Chapter 20 Rheumatologic Disorders

RHEUMATOLOGIC
DISORDERSC H A P T E R 2 0
M O D I F I E D BY : M E G A N S I M P S O N

RHEUMATOLOGIC
DISORDERS
• Rheumatologic (or rheumatoid) disease is much more than
“arthritis” and encompass a large group of disorders of the
rheumatic diseases that affect bones, joints, and muscles
– Some of the more common types include rheumatoid
arthritis (RA), osteoarthritis (OA), psoariatic arthritis(pRA),
systemic lupus erythematosus (SLE), juvenile rheumatoid
arthritis (jRA), scleroderma (SD), Sjögren syndrome (SS),
gout, ankylosing spondylitis, Lyme disease, giant cell
arteritis (or temporal arteritis) and fibromyalgia syndrome
(FMS)

RHEUMATOLOGIC
DISORDERS (CONT’D)
• 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
– Arthritis costs the American economy more than
$20 billion annually, and nearly 30 million
workdays are lost per year

CATEGORIES OF
RHEUMATOLOGIC DISORDERS
• Rheumatologic diseases can be classified into nine
categories, defined by the predominantly affected
tissues, such as joint, synovium, cartilage, or
connective tissues
– Recognition of the pattern of predominant tissue
involvement can direct attention toward the
disease primarily associated with that tissue
– At each point in the evaluation (history, physical
examination, and laboratory testing), it is
important to identify the tissues involved

PATHOPHYSIOLOGY AND
COMPLICATIONS
• The structures that are commonly involved in
rheumatologic 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

PATHOPHYSIOLOGY AND
COMPLICATIONS (CONT’D)
• 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
– Synovial fluid 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

PATHOPHYSIOLOGY AND
• 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 the joint

PATHOPHYSIOLOGY AND
• 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

PATHOPHYSIOLOGY AND
• Osteoarthritis is a non-inflammatory, degenerative disease that
begins in the cartilage and leads to cartilage loss, subchondral
new bone formation, and marginal bony overgrowth
– 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 rising from the joint itself
– Fibromyalgia is characterized by soft tissue pain with local
tenderness in specific points but without abnormal blood

RHEUMATOID ARTHRITIS
• 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 varies widely from patient to patient and from
time to time within the same patient
– Disease onset usually occurs between ages 35 and 50
years, and is more prevalent in women than in men by
a 3:1 ratio
– Prevalence estimates range from 1% to 2% of the
population

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
– One specific causative gene has not been identified
– 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

PATHOPHYSIOLOGY AND
COMPLICATIONS
• With RA, the fundamental abnormality involves
microvascular endothelial cell activation and injury
– 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

PATHOPHYSIOLOGY AND
• Eventually, granulation tissue covers the articular surfaces
and destroys the cartilage and subchondral bone through
enzymatic activity
– 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

PATHOPHYSIOLOGY AND
• 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

PATHOPHYSIOLOGY AND
• 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

PATHOPHYSIOLOGY AND
• 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

PATHOPHYSIOLOGY AND
The long-term prognosis for individuals with abrupt
onset of disease is similar to that for those 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 managed
to allow a normal or nearly normal life

PATHOPHYSIOLOGY AND
• 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
– Many complications accompany RA, including skin
ulcers, muscle atrophy, keratoconjunctivitis sicca
(Sjögren syndrome), digital gangrene, TMJ
involvement, pulmonary interstitial fibrosis,
pericarditis, amyloidosis, anemia, thrombocytopenia,
neutropenia, and splenomegaly (Felty syndrome)

CLINICAL PRESENTATION
• The usual onset of RA is gradual and subtle, and the
disorder is commonly preceded by a prodromal syndrome
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

(CONT’D)
• 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

(CONT’D)
• Extra-articular manifestations include rheumatoid nodules,
vasculitis, skin ulcers, Sjögren syndrome, interstitial lung
disease, pericarditis, cervical spine instability, entrapment
neuropathies, and ischemic neuropathies
– The American Rheumatism Association’s criteria for
diagnosis and classification of RA for clinical trials and
epidemiologic studies (89% specificity, 91-94%
sensitivity) 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

LABORATORY AND
DIAGNOSTIC 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 in 85% of affected
patients, and a hypochromic microcytic anemia
– In patients with Felty syndrome (RA with
splenomegaly), a marked neutropenia may be present

LABORATORY AND
DIAGNOSTIC FINDINGS
(CONT’D)
• Antibodies to cyclic citrullinated proteins (CCPs) are
helpful in the diagnosis of RA
– 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, allowing for earlier diagnosis
and intervention

LABORATORY AND
DIAGNOSTIC FINDINGS
(CONT’D)
• The American College of Rheumatology has established
criteria for the diagnosis of RA, the classification of
severity by radiography, functional classes, and the
definition of remission
– The diagnosis of RA cannot be made until the disease
has been present for at least several weeks
– Many extra-articular features of RA, the characteristic
symmetry of inflammation, and the typical serologic
findings may not be evident during the first few
months after disease onset
– Therefore, the diagnosis of RA usually is presumptive

LABORATORY AND
DIAGNOSTIC FINDINGS
(CONT’D)
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

MEDICAL MANAGEMENT
• Treatment of RA focuses on use of anti-inflammatory
drugs and disease-modifying antirheumatic drugs
(DMARDs), which are helpful in controlling disease and
limiting joint damage
– The treatment approach to RA is, by necessity, mostly
palliative because no cure as yet exists for the disease
and the ultimate aim of management is to achieve
disease remission and maintain or regain functional
activity

MEDICAL MANAGEMENT
(CONT’D)
• 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
– 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

MEDICAL MANAGEMENT
(CONT’D)
• 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 personnel 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
– Remission is elusive, so more practical treatment goals
are to reduce joint inflammation and swelling, relieve
pain and stiffness, and encourage normal function

MEDICAL MANAGEMENT
(CONT’D)
• Management of RA is accomplished through a basic
treatment program that consists of patient education, rest,
exercise, physical therapy, and various nonsteroidal anti-
inflammatory drugs (NSAIDs) and disease modifying anti-
rheumatic agents (DMARDs)
– The major goals of therapy are to reduce joint
damage; relieve pain, swelling, and fatigue; improve
joint function; and prevent disability and disease-
related morbidity
– These goals are constant throughout the disease
course, although emphasis may shift to address
specific patient needs

