here.

Rheumatoid Arthritis

Definition

Incidence and Prevalence

Rheumatoid arthritis (RA) is an autoimmune disease of unknown origin that is characterized by symmetric inflammation of joints, especially of the hands, feet, and knees. Severity of the disease varies widely from patient to patient and from time to time within the same patient. Prevalence is somewhat difficult to determine because of lack of well-defined markers of the disease; however, estimates range from 1% to 2% of the population. Disease onset usually occurs between ages 35 and 50 years. RA is more prevalent in women than in men by a 3 : 1 ratio.1

Etiology

The cause of RA is unknown; however, evidence seems to implicate an interrelationship of infectious agents, genetics, and autoimmunity. One theory suggests that a viral agent alters the immune system in a genetically predisposed person, leading to destruction of synovial tissues. Although the disease can occur within families, suggesting a genetic component, one specific causative gene has not been identified.24 Nevertheless, many people who develop RA have a genetic predisposition that occurs in the form of a tissue marker called HLA-DR4; however, not everyone with this tissue type develops the disease.25

Pathophysiology and Complications

With RA, the fundamental abnormality involves microvascular endothelial cell activation and injury.25 Primary changes occur within the synovium, which is the inner lining of the joint capsule (Figure 20-1). Edema of the synovium occurs, followed by thickening and folding. This excessive tissue, composed of proliferative and invasive granulation tissue, is referred to as pannus. In addition, marked infiltration of lymphocytes and plasma cells into the capsule occurs. Eventually, granulation tissue covers the articular surfaces and destroys the cartilage and subchondral bone through enzymatic activity (Figure 20-2). This process also extends to the capsule and ligaments, causing distention and rupture. New bone or fibrous tissue then is deposited, resulting in fusion or loss of mobility.25

image

FIGURE 20-1 The joint surface (top) has lost its cartilage and consists of granulation tissue with scar tissue. Subchondral bone shows degenerative changes and areas of necrosis.

(Courtesy A. Golden, Lexington, Kentucky.)

image

FIGURE 20-2 A micrograph of a pannus resulting from severe synovitis in rheumatoid arthritis. The pannus is eroding articular cartilage and bone (arrow).

(Courtesy Richard Estensen, MD, Minneapolis, Minnesota.)

A likely sequence of events begins with a synovitis that stimulates immunoglobulin G (IgG) antibodies. These antibodies form antigenic aggregates in the joint space, leading to the production of rheumatoid factor (autoantibodies). Rheumatoid factor then complexes with IgG complement, a process that produces an inflammatory reaction that injures the joint space.25

An associated finding in 20% of patients with RA is the presence of subcutaneous nodules, which are commonly found around the elbow and finger joints. These nodules are thought to arise from the same antigen-antibody complex that is found in the joint. Vasculitis confined to small- and medium-sized vessels also may occur and probably is caused by the same complex.25

RA is a pleomorphic disease with variable expression. The most progressive period of the disease occurs during the earlier years; thereafter, it slows. Onset is gradual in more than 50% of patients, and as many as 20% follow a monocyclic course that abates within 2 years. Another 10% experience relentless crippling that leads to nearly complete disability. The remainder follows a polycyclic or progressive course.25 The long-term prognosis for people with abrupt onset of disease is similar to that for people with gradual disease onset. The course and severity of RA are unpredictable, but the disorder is characterized by remissions and exacerbations. For most patients, however, the disease is a sustained, lifelong problem that can be controlled or modified to allow a normal or nearly normal life.25

The life expectancy of persons with severe RA is shortened by 10 to 15 years. This increased mortality rate usually is attributed to infection, pulmonary and renal disease, and gastrointestinal bleeding.25

Many complications may accompany RA. Included among these are digital gangrene, skin ulcers, muscle atrophy, keratoconjunctivitis sicca (Sjögren syndrome), TMJ involvement, pulmonary interstitial fibrosis, pericarditis, amyloidosis, anemia, thrombocytopenia, neutropenia, and splenomegaly (Felty syndrome).25