MEDICAL MANAGEMENT
(CONT’D)
• 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
• Anti-inflammatory properties have been noted for several
disease-modifying antirheumatic drugs (DMARDs), which
are used principally to control disease and to limit joint
damage
• Corticosteroids are powerful, nonspecific inhibitors of
cytokines and have been demonstrated to effectively
delay joint erosion

MEDICAL MANAGEMENT
(CONT’D)
• NSAIDs, including aspirin, constitute the cornerstone of
treatment
– 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 optimal
sequencing of DMARDs remains a source of debate
– 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 cyclooxygenase inhibitors, namely, celecoxib;
ibuprofen; naproxen; sulindac; tolmetin; fenoprofen;
piroxicam; diclofenac; flurbiprofen; diflunisal; etodolac,
and nabumetone

MEDICAL MANAGEMENT
(CONT’D)
• 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)
– Celecoxib, a COX-2 inhibitor, is designed to be safer
for the stomach

MEDICAL MANAGEMENT
(CONT’D)
• Corticosteroids, including prednisone, prednisolone and
methylprednisolone, are potent and quick-acting anti-
inflammatory medications
– These medications provide immediate control of
inflammation while waiting for NSAIDs and DMARDs
take effect
– Because of the risk of side effects with corticosteroids,
they are prescribed for as short a time as possible and
in doses as low as possible

MEDICAL MANAGEMENT
(CONT’D)
• The most commonly used DMARD for RA is methotrexate
– Other frequently utilized DMARDs include
hydroxychloroquine, sulfasalazine, leflunomide and
azathioprine
– An individual diagnosed with RA is likely to be
prescribed a DMARD fairly early in the course of their
disease, as studies have demonstrated that starting
these drugs early can help prevent irreparable joint
damage

MEDICAL MANAGEMENT
(CONT’D)
• Biologic agents are highly targeted DMARDs that in many
ways have revolutionized the management of RA
– Biologics have been shown to help slow progression
of rheumatoid arthritis when all other treatments have
failed to do so
– Aggressive rheumatoid arthritis treatment is known to
help prevent long-term disability from RA
– Among the biologics approved for RA: abatacept,
adalimumab, anakinra, certolizumab pegol, etanercept,
infliximab, golimumab, and rituximab

MEDICAL MANAGEMENT
(CONT’D)
• The biologic agents etanercept and infliximab have been
shown to be highly effective in the treatment of patients
with early RA relative to the “gold standard” agent,
methotrexate
– Etanercept has been shown to significantly reduce
symptoms of RA and more effectively slow joint
damage when compared with methotrexate
– Infliximab, when used with methotrexate, significantly
reduced RA symptoms and slowed joint damage to a
greater extent than that achieved with methotrexate
therapy alone

MEDICAL MANAGEMENT
(CONT’D)
• Etanercept and infliximab are administered by injection or
intravenous (IV) infusion and usually have side-effects
– The most common side effects seen with biologics is
pain and rash at the injection site, occurring in less
than 30% of patients
– Symptoms of infusion reactions include flu-like illness,
fever, chills, nausea, and headache
– Biologics have been implicated in increased infections;
one study found that patients taking high-dose
biologics were nearly 2.5 times more likely to have a
serious infection than controls

MEDICAL MANAGEMENT
(CONT’D)
• Tofacitini is a JAK inhibitor, a janus-associated kinase
inhibitor which disrupts cytokine and growth factor
signaling pathways, thereby effectively reducing
inflammation

MEDICAL MANAGEMENT
(CONT’D)
A potential long-term complication of chronic
rheumatoid arthritis is the ultimate destruction of
particular joint structures to the degree that the
joint must be replaced
Patients whom have recently received a prosthetic joint
are at increased risk of a thromboembolic event within a
month of the implant
They are also more likely to have a pulmonary embolism
for several years following their implant
When patients with prosthetic joints are encountered in
dental practice, a question regarding the need for
antibiotic prophylaxis to prevent infection of the
prosthesis can arise

DENTAL MANAGEMENT
• Dental appointments should be kept as short as possible,
and the patient should be allowed to make frequent
position changes if needed
– 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

DENTAL MANAGEMENT
(CONT’D)
• The most significant complications associated with RA are
drug-related
– Aspirin and other NSAIDs can interfere with platelet
function and cause prolonged bleeding (however, this
effect is not found to be of clinical significance)
– A patient taking both aspirin and a corticosteroid may
be at greater risk for bleeding
– Patients usually can be treated, so long as curettage or
surgery is performed conservatively in small segments,
with attention to good techniques

DENTAL MANAGEMENT
(CONT’D)
• Patients taking gold salts, penicillamine, sulfasalazine, or
immunosuppressive agents are susceptible to bone
marrow suppression
– This can result in anemia, agranulocytosis, and
thrombocytopenia
– If corticosteroids are used for prolonged periods, the
potential for adrenal suppression exists

LATE PROSTHETIC JOINTS
• A potential long-term complication of rheumatoid arthritis
is the ultimate destruction of particular joint structures to
the degree that the joint must be replaced with synthetic
materials
– Wound contamination or skin infection (Staphylococci)
appears to be the source of the vast majority of late
prosthetic joint infections (LPJI)
– A few cases have been remotely associated with
bacteria (Streptococci) found in the oral cavity

(CONT’D)
• An ADA Council on Scientific Affairs developed an
evidence-based clinical practice guideline (CPG) on
prophylactic antibiotic use in patients with prosthetic
joints undergoing dental procedures
– The panel identified 4 case-control studies and judged
that the current best evidence failed to demonstrate
an association between dental procedures and
prosthetic joint infection (PJI)
– The panel also presented information about antibiotic
resistance, adverse drug reactions, and costs
associated with prescribing antibiotics for prosthetic
joint infection prophylaxis

(CONT’D)
• An important study evaluated both preoperative and
postoperative factors associated with PJI
– The most clinically relevant of these factors were
postoperative, especially wound drainage after
arthroplasty
– Other postoperative factors associated with PJI were
wound hematoma after arthroplasty, and
postoperative urinary tract infection
– Patients at the highest risk of developing PJI had
drainage, an infection, or both after arthroplasty
– Preoperative factors including prior
operation/arthroplasty on the index joint, diabetes

(CONT’D)
• 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

(CONT’D)
• In 2010, the American Academy of Oral Medicine (AAOM)
published a position paper in the Journal of the American
Dental Association (JADA)
– 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