Clinical Presentation

Signs and Symptoms

The usual onset of RA is gradual and subtle (Table 20-2), and the disorder is commonly preceded by a prodromal phase of general fatigue and weakness with joint and muscle aches. Characteristically, these symptoms come and go over varying periods. Then, painful joint swelling, especially of the hands and feet, occurs in several joints and progresses to other joints in a symmetric fashion (Figure 20-3). Joint involvement persists and gradually progresses to immobility, contractures, subluxation, deviation, and other deformities. Characteristic features include pain in the affected joints aggravated by movement, generalized joint stiffness after inactivity, and morning stiffness that lasts longer than 1 hour. The joints most commonly affected are fingers, wrists, feet, ankles, knees, and elbows. Multiple joint changes noted in the hands include a symmetric spindle-shaped swelling of the proximal interphalangeal (PIP) joints, with dorsal swelling and characteristic volar subluxation of the metacarpophalangeal (MCP) joint (see Figure 20-3). The TMJ is reported to be involved in up to 75% of patients.26 Because of the variable rate of progression and pain intensity, the median period between onset of symptoms of RA and its diagnosis is 36 weeks.1,7

TABLE 20-2 Comparison of Rheumatoid Arthritis and Osteoarthritis

Rheumatoid Arthritis Osteoarthritis
Multiple symmetric joint involvement Usually one or two joints (or groups) involved
Significant joint inflammation Joint pain usually without inflammation
Morning joint stiffness lasting longer than 1 hour Morning joint stiffness lasting less than 15 minutes
Symmetric, spindle-shaped swelling of proximal interphalangeal joints and volar subluxation of metacarpophalangeal joints and Bouchard’s nodes of proximal interphalangeal joints Heberden’s nodes of distal interphalangeal joints
Systemic manifestations (fatigue, weakness, malaise) No systemic involvement
image

FIGURE 20-3 Hands of a patient with advanced rheumatoid arthritis.

(From Damjanov I: Pathology for the health professions, ed 4, St. Louis, 2012, Saunders.)

Extraarticular manifestations include rheumatoid nodules, vasculitis, skin ulcers, Sjögren syndrome, interstitial lung disease, pericarditis, cervical spine instability, entrapment neuropathies, and ischemic neuropathies.8 The American Rheumatism Association has developed revised criteria for the diagnosis and classification of RA to be used in clinical trials and epidemiologic studies (Box 20-1). These criteria have high specificity (89%) and sensitivity (91% to 94%) compared with control subjects when used to classify patients with RA. For the diagnosis of RA to be made, four of seven criteria must be met.25

image

Box 20-1

Criteria for the Diagnosis of Rheumatoid Arthritis*

Morning stiffness

Arthritis of three or more joint areas

Arthritis of hand joints

Symmetric arthritis

Rheumatoid nodules

Serum rheumatoid factor

Radiographic changes

Adapted from Arnett FC, et al: The American Rheumatism Association 1987 revised citeria for the classification of rheumatoid arthritis, Arthritis Rheum 31:315-324, 1988.

* At least four must be present for a diagnosis of rheumatic arthritis.

image

Laboratory Findings

No laboratory tests are pathognomonic or diagnostic of RA, although they are used in conjunction with clinical findings to confirm the diagnosis. Laboratory findings most commonly seen in RA include an increased erythrocyte sedimentation rate (ESR), the presence of C-reactive protein (CRP), a positive result on rheumatoid factor assay in 85% of affected patients, and a hypochromic microcytic anemia. In patients with Felty syndrome (RA with splenomegaly), a marked neutropenia may be present.25

Antibodies to cyclic citrullinated proteins (CCPs) are autoantibodies, which are important in the diagnosis of RA.9 Anti-CCP antibodies are highly associated with RA. They occur in 70% to 80% of patients with RA as well as in some other forms of inflammatory arthritis. These antibodies may appear before any signs or symptoms of RA and therefore may prove beneficial as early screening markers for earlier diagnosis and intervention of RA.9

Diagnosis

The American College of Rheumatology has established criteria for the diagnosis of RA (see Box 20-1), the classification of severity by radiography, functional classes, and the definition of remission. Although they were not designed for managing individual patients, these criteria are useful as a frame of reference and for describing clinical phenomena.1,10

By definition, the diagnosis of RA cannot be made until the disease has been present for at least several weeks. Many extraarticular features of RA, the characteristic symmetry of inflammation, and the typical serologic findings may not be evident during the first month or two after disease onset. Therefore, the diagnosis of RA usually is presumptive early in its course.