(CONT’D)
• Three options for the dentist when dealing with patients
with joint replacement regarding antibiotic prophylaxis
– Informed consent
– Base clinical decisions on the 2003 ADA/AAOS
consensus statement
– Consultation with the patient’s orthopedic surgeon to
recommend following the 2003 guidelines until a new
joint consensus statement is approved

2015 SUMMARY OF THE
ADA AND AAOS (CONT’D)
• In January 2015, the results of the ADA/American
Academy of Orthopedic Surgeons (AAOS) task force,
along with rationale and clinical guidelines, were
published in JADA
– The general recommendation is that patients with
prosthetic joints ARE NOT recommended to receive
prophylactic antibiotics prior to dental treatment

2015 SUMMARY OF THE
There are caveats and exceptions which must be taken into
account in making the decision to prescribe prophylactic
antibiotics prior to dental treatment
Those factors may include other systemic co-morbid
conditions which may render the individual patient
susceptible to infection, prior or existing infection of
the prosthetic joint, etc.
A careful, comprehensive review of the patient’s
medical conditions and status and possible consultation
with the physician may be in order

2015 SUMMARY OF THE
A further recommendation was: “In cases where antibiotic
prophylaxis is deemed necessary by the orthopedic surgeon,
it is appropriate for them to recommend the appropriate
antibiotic and when reasonable, to write the prescription….”
Due to the risk of potential complications, it is best to
defer elective dental treatment for at least 30 days
following a total joint replacement

TREATMENT PLANNING
MODIFICATIONS
• Treatment planning modifications are dictated by the
patient’s physical disabilities
– RA is a progressive disease that ultimately may lead to
severe disability and crippling in some patients, which
can make providing dental care difficult
– The dentist should be diligent in providing ongoing
preventive care and should attempt to identify and
treat or eliminate potential problems before the
disease progresses

TREATMENT PLANNING
MODIFICATIONS (CONT’D)
• Disabled patients may have significant difficulty cleaning
their teeth
– Cleaning aids may be recommended
– If replacement of missing teeth is desired,
consideration should be given to fabrication of a
removable prosthesis
– If a fixed prosthesis is desired, the realistic potential to
keep it clean must be a significant factor in design
– A patient with marked systemic disability or limited or
painful jaw function should not be subjected to
prolonged or extensive treatment

ORAL COMPLICATIONS
AND MANIFESTATIONS
• The most significant complication of the oral and
maxillofacial complex in RA is TMJ involvement, which is
found in up to 45% to 75% of patients with RA
– Fibrosis or bony ankylosis can occur
– Clinically, patients may present with tenderness over
the lateral pole of the condyle, crepitus, limited
opening
– Radiographic changes initially may show increased
joint space due to inflammation in the joint

ORAL COMPLICATIONS AND
MANIFESTATIONS (CONT’D)
• A potential dental complication is the development of an
anterior open bite, caused by destruction of the condylar
heads and loss of condylar height
– Although palliative treatment such as interocclusal
splints, physical therapy, and medication may prove to
be helpful, surgical intervention often becomes
necessary to decrease pain, improve appearance, or
restore function

• An additional complication that may be seen in patients
with RA is severe stomatitis that occurs after the
administration of drugs such as gold compounds,
penicillamine, or immunosuppressive agents
– Stomatitis may be an indication of drug toxicity and
should be reported to the physician
– Treatment should include consideration for changing
the offending drug, and palliative mouth rinses,
diphenhydramine elixir, or a topical emollient such as
Orabase

QUESTIONS TO ASK PATIENT
WITH RA
• How long ago were you diagnosed with RA?
• What symptoms do you experience with RA?
• What medications are you taking to treat RA?
• Do you experience any fatigue or muscle weakness?
• Do you prefer to lay supine or semi-supine?
• How often will you need to move and exercise your joints
throughout the appointment to prevent pain from occurring?
57

PRODUCTS TO RECOMMEND
TO PATIENT WITH RA
• Fluoride treatment and recommendation of fluoridated
products if patient is taking medication that may cause
xerostomia.
• Floss reacher if patient has limited movement in hands.
• Power brush for difficulty brushing with manual brush.
• Non-alcoholic fluoridated mouth rinses.
• Occlusal splints to decrease joint loading.
58

OSTEOARTHRITIS
• Osteoarthritis (OA), also called degenerative joint disease,
is the most common form of arthritis
– Almost everyone older than 60 years of age develops
OA to some degree
– Most affected persons are minimally symptomatic
(however, approximately 17 million people in the U.S.
have OA to the extent that it results in pain
– OA is the leading cause of disability for the elderly

OSTEOARTHRITIS (CONT’D)
• OA usually affects often-used joints, such as hips, knees,
feet, spine, and hands
– The TMJ also may be affected
– Women are afflicted twice as often as men, however,
men are afflicted at an earlier age
– It is generally a disease of middle to older age, first
appearing after the age of 40
– Racial differences have been noted in the prevalence
of OA and in the pattern of joint involvement

ETIOLOGY AND
EPIDEMIOLOGY
• OA has been thought to result from normal wear and tear
on joints over a long period
– Other factors are now believed to be of significance
– Preexisting structural joint abnormalities, intrinsic
aging, metabolic factors, genetic predisposition,
obesity leading to overloaded joints, and macrotrauma
or microtrauma are considered causative or
contributory factors in the origin of the disease
– It is estimated that 12% of the US population has OA

PATHOPHYSIOLOGY AND
COMPLICATIONS
• In the early stages of the disease, the articular cartilage
actually becomes thicker than normal, and water content and
the synthesis of proteoglycans are increased
– Ultimately, however, the joint surface thins and
proteoglycan concentration decreases, leading to
softening of the cartilage
– Progressive splitting and abrasion of cartilage down to
the subchondral bone occur
– The exposed bone becomes polished and sclerotic,
resembling ivory (eburnation)
– New bone forms in the non-weight-bearing part of the
joint, creating osteophytes (or spurs), often covered by
cartilage that augment the degree of deformity

PATHOPHYSIOLOGY AND
• In contrast with RA, OA has a more favorable prognosis
and less serious complications, depending on the joint or
joints involved
– The two most important complications associated with
OA are pain and disability
– Although RA is a more serious disease, OA has a 30-
fold greater economic impact, resulting in 68 million
lost workdays per year compared with 2 million for RA
– Primary generalized osteoarthritis, characterized by
involvement of three or more joints or groups of
joints, occurs most often in women