Although extraarticular manifestations may dominate in some patients, documentation of an inflammatory synovitis is essential for a diagnosis. Inflammatory synovitis can be documented by demonstration of synovial fluid leukocytosis, defined as white blood cell (WBC) counts greater than 2000/µL, histologic evidence of synovitis, or radiographic evidence of characteristic erosions.57,9,10

Medical Management

The treatment approach to RA is, by necessity, palliative because no cure as yet exists for the disease. The ultimate aim of management is to achieve disease remission for the patient. Remission is elusive, however, so more practical treatment goals are to reduce joint inflammation and swelling, relieve pain and stiffness, and facilitate and encourage normal function.8 These goals are accomplished through a basic treatment program that consists of patient education, rest, exercise, physical therapy, and aspirin or other nonsteroidal antiinflammatory drugs (NSAIDs).25

When an understanding of the determinants of disease outcome is acquired, a treatment strategy that will be useful and acceptable to the individual patient can be devised. These determinants include presence of rheumatoid factor, early onset of severe synovitis with functional limitation, joint erosions, persistent elevation of ESR or CRP, presence of extraarticular manifestations, and a family history of severe RA.11,12

The major goals of therapy are to relieve pain, swelling, and fatigue; improve joint function; stop joint damage; and prevent disability and disease-related morbidity. These goals are constant throughout the disease course, although emphasis may shift to address specific patient needs. For example, some patients with advanced joint damage experience minimal swelling or constitutional symptoms and benefit most from physical therapy, joint reconstruction, and pain control. Most patients, however, require continued efforts to control the inflammatory process through disease-modifying therapy.1,12

Drugs for the management of RA have been traditionally, but imperfectly, divided into two groups: those used primarily for the control of joint pain and swelling, and those intended to limit joint damage and improve long-term outcome (Table 20-3). Symptoms of pain and swelling in RA are mediated, at least in part, by intense cytokine activity. NSAIDs inhibit proinflammatory prostaglandins and are effective treatments for pain, swelling, and stiffness, but they have no effect on the disease course or on risk of joint damage. On the other hand, antiinflammatory properties have been noted for several disease-modifying antirheumatic drugs (DMARDs), which are used principally to control disease and to limit joint damage.25 These drugs include methotrexate and biologic response modifiers with actions targeted against specific cytokines, such as tumor necrosis factor-α (TNF-α). Corticosteroids are powerful, nonspecific inhibitors of cytokines and, in some studies that compared them with placebo, are reported to effectively delay joint erosion.17

TABLE 20-3 Drugs Used in the Management of Rheumatoid Disorders and Systemic Lupus Erythematosus

Drug(s) (Trade Name) Dental and Oral Considerations
Salicylates
Aspirin, Ascriptin, Bufferin, Anacin, Ecotrin, Empirin Prolonged bleeding but not usually clinically significant
Nonsteroidal Antiinflammatory Drugs (NSAIDs)
Ibuprofen (Motrin), fenoprofen (Nalfon), indomethacin (Indocin), naproxen (Naprosyn), meclofenamate (Meclomen), piroxicam (Feldene), sulindac (Sulindac), tolmetin (Tolectin), diclofenac (Voltaren), flurbiprofen (Ansaid), diflunisal (Dolobid), etodolac (Lodine), nabumetone (Relafen), oxaprozin, ketorolac Prolonged bleeding but not usually clinically significant; oral ulceration, stomatitis
Cyclooxygenase (COX)-2 Inhibitors
Celecoxib
Rofecoxib
None
Tumor Necrosis Factor-α Inhibitors
Etanercept
Infliximab
None
Injectable Glucocorticoids
Triamcinolone hexacetonide Adrenal suppression, masking of oral infection, impaired healing
Triamcinolone acetonide
Prednisolone tebutate
Methylprednisolone acetate
Dexamethasone acetate
Hydrocortisone acetate
Triamcinolone diacetate
Betamethasone sodium phosphate and acetate
Dexamethasone sodium phosphate
Prednisolone sodium phosphate
Systemic Glucocorticoids
Hydrocortisone, cortisone, prednisone, prednisolone, dexamethasone, methylprednisolone (Deltasone, Meticorten, Orasone, Articulose-50, Delta-Cortef, Medrol) Adrenal suppression, masking of oral infection, impaired healing
Disease-Modifying Antirheumatic Drugs (DMARDs)
Antimalarial Agents
Hydroxychloroquine, quinine, chloroquine (Plaquenil) None
Penicillamine
Cuprimine, Depen None
Gold Compounds
Gold sodium thiomalate (Auranofin), aurothioglucose (Myochrysine Ridaura, Solganal) Increased infections, delayed healing, prolonged bleeding, oral ulcerations
Aralen Increased infections, delayed healing, prolonged bleeding, glossitis, stomatitis
Sulfasalazine
Azulfidine Increased infections, delayed healing, prolonged bleeding, intraoral pigmentation
Immunosuppressives
Azathioprine, cyclophosphamide Increased infections, delayed healing, prolonged bleeding
Methotrexate, cyclosporine, chlorambucil (Imuran, Cytoxan, Rheumatrex) Increased infections, delayed healing, prolonged bleeding, stomatitis