• The primary symptom of OA is pain localized to one or
two joints
– The pain is described as a dull ache accompanied by
stiffness that is typically worse in the morning or after
a period of inactivity
– The pain and stiffness usually last no longer than 15
minutes
– Joint noises or grinding sounds (crepitus) may be
detected with movement

(CONT’D)
• The most common sign of OA is appearance of painless
bony growths on the medial and lateral aspects of the
proximal interphalangeal joints, called Heberden’s nodes
– When these enlargements occur on the distal
interphalangeal joints, they are called Bouchard’s
nodes
– On occasion, some pain may be associated with these
nodes

HEBERDEN’S & BOUCHARD’S
NODES
66

(CONT’D)
• Depending on which joint or group of joints is involved,
patients may experience varying degrees of incapacitation
• Hip and knee joints are particularly troublesome and are a
common source of disability

(CONT’D)
• Radiographic signs of OA include narrowing of the joint
space, articular surface irregularities and remodeling, and
osteophytes or spurs
– In addition, subchondral sclerosis (eburnation) and
ankylosis may be seen
– Symptoms often are not well correlated with
radiographic signs

LABORATORY AND
DIAGNOSTIC FINDINGS
• Laboratory findings in OA are essentially unremarkable
– The ESR usually is normal, except for a mild elevation
in primary generalized cases

MEDICAL MANAGEMENT
• The management of OA is palliative, and drug therapy is
limited to analgesics
– Acetaminophen frequently is effective and
recommended as a first-line drug, with aspirin or
NSAIDs employed when it is ineffective
– Narcotic analgesics and intra-articular steroid
injections are used only for acute flares for short
periods
– Patient education, physical therapy, mild exercise,
weight reduction, and joint protection are all
important aspects of management
– Surgery, including joint replacement, may be required
to improve function or relieve pain

DENTAL MANAGEMENT
• Oral Complications and Manifestations
– The TMJ may be affected and TMJ pain caused by OA
may occur
– The usual finding in patients with OA of the TMJ is the
onset of unilateral preauricular aching and pain with
stiffness after a period of inactivity that decreases with
mild activity supports, as well as scheduling short
appointments
– Severe pain may be elicited on wide opening, and pain
occurs with normal function and worsens during the
day

DENTAL MANAGEMENT
(CONT’D)
– In most cases, osteoarthritic pain in the TMJ resolves
within 8 months of onset
– Radiographic changes include decreased joint space,
sclerosis, remodeling, and osteophytes
– No correlation exists between TMJ symptoms and
radiographic or histologic signs of OA
– There is a relationship between TMJ disk displacement
and OA
– Most patients with disk displacement, whether
reducing or nonreducing, can be treated successfully
with conservative, reversible therapies

DENTAL MANAGEMENT
(CONT’D)
– Treatment of OA of the TMJ consists of
acetaminophen, aspirin or NSAIDs, muscle relaxants,
approaches to limit jaw function, physical therapy
(heat, ice, ultrasound, controlled exercise), and occlusal
splints to decrease joint loading
– Conservative therapy is successful in controlling
symptoms in most cases, however, should pain or
dysfunction be severe and persistent, TMJ surgery may
be necessary

WITH OA
• How long ago were you diagnosed with OA?
• What symptoms do you experience with OA?
• Do you have pain in your jaw when opening and closing?
• What medications are you taking to treat OA?
74

TO PATIENT WITH OA
xerostomia.
• Floss reacher if patient has limited movement in hands.
• Non-alcoholic mouth rinses.
• Occlusal splint to decrease joint loading.
75

SYSTEMIC LUPUS
ERYTHEMATOSUS
There are two types of lupus erythematosus (LE): discoid
(DLE), which predominantly affects the skin, and a more
generalized systemic form (SLE), which affects multiple
organ systems
Most patients with DLE have very few systemic
manifestations, and the course tends to be benign
SLE involves the skin and many other organ systems
and is the more serious form

ETIOLOGY
The etiology of SLE is unknown, although it is clearly an
autoimmune disease
A strong familial aggregation exists with a much higher
frequency noted among first-degree relatives of patients
Studies of patients with SLE suggest that the disease is
caused by genetically determined immune abnormalities
that can be triggered by exogenous and endogenous
factors
Among these triggering factors are infectious agents,
stress, diet, toxins, drugs, and sunlight

EPIDEMIOLOGY
SLE is a prototypical autoimmune disease that
predominantly affects women of childbearing age
with a female-to-male ratio of 6:1 to 10:1
The disease is more common and more severe among
African Americans and Hispanics compared with
Caucasians
A defining feature of SLE is the presence of antibodies
directed against one or more components of cell nuclei
(antinuclear antibodies), with certain disease
manifestations associated with the presence of one or
more of these different antinuclear antibodies

PATHOPHYSIOLOGY AND
COMPLICATIONS
In SLE, antibody and immune complex deposition leads to
inflammation and vasculopathy
Circulating autoantibodies form antigen-antibody
complexes, which are deposited in a wide variety of
tissues and organs

PATHOPHYSIOLOGY AND
Despite advances in diagnosis and management,
complications attributable to SLE or its treatment continue
to cause substantial morbidity
Complications of SLE include; infection, coronary artery
disease, renal and pulmonary disease and osteonecrosis
The leading causes of death in patients with SLE are
infectious complications and clinical manifestations
related to lupus itself, such as acute vascular neurologic
events, renal failure, and cardiovascular or pulmonary
involvement

Because of the widespread involvement of SLE, multiple
manifestations are observed in many tissues and organs
The typical presentation is a female with polyarthritis and
a butterfly-shaped erythematous rash across the nose
and cheeks
The clinical presentation varies widely from mild to
severe and depends largely on the extent and type of
organ involvement

(CONT’D)
Arthritis is the most common manifestation of SLE, affecting
nearly three-quarters of patients
It affects the small joints and is migratory, with the pain
typically out of proportion compared with clinical signs
The classic butterfly rash is found in only about one third
of patients with SLE (a rash on the upper trunk or areas
of exposed skin is more common

(CONT’D)
Serious renal abnormalities occur in less than one third of patients
with SLE, but is the best clinical indicator of a poor prognosis
Autoimmune hepatitis may occur, but it is not transmissible
though it may result in liver damage
Neuropsychiatric symptoms are common and include organic
brain syndrome, psychosis, seizures, stroke, movement disorders,
and peripheral neuropathy
Thromboembolism associated with antiphospholipid antibody is
an important cause of abnormalities in the central nervous system
Pulmonary manifestations include pleuritis, infection, pulmonary
edema, pneumonitis, and pulmonary hypertension