NSAIDs, especially aspirin, constitute the cornerstone of treatment. Aspirin may be prescribed in large doses on an individual basis. A common approach is to start a patient on three 5-grain tablets four times a day, then to adjust the dosage on the basis of patient response. The most common sign of aspirin toxicity is tinnitus. Should this occur, dosage is decreased. In addition to aspirin, many NSAIDs are available for use (see Table 20-3). Some of the more common NSAIDs include cyclooxygenase (COX)-2 inhibitors, namely, celecoxib (Celebrex); ibuprofen (Motrin, Advil, Rufen, Nuprin); naproxen (Naprosyn, Aleve); sulindac (Clinoril); tolmetin (Tolectin); fenoprofen (Nalfon); piroxicam (Feldene); diclofenac (Voltaren); flurbiprofen (Ansaid); diflunisal (Dolobid); etodolac (Lodine), and nabumetone (Relafen).17

All NSAIDs can cause a qualitative platelet defect that may result in prolonged bleeding, especially when given in high doses. The effects of aspirin are irreversible for the life of the platelet (10 to 12 days); thus, this effect continues until new platelets have replaced the old. The effect of the other NSAIDs on platelets is reversible and lasts only as long as the drug is present in the plasma (see Chapter 24).17

In addition to NSAIDs, a variety of other drugs can be used to treat patients with RA (see Table 20-3). Many of these drugs cause blood dyscrasias that may lead to more frequent infection, delayed healing, and prolonged bleeding.17

DMARDs, which commonly are employed in the treatment of patients with RA, are classified in various groups, each of which consists of multiple drugs (e.g., antimalarial agents, penicillamine, gold compounds) (see Table 20-3).17 Conventional DMARDs include methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, and gold injections. These drugs can be helpful in slowing down the damaging component of the disease process; however, the precise modes of action are still subject to research. The optimal sequencing of DMARDs remains a source of debate, and whether patients should be started on combinations of therapies or a single DMARD is also contentious.8

Gold compounds may be effective in decreasing inflammation and retarding the progress of the disease, but the incidence of associated toxicity is high, and dermatitis with mucosal ulceration, proteinuria, neutropenia, and thrombocytopenia may result. Antimalarial drugs (e.g., chloroquine, hydroxychloroquine) are also used to treat patients with RA; they are usually given in combination with aspirin or corticosteroids.17 Adverse effects include severe eye damage and blue-black intraoral pigmentation. Penicillamine also is used in the treatment of patients with RA. Both the antimalarials and penicillamine, however, are associated with significant toxicity—a fact that limits their use. Corticosteroids (e.g., prednisone, prednisolone) frequently are useful in controlling acute symptoms; however, because of multiple adverse effects, long-term usage is avoided if possible. One of the more potentially significant associated adverse effects is secondary adrenal suppression (see Chapter 15).1,3,7

In cases of refractory disease, immunosuppressive therapy has been used successfully and may include methotrexate, cyclophosphamide, or azathioprine. These drugs may produce significant adverse effects, including severe oral ulceration. Methotrexate also may cause hepatic toxicity. COX-2 inhibitors and TNF-α inhibitors have recently proved effective in relieving the symptoms of RA (see Table 20-3). Although COX-2 inhibitors (e.g., celecoxib [Celebrex]1,13) have shown considerable efficacy in relieving inflammatory pain associated with RA, problems have been reported with these agents, and myocardial infarction has occurred in patients who have used these treatments over the long term.17 Celebrex carries with it warnings regarding potential heart problems that are provided to long-term users. Standard NSAIDs inhibit both cyclooxygenases (COX-1 and COX-2)—the enzymes involved in production of prostaglandins. Whereas COX-2 is active on demand, COX-1 is critical for normal cellular function.1 A complication that may result from the use of NSAIDs for arthritis (and other conditions) is the adverse effect of gastrointestinal distress. Because COX-2 inhibitors are selective for this enzyme, they produce fewer gastrointestinal adverse effects.17 As treatment options for RA become more effective and more complex, greater attention will be paid to the costs of drug treatments and associated adverse effects with respect to disease control and remission. Drugs that improve the long-term outcomes of disease will be prescribed more frequently, and efforts will be made to limit the use of NSAIDs in persons who are coping with joint pain and swelling.17