(CONT’D)
Cardiac involvement is common and consists of
pericarditis, myocarditis, endocarditis, and coronary
artery disease
Valvular abnormalities can be identified by
echocardiography in 25% of patients but rarely result in
serious valvular dysfunction
Approximately 4% of patients had cardiac valve
abnormalities that placed them in the moderate risk
group for endocarditis
However, no cases demonstrated a relationship between
endocarditis and SLE

LABORATORY AND DIAGNOSTIC
FINDINGS
The antinuclear antibody test is the best screening
test for SLE because it yields a positive result in
95% of patients
A positive result also occurs in patients with other
rheumatic diseases
Hematologic abnormalities include hemolytic anemia,
leukopenia, lymphopenia, and thrombocytopenia
Leukopenia in SLE usually is not associated with
recurrent infection, but autoimmune thrombocytopenia
occurs in as many as 25% of patients with SLE and may
be severe

LABORATORY AND DIAGNOSTIC
FINDINGS (CONT’D)
A variety of clotting abnormalities may be seen (the most
common of these is the lupus anticoagulant, which is
associated with elevated partial thromboplastin time (PTT)
This can indicate the presence of antiphospholipid
antibodies
The ESR often is elevated, but this does not reflect
disease activity
With active nephritis, proteinuria is present, as are
hematuria and cellular or granular casts

MEDICAL MANAGEMENT
SLE treatment utilizes many of the medications
used to treat other rheumatologic disorders, but
with a greater degree of observation for renal,
cardiac and clotting abnormalities
Patients with SLE are advised to avoid sun exposure
because sunlight may trigger onset or exacerbation of
the disease
Aspirin and NSAIDs are often used for mild disease,
antimalarials for dermatologic disease, glucocorticoids
for more severe symptoms, and cytotoxic agents for
symptoms unresponsive to other therapies or as
adjuncts in severe disease

MEDICAL MANAGEMENT
(CONT’D)
A specific set of quality indicators to evaluate the
monitoring of SLE patients in routine clinical practice
has been developed recently
These quality indicators have been integrated into the
recently developed EULAR recommendations for monitoring
SLE patients in routine clinical practice and observational
studies
Eleven quality indicators (QIs) have been developed referring
to the use of validated activity and damage indices in routine
clinical practice, general evaluation of drug toxicity,
evaluation of comorbid conditions, eye evaluation, laboratory
assessment, evaluation of the presence of chronic viral
infections, documentation of vaccination, and antibody
testing at baseline

DENTAL MANAGEMENT
Because SLE is such a varied disease with so many
potential problems caused by the disease or its
treatment, pretreatment consultation with the
patient’s physician is advised
The leukopenia that is common in SLE usually is not
associated with a significant increase in infection
(however, when combined with corticosteroid or
cytotoxic drugs, the likelihood of infection is increased
In patients who are taking a corticosteroid or cytotoxins
who also have leukopenia, the use of prophylactic
antibiotics for periodontal and oral surgical procedures
may be considered

DENTAL MANAGEMENT (CONT’D)
Abnormal bleeding due to thrombocytopenia is a potential
problem in some patients with SLE
A coagulation profile that especially notes the platelet
count and PTT should be obtained
A platelet count lower than 50,000/ml may indicate
inadequate platelet activity and potential bleeding
problems
Typically an elevated PTT associated with the lupus
anticoagulant is not a risk factor for increased bleeding

Cardiac valvular abnormalities are found in 25% to
50% of patients with SLE and often are not clinically
detectable but the potential exists for bacterial
endocarditis resulting from physiologic bacteremia
The American Heart Association 2007 guidelines for
endocarditis prevention do not recommend antibiotic
prophylaxis for patients with valvular disease associated with
SLE when receiving invasive dental procedures
Patients with SLE-associated renal failure have the potential
for altered drug metabolism, hematologic disorders, and
infection

TREATMENT PLANNING
CONSIDERATIONS
No specific treatment planning modifications are required
Consideration should be given to physical disabilities
related to arthritis and myalgia
Systemic complications such as renal impairment and
cardiac problems such as arrhythmias and valvular
defects may occur

MANIFESTATIONS
Oral lesions of the lips and mucous membranes have been
reported to occur in up to 5% to 25% of patients with SLE
These lesions are rather nonspecific and may be
erythematous with white spots or radiating peripheral
lines (they also may occur as painful ulcerations)
When they occur on the lip, a silvery, scaly margin,
similar to that seen on the skin, may develop

94
Ulceration of
buccal mucosa in
patient with SLE
Butterfly rash in
patient with SLE

Other oral manifestations of SLE may include xerostomia
and hyposalivation, dysgeusia, and glossodynia
The dentist should always remain alert to oral eruptions
and lesions associated with medications used to treat
SLE, as these may be a sign of toxicity

WITH SLE
• When were you diagnosed with SLE?
• What other complications do you suffer from with this disease?
– Infection, coronary artery disease, renal and pulmonary disease and
osteonecrosis?
• For patients with leuokopenia – Are you taking corticosteroids
or cytotoxins?
• Do you know your most recent platelet count and partial
thromboplastin time PTT?
96

TO PATIENT WITH SLE
• Fluoride treatment at dental office to reduce risk of caries.
• Dry mouth products such as Biotene if patient suffers from
xerostomia.
• Power brush if patient suffers from limited hand dexterity due to
arthritis.
• Water flosser if patient suffers from limited hand dexterity due
to arthritis.
97

SJӦGREN SYNDROME
Sjögren syndrome (SS) is an autoimmune disease
complex classified among the many rheumatic
diseases that cause exocrinopathy and affect the
salivary and lacrimal glands
SS is characterized by a triad of clinical conditions that
consists of keratoconjunctivitis sicca, xerostomia, and a
connective tissue disease (usually RA)
SS manifests in two different forms: primary SS and
secondary SS

SJӦGREN SYNDROME (CONT’D)
Primary SS (SS-1) manifests clinically with the primary
ocular complication of keratoconjunctivitis sicca: in the
oral cavity, it is associated with various levels of
salivary gland dysfunction
Secondary SS (SS-2) manifests as the presence of
keratoconjunctivitis sicca or xerostomia in the
presence of a diagnosed systemic connective tissue
disease
The connective tissue disorder from which SS develops most
commonly is RA