A group of drugs have been developed, labeled “biologic,” because they consist of monoclonal antibodies and soluble receptors that specifically modify the disease process by blocking key protein messenger molecules (such as cytokines) or cells (such as B lymphocytes). The development of biologic drugs has been based on an increasing understanding of the disease process. The key drivers of RA include cytokines such as TNF-α, interleukin 1 (IL-1), and interleukin 6 (IL-6). An IL-1 receptor antagonist called anakinra had been appraised by the National Institute for Health and Clinical Excellence (NICE) and rejected for use in the National Health Service as not being cost-effective.8

The newer biologic agents etanercept and infliximab (and other TNF-α inhibitors) have been shown to be highly effective in the treatment of patients with early rheumatoid arthritis relative to the “gold standard” agent, methotrexate.17 Although costly and difficult to administer (requiring an injectable route), etanercept (e.g., Enbrel, Immunex) has been shown to significantly reduce symptoms of RA and to more effectively slow joint damage when compared with methotrexate. Likewise, infliximab (Remicade), which also is costly and requires administration by the intravenous route, when used with methotrexate significantly reduced RA symptoms and slowed joint damage to a greater extent than that achieved with methotrexate therapy alone. Although these biologic agents are novel and show great promise, they have had limited widespread use in RA therapy.17

Combination Therapies

In people with moderate to severe disease activity, methotrexate often is used in combination with other agents.17 In patients who have acute and severe disease, initial therapy often consists of a combination of DMARDs, corticosteroids, and NSAIDs. Combinations of DMARDs also are used to improve disease control; approximately 50% of people with RA who are treated by rheumatologists are prescribed combination therapies with two or three DMARDs. The combination of methotrexate, hydroxychloroquine, and sulfasalazine is among the most popular regimens, although study results are not readily duplicated among prescribing physicians.17 Other successful combination therapies include methotrexate used with such agents as cyclosporine, TNF-α antagonists, leflunomide, and azathioprine.17 Surgical management of severely deformed or dysfunctional joints often is necessary and may involve a variety of procedures, including arthroplasty, reconstruction, synovectomy, and total joint replacement.17

Clinical tools for monitoring the patient’s well-being and the efficacy of therapy include self-assessment of the duration of morning stiffness and severity of fatigue, as well as functional, social, emotional, and pain status, as measured by a health assessment questionnaire. A patient-derived global assessment based on a visual analog scale is a simple and effective means of recording patient well-being. The number of tender and swollen joints is a useful measure of disease activity, as is the presence of anemia, thrombocytosis, and elevated ESR or CRP. Serial radiographs of target joints, including the hands, are useful in assessing disease progression.1,7

Patient education is essential early in the disease course and on an ongoing basis. Patients are best served by a multidisciplinary approach with early referral to a rheumatologist and other specially trained medical personnel, including nurses, counselors, and occupational and physical therapists who are skilled and knowledgeable about RA. Appropriate medical care of patients with RA encompasses attention to smoking cessation, immunizations, prompt treatment of infections, and management of comorbid conditions such as diabetes, hypertension, and osteoporosis.1,7

Dental Management

Medical Considerations

Because patients may have multiple joint involvement with varied degrees of pain and immobility, dental appointments should be kept as short as possible, and the patient should be allowed to make frequent position changes as needed (Box 20-2). The patient also may be more comfortable in a sitting or semisupine position, as opposed to a supine one. Physical supports, such as a pillow or a rolled towel, may be used to provide support for deformed limbs, joints, or neck.

image

Box 20-2 Dental Management

Considerations in Patients with Rheumatoid Disorders

P

Patient Evaluation/Risk Assessment (see Box 1-1)

Evaluate and determine whether rheumatoid or joint disorder exists.

Obtain medical consultation if disease is poorly controlled or undiagnosed, or if the diagnosis is uncertain.