EPIDEMIOLOGY
The prevalence of SS in the adult population is
estimated to be around 2.7%, and the prevalence
of SS in the U.S. is estimated at more than 2.5
million
SS has now become the second most common
rheumatoid disorder
SS is primarily a disease of women—more than 90% of
all patients with SS are female
SS typically manifests during the fourth or fifth decade
of life, although the condition usually progresses
insidiously over several years, often remaining
unrecognized

ETIOLOGY
The precise cause of SS is unknown
One theory is that the disease results from
complications of viral infection with EBV
Exposure to or reactivation of EBV elicits expression of
the HLA (human lymphocyte antigen) complex (this is
recognized by the T cell (CD4+) lymphocytes and
results in the release of cytokines (tumor necrosis factor
[TNF]), interleukin 2 [IL-2], interferon-γ [IFN-γ], and
others
Chronic inflammation, infiltration of lymphocytes, and
ultimate destruction of exocrine gland tissue follow

PATHOPHYSIOLOGY AND
COMPLICATIONS
SS is a chronic, progressive autoimmune disorder that is
characterized by exocrinopathy and generalized
lymphoproliferation that primarily affect the salivary and
lacrimal glands
It can affect the pancreas, biliary tract, and lungs
A genetic marker, HLA-DR4, has been identified as
specific for SS
Activation of the interferon pathway is important in SS

PATHOPHYSIOLOGY AND
Labial salivary gland histopathologic examination has
been accepted almost universally as the prima facie
diagnostic indicator for definitive diagnosis of SS
The classic histopathologic feature of the minor salivary
glands in SS is seen as lymphocytic infiltration that includes
benign lymphosialadenopathy
This benign lymphosialadenopathy may manifest as parotid
hypertrophy, particularly in patients with primary SS
As the inflammatory process progresses, fibrosis and atrophy
of the salivary glands occur, and hyposalivation progresses

PATHOPHYSIOLOGY AND
Lymphomas occur in SS-1 patients at a rate higher
than in the general population
Progression to lymphoma in patients with SS is thought to be
related to chronic inflammatory challenge
In the presence of continued and chronic inflammation
(mediated first by type 1 cytokines [TNF-α, IL-2, IFN-γ] and
then later by type 2 cytokines [IL-4, IL-6, and IL-10]), B cells
undergo oligoclonality and sometimes, eventually,
monoclonality
Patients with SS may then manifest non-Hodgkin lymphoma

PATHOPHYSIOLOGY AND
Clinical findings associated with lymphoma include
anemia, cryoglobulinemia, lymphopenia, cutaneous
vasculitis, and peripheral neuropathy
Lymphadenopathy is common (86%) and is associated with
enlarged cervical and axillary nodes
Evidence suggests that initial transformation to lymphoma
occurs in the salivary glands, and that the presence of B cell
monoclonality in labial minor salivary glands (LMSG) tissue is
associated with progression to malignancy
IL-6 and TNF-α are associated with lesions that undergo
transformation to lymphoma

SS is characterized by eye dryness, hyposalivation, and
enlargement of the parotid glands
Secondary outcomes of persistent oral dryness are
angular cheilosis, dysgeusia (taste dysfunction),
secondary infection, and a significantly increased caries
rate

SALIVARY GLAND DYSFUNCTION
AND HYPOSALIVATION
Saliva in normal quantity and composition is rich in
constituents that have potent antimicrobial, antacid,
lubricative, and homeostatic properties
Saliva contains approximately 60 important protective
constituents, including immunoglobulins, electrolytes,
buffers, antimicrobial enzymes, digestive enzymes, and
many others
When saliva is diminished in quantity or altered in
composition, deterioration of oral soft and mineralized
tissues may occur

SALIVARY GLAND DYSFUNCTION
AND HYPOSALIVATION (CONT’D)
Patients with SS have difficulty tasting, tolerating,
and swallowing certain foods
Dietary intake of certain nutrients may be inadequate in
these patients
Saliva has been shown to be rich in proteins that have
potent antifungal properties, so it plays an important
role in host defense and protection from yeasts such as
Candida
Thus, with reduced salivary flow in SS, Candida
infections are very common
Studies also have shown that patients with SS more
frequently exhibit periodontal disease, especially loss of
clinical attachment

LABORATORY AND
DIAGNOSTIC FINDINGS
Precise diagnostic criteria for SS remain controversial,
although specific laboratory tests are available for the
major diagnostic categories of salivary and tear production,
histopathologic changes, and serologic inflammatory
markers
Several published criteria (ACR, etc.) are available for
the diagnosis of SS with values that are slightly
different

LABORATORY AND
DIAGNOSTIC FINDINGS
(CONT’D)
Hypergammaglobulinemia is the most frequent
laboratory finding (80%) among patients with SS
Hyperactivity of B lymphocytes results in increased
rheumatoid factor antibodies, antinuclear antibodies (ANA),
and antibodies against organ-specific antigens, such as
salivary duct epithelia or thyroid tissue
The ANA also may be found in other autoimmune disorders
Elevated ESR, mild anemia (approximately 25%), and
leukopenia (approximately 10%) also are found in patients
with SS

SIALOMETRY
Sialometry is useful as an initial screening tool for
hyposalivation associated with SS and as an assessment for
the level of severity of SS
To be valuable as a diagnostic technique, salivary flow
collection must be performed precisely according to the
type of gland and over a period of at least 5 minutes
(often up to 15 minutes)

DENTAL MANAGEMENT
Patient management for SS traditionally has been palliative
and preventive, as there is no known cure
Relief of the primary symptoms of dryness (oral and
ocular) and the secondary burning and discomfort is
the main goal
Restoration and maintenance of a normal homeostatic
oral environment is a secondary goal

Therapy for the oral component of SS may be classified
into three major categories
– Provision of moisture and lubrication by stimulation or
simulation
– Treatment of secondary mucosal conditions (such as
mucositis or candidiasis)
– Prevention of oral disease, and provision of
maintenance and general support (such as nutrition)

MOISTURE AND LUBRICATION
Patients with SS should be counseled to drink plenty
of water (8 to 10 glasses per day) and to avoid
diuretics such as caffeine, tobacco, and alcoholic
beverages
Certain medications (more than 400) may contribute to and
compound the xerostomia, so some may need to be
modified or avoided, if possible
Although salivary substitutes, oral moisturizers, and artificial
salivas may provide some relief for the xerostomia
experienced by patients with SS, by and large, they are
inadequate