Potential Issues/Factors of Concern

A
Analgesics If patient is taking aspirin or another NSAID or acetaminophen, be aware of dosing and the possibility that pain may be refractory to some analgesics; dosing and/or analgesic choices may need to be modified in consultation with the physician.
Antibiotics Provide antibiotic prophylaxis in accordance with ADA (2003) guidelines (see Boxes 20-3 and 20-4).
Anesthesia No issues.
Anxiety No issues.
Allergy Allergic reactions or lichenoid reactions are possible in patients taking many medications.
B
Bleeding Excessive bleeding may occur if major surgery performed on patients who take aspirin or other NSAIDs. Bleeding usually is not clinically significant and can be controlled with local hemostatic measures.
Blood pressure No issues.
C
Chair position Ensure comfortable chair position. Consider shorter appointments and use supports as needed (e.g., pillows, towels).
D
Devices Patients who have a prosthetic joint replacement should be managed according to ADA (2003) guidelines (see Boxes 20-3 and 20-4).
Drugs Obtain blood cell count with differential if surgery is planned for patients taking gold salts, penicillamine, antimalarials, or immunosuppressives. If patient is taking corticosteroids—secondary adrenal suppression is possible (see Chapter 15).
E
Equipment No issues.
Emergencies If surgery is performed, supplemental techniques may be necessary to control bleeding.
F
Follow-up Routine follow-up evaluation is appropriate.

ADA, American Dental Association; NSAIDs, Nonsteroidal antiinflammatory drug.

image

The most significant complications associated with RA are drug-related (see Table 20-3). Aspirin and other NSAIDs can interfere with platelet function and cause prolonged bleeding; however, this effect generally is not found to be of clinical significance. A patient who is taking both aspirin and a corticosteroid may be at greater risk for bleeding. The risk is not great, however, and patients usually can be treated, so long as curettage or surgery is performed conservatively in small segments, with attention to good techniques (see Chapter 24).1416

Patients who are taking gold salts, penicillamine, sulfasalazine, or immunosuppressive agents are susceptible to bone marrow suppression, which can result in anemia, agranulocytosis, and thrombocytopenia. As a rule, these patients should be followed closely by their physician for detection of this problem. If a patient has not undergone recent laboratory testing, a complete blood cell count with a differential white blood cell count should be ordered. Abnormal results should be discussed with the physician. If corticosteroids are used for prolonged periods, the potential for adrenal suppression exists. Management of this problem is discussed in Chapter 15. Corticosteroids may induce a number of adverse effects, which are presented in Table 20-3.

Prosthetic Joints

A potential long-term complication of chronic rheumatoid arthritis (also osteoarthritis14 and other types, including fractures that do not heal and avascular necrosis) is the ultimate destruction of particular joint structures to the degree that the joint must be replaced with synthetic materials. Patients with prosthetic joints (most commonly, hip and knee replacement, followed by shoulder, elbow, wrist, and ankle) often are encountered in dental practice; when this occurs, a question arises concerning the need for antibiotic prophylaxis to prevent infection of the prosthesis. This is a legitimate concern; however, whether bacteremia resulting from dental procedures can cause prosthetic joint infection (PJI) is the primary issue. This issue has been debated for many years, although scientific data for decision making are lacking. Recommendations to place dental patients on prophylactic antibiotics have been made empirically by orthopedic surgeons, although little evidence suggests that dentally induced bacteremia may cause PJI.15

Although reports in the literature weakly associate PJI with dentally induced bacteremia, authors have questioned the validity of these reports. It appears that wound contamination or skin infection is the source of the vast majority of infections.15 Even the few cases of PJI caused by presumably oral bacteria were more likely to result from physiologically occurring bacteremia or bacteremia caused by acute or chronic infection than from invasive dental procedures.15

Unfortunately, however, many orthopedic surgeons have persisted in requesting that patients continue to receive antibiotic prophylaxis for all dental procedures.1618

In an effort to clarify the issue, in 1997 and updated in 2003, an advisory statement made jointly by the American Dental Association (ADA) and the American Academy of Orthopedic Surgeons (AAOS) was published.19 The 2003 advisory statement concluded that scientific evidence does not support the need for antibiotic prophylaxis for dental procedures to prevent late prosthetic joint infection (LPJI). It further stated that antibiotic prophylaxis is not indicated for dental patients with pins, plates, and screws, nor is it routinely indicated for most patients with total joint replacement. The statement did indicate, however, that antibiotic prophylaxis can be considered for patients whose joint replacement has been in place for less than 2 years and for patients at increased risk for infection who are undergoing invasive dental procedures (see Box 20-3). No evidence suggests that even these patients are at increased risk for infection from dentally induced bacteremia, and in fact, the microbiology of LPJI in these patients is the same in other patients with LPJI.17

image

Box 20-3 High-Risk Patients with Prosthetic Joints

Immunocompromised/Immunosuppressed Patients

Inflammatory arthropathies: rheumatoid arthritis; systemic lupus erythematosus; disease-, drug-, or radiation-induced immunosuppression