MOISTURE AND LUBRICATION
(CONT’D)
Pharmacologic stimulation of the salivary glands can be
quite successful
Systemic administration of pilocarpine or cevimeline
effectively stimulates only the salivary acinar tissue,
which remains functional
Other pharmacologic sialagogues, such as bethanechol
chloride, bromhexine, and anethole trithione, have been
shown to stimulate salivary flow, but none has been
approved by the FDA

ORAL COMPLICATIONS
AND MANIFESTATIONS
One of the most significant oral complications of Sjögren
disease and xerostomia is the tremendous increased
incidence of caries
Recommendations for patients with Sjögren disease
with dry mouth include
Topical daily fluoride
Increasing saliva through gustatory, masticatory, or
pharmaceutical stimulation
Chlorhexidine administered as varnish, gel, or rinse
Nonfluoride remineralizing agents as an adjunct
therapy

ORAL COMPLICATIONS
AND MANIFESTATIONS (CONT’D)
Among the oral symptoms most commonly
associated with SS is glossodynia (burning
tongue)
The tongue often becomes depapillated and fissured
and develops a scrotal appearance
Pain and burning may be spontaneous or may be
elicited with acidic or spicy food
The tongue is commonly infected (in as many as 83%)
with C. albicans in patients with SS
Not only must the acute candidial infection be treated,
but some type of maintenance therapy must be
provided to prevent recurrence of the fungal infection

ORAL COMPLICATIONS
AND MANIFESTATIONS
As long as the oral environment is adversely affected by
hyposalivation, susceptibility to recurrence of the oral
infection and continued deterioration remains
Clinical follow-up evaluation and some phased
maintenance therapy may be necessary
Generally, these oral mucosal conditions are treated as
if they occurred independently

PREVENTION AND
MAINTENANCE
The patient with SS may have less than 5% of the normal
quantity of saliva to protect the oral cavity
The risk for caries as well as enamel erosion is
extremely high
Meticulous oral hygiene with minimally abrasive
fluoridated dentifrices and irrigation devices is
paramount
In the xerostomic environment, abrasion of the tooth
surface should be minimized as much as possible

WITH SS
• What symptoms do you experience with SS?
• What medications and/or supplements are you currently taking
to treat SS?
• How much water are you drinking per day?
120

TO PATIENT WITH SS
• Minimally abrasive, fluoridated toothpaste (Fluoridex)
• Non-alcoholic, dry mouth rinses (Biotene)
• Saliva stimulating aids such as xylitol gum
• Power brush to aid in sufficient removal of bacterial plaque
biofilm
121

PSORIATIC ARTHRITIS
• Psoriatic arthritis (PsA) is an inflammatory arthritis
associated with the inflammatory skin condition, psoriasis
– Although most cases arise in patients with established
cutaneous disease, some patients (particularly
children) have arthritis that antedates the appearance
of the skin lesions
– Although the extent of psoriatic skin disease correlates
poorly with the development of arthritis, the risk for
PsA increases with a family history of PsA

EPIDEMIOLOGY
PsA is estimated to occur in 0.1- 1.0 % of the population in
the U.S.
PsA develops in 5% to 7% of patients with psoriasis
The age at onset can range from 30 to 55 years, with an
equal predilection for women and men

PATHOPHYSIOLOGY AND
COMPLICATIONS
• The genetic associations with PsA are complex
– No etiologic agent has been proved in PsA, although
some investigators have proposed that the disease
process represents ReA in response to cutaneous
bacteria
– There is the potential for aggressive osteolysis, fibrous
ankylosis, and heterotopic new bone formation to
occur in PsA
– The coexistence of human immunodeficiency virus
(HIV) and PsA in some patients seems to set the stage
for an aggressive course of joint destruction

PATHOPHYSIOLOGY AND
• PsA has a variable manifestation and disease course, but
clinical patterns have been identified in prospectively
monitored cohorts of patients
– The most common form is an asymmetric oligoarthritis
that may involve both larger and smaller joints
– In the second subset, there is selective targeting of the
distal interphalangeal joint
– The third subset has a symmetrical polyarthritis that
mimics RA in many ways, except for the absence of
rheumatoid nodules and rheumatoid factor
– The fourth clinical variant is psoriatic spondylitis
– Finally, arthritis mutilans affects large and small joints

PATHOPHYSIOLOGY AND
• Radiographic changes in PsA involve soft tissue swelling
(particularly, in the case of dactylitis), erosions, and
periostitis
– Axial involvement may lead to the appearance of
asymmetric sacroilitis with syndesmophytes that are
bulky, asymmetric, and nonmarginal
– The classic “pencil-in-cup” deformity may be seen in
patients with distal interphalangeal joint disease or
arthritis mutilans
– Acroosteolysis is noted in a minority of patients and
reflects an aggressive erosive process

MEDICAL MANAGEMENT
• Abatacept is a modified antibody for the management of
psoriatic arthritis has proved in clinical trials to be an
effective treatment
– Abatacept selectively inhibits T cell activation via
competitive binding to CD80 or CD86, and decreases
serum levels of cytokines and inflammatory proteins
implicated in the pathogenesis of PsA
– Abatacept is an approved treatment for chronic
inflammatory conditions such as RA and juvenile
idiopathic arthritis, in which T cells are involved in the
pathophysiologic progression of the disease

DENTAL MANAGEMENT
• Dental management and treatment planning
modifications for PsA are very similar to that for RA
– The exception may be the skin involvement as well as
the choice and/or combination of immunosuppressive
drugs
– The dentist must make a careful assessment of the
severity of disease and medical management of the
patient’s condition

GIANT CELL ARTERITIS
• Giant cell arteritis (GCA) is a systemic vasculitis involving
medium-sized and large arteries, most commonly the
extracranial branches of the carotid artery
– This inflammatory disorder affects women more often
than men, almost exclusively after 50 years of age, and
the average age is 72 years
– Histologically, GCA is represented by a mononuclear
cell infiltrate of T cells and macrophages, which
penetrates through the wall of arteries (typically the
temporal artery)