Other Patients

Insulin-dependent (type 1) diabetes

First 2 years after joint replacement

Previous prosthetic joint infections

Malnourishment

Hemophilia

image

A more appropriate interpretation is that these patients are at increased risk for LPJI from the usual sources such as wound contamination and acute infection from distant sites. The advisory statement also is clear that the final decision on whether to provide antibiotic prophylaxis lies with the dentist, who must weigh perceived potential benefits against risks. The advisory statement provides suggested antibiotic regimens, should the practitioner elect to provide antibiotic prophylaxis (see Box 20-4).19

image

Box 20-4 Suggested Antibiotic Prophylaxis Regimens

Patients Not Allergic to Penicillin: Cephalexin, Cefradine, or Amoxicillin

2 g orally 30 minutes to 1 hour before the dental procedure

Patients Not Allergic to Penicillin and Unable to Take Oral Medications: Cefazolin or Ampicillin

Cefazolin 1 g or ampicillin 2 g intramuscularly or intravenously 30 minutes to 1 hour before the dental procedure

Patients Allergic to Penicillin: Clindamycin

600 mg orally 30 minutes to 1 hour before the dental procedure

Patients Allergic to Penicillin and Unable to Take Oral Medications: Clindamycin

600 mg intravenously 30 minutes to 1 hour before the dental procedure

image

In 2009 the AAOS published an information statement that added a great deal of confusion to the dental management of patients with joint replacements. Antibiotic prophylaxis was suggested for all patients with joint replacements for dental procedures that produced bacteremia. This statement was made without input from the ADA and appeared to negate the 2003 advisory statement of the ADA and AAOS.16

In 2010 the American Academy of Oral Medicine (AAOM) published a position paper in the Journal of the American Dental Association (JADA).20 It strongly recommended that the ADA, AAOS, and the Infectious Disease Society of America (IDSA) meet to develop evidence-based recommendations for the dental management of patients with joint replacements. Until this occurs, the AAOM position paper recommended three options for the dentist when dealing with patients with joint replacements regarding antibiotic prophylaxis:

1 Informed consent

2 Base clinical decisions on the 2003 ADA/AAOS consensus statement

3 Consultation with the patient’s orthopedic surgeon to recommend following the 2003 guidelines until a new joint consensus statement is approved. If the orthopedist elects to recommend antibiotic prophylaxis for a patient who would not receive it on the basis of the 2003 guidelines, the orthopedist can write the prescription for the desired antibiotic.20

In November 2010 the ADA, AAOS, and IDSA began a series of meetings with the goal of developing an evidence-based recommendation for the dental management of patients with joint replacements. The process was estimated to take about 1 year. Until this recommendation is available, then, the dentist should consider one of the options suggested in the AAOM position paper.

A study that should have a great influence on the future recommendations of the ADA, AAOS, and IDSA was reported from the Mayo Clinic. The investigators concluded that dental procedure bacteremias were not associated with the onset of LPJIs and that antibiotic prophylaxis did not prevent PJIs.21

Treatment Planning Modifications

Treatment planning modifications are dictated by the patient’s physical disabilities. A patient with marked systemic disability or limited or painful jaw function due to TMJ involvement should not be subjected to prolonged or extensive treatment, such as complicated crown and bridge procedures. If replacement of missing teeth is desired, consideration should be given to fabrication of a removable prosthesis because of the decreased chair time needed for mouth preparation and the ease of cleaning of the appliance. If a fixed prosthesis is desired, the realistic potential to keep it clean must be a significant factor in design. Unpredictable, progressive, or abrupt changes in occlusion are possible because of erosion of the condylar head. Therefore, the dentist and the patient should take these potential occlusal changes into consi/>

Only gold members can continue reading. Log In or Register to continue

Jan 4, 2015 | Posted by in General Dentistry | Comments Off on 20: Rheumatologic and Connective Tissue Disorders
Premium Wordpress Themes by UFO Themes