GIANT CELL ARTERITIS
(CONT’D)
• Because of the occlusive nature of the narrowing of the
vascular lumen, cranial pain, blindness, transient ischemic
attacks (TIAs), and other strokes are common
complications
– Symptoms and signs of GCA include excessive
sweating, fever, malaise, anorexia, headaches, scalp
tenderness, muscle aches, and jaw pain
– A typical temporal artery affected by GCA shows
characteristics such as panmural mononuclear
inflammatory infiltrate, destruction of the internal and
external elastic laminae, and concentric intimal
hyperplasia

MEDICAL MANAGEMENT
The universal treatment for GCA is glucocorticoid therapy.
Prednisone (60 mg per day) is the usual initial therapy.
Once the immune response has subsided and
symptoms diminish, the prednisone may be reduced by
10% per week. However, therapy may need to be
resumed when symptoms return
Adjunctive therapy with aspirin also is quite helpful. The
primary rationale for aspirin therapy is to reduce
ischemic events in the obstructed vessels

DENTAL MANAGMENT
• From a dental perspective, GCA is significant for several
reasons
– Major manifestations are temporal headaches and jaw
claudication
– Orofacial manifestations of GCA can lead to a
misdiagnosis as temporomandibular disorder
– GCA should be included in the differential diagnosis of
orofacial pain in elderly persons on the basis of
knowledge of related signs and symptoms, including
masticatory muscle pain, hard “end-feel” limitation of
range of motion, and temporal headache

LYME DISEASE
Lyme disease is a multisystemic inflammatory disease
caused by the tickborne spirochete Borrelia burgdorferi
The classical pattern of Lyme disease is a characteristic
macular skin rash (erythema migrans) that appears
within a month of the tick (Ixodes dammini) bite
Several different manifestations, including neurologic,
articular, and cardiac manifestations, may follow

EPIDEMIOLOGY
Lyme disease has been reported in North America, Europe,
and Asia
In the U.S., more than 90% of all cases of Lyme disease
have been reported in only eight states
Difference in the organism and in the immunogenetics
of the affected population may explain the differences
in clinical presentation of Lyme disease

PATHOPHYSIOLOGY AND
COMPLICATIONS
Precisely how B. burgdorferi causes Lyme disease is not
clear
Vasculitis has been implicated in some cases of
peripheral neuropathy, and a vascular lesion resembling
endarteritis obliterans has been identified in the
meninges and synovium of patients with Lyme disease

PATHOPHYSIOLOGY AND
The clinical manifestations of Lyme disease can be divided
into three phases
Early localized disease includes erythema migrans and
associated findings
The primary clinical manifestations of the early
disseminated phase are cardiac and neurologic
problems
In the late disease stage, musculoskeletal problems are
the primary manifestation

PATHOPHYSIOLOGY AND
Late neurologic manifestations of Lyme disease, called
tertiary neuroborreliosis, consist of encephalopathy,
neurocognitive dysfunction, and peripheral neuropathy
Symptoms may be subtle and reported as headache
and fatigue, in addition to cognitive, mood, and sleep
disturbances
Neuropsychological testing may be useful in
confirming the diagnosis
Fibromyalgia is common in patients with Lyme disease

LABORATORY AND DIAGNOSTIC FINDINGS
The diagnosis of Lyme disease is based on clinical
findings, but serologic testing is important and
necessary
Current practice is to confirm all enzyme-linked
immunosorbent assay (ELISA) results with Western blot
analysis
Many other conditions may mimic Lyme disease
(therefore, laboratory testing should be performed for a
more precise, definitive diagnosis
Antibody responses may be undetectable in infections of
less than 6 weeks’ duration, and early antibiotic therapy
based on symptoms may render the infected patient
seronegative

MEDICAL MANAGEMENT
Antibiotic therapy is effective for the treatment of patients
with B. burgdorferi infection
Prompt antibiotic therapy when early symptoms are
reported usually prevents progression to later stages of
Lyme disease
In the late disseminated stages of Lyme disease,
intravenous antibiotics may be necessary
Some patients with arthritis are refractory to antibiotic
therapy
These patients may benefit from intra-articular
corticosteroid injections or hydroxychloroquine

DENTAL MANAGEMENT
The major dental consideration in Lyme disease is the
identification of unusual symptoms in the absence of a
clear medical condition
Symptoms of fatigue, malaise, arthralgia, neuritis, or
neuralgia, including facial palsy, may indicate the
possibility of Lyme disease and the need for referral for
proper medical diagnosis

FIBROMYALGIA
• Fibromyalgia (FM) is the most common cause of chronic
pain in the U.S.
– The diagnosis of FM is typically difficult and lengthy
because there are so many other potential causes for
the widespread pain
– Chronic (several years) diffuse (muscle) pain
accompanied by fatigue, sleep disturbance, and
neuropathies (or other neurologic symptoms) are all
cardinal symptoms of FM
– FM affects up to 4% of the population, primarily
women

EPIDEMIOLOGY AND
• In 1990, the American College of Rheumatology adopted
diagnostic classification criteria for FM
– To meet the diagnostic criteria, there must be chronic
(present for more than 3 months) widespread pain in
all four quadrants of the body, and 11 of 18 points
must be painful on application of only 4-kg pressure

MEDICAL MANAGEMENT
• Successful management of FM requires a thorough
analysis of the patient’s biopsychosocial issues
– Management of central sensitization using
heterocyclic antidepressant agents (HCA) is beneficial
– Serotonin reuptake inhibitors (SSRIs) exhibit a modest
pain benefit in patients with FM
– Anticonvulsant medications are effective and are being
utilized more frequently in the treatment of FM
– Opioids also are commonly used in FM, but long-term
trials are lacking, and these should not be the first
choice of therapy

DENTAL MANAGEMENT
• The major discomfort with FM is muscle pain
– Depending on which muscles are involved, patients
may not be comfortable in a supine position in the
dental chair
– Consideration should be given to providing a more
upright chair position, using neck, back, and leg
supports, and scheduling short appointments

DENTAL MANAGEMENT
(CONT’D)
• The American College of Rheumatology has established
specific diagnostic criteria for FM, however there is a
strong psychological component
– Often patients with FM are treated with anxiolytic
drugs (benzodiazepines) or antidepressants (tricyclics)
– Patients are often very focused on their chronic
symptoms and develop central sensitization

MANIFESTATIONS
• Patients affected with FM may experience TMD-like
features resulting in severe pain upon wide opening, and
pain occurring even with normal function, which worsens
throughout the day
– Adjacent muscle splinting and spasm may occur
– Crepitus is a common finding in the affected joint

• The regional pain found with myofascial pain syndrome
(MFP) needs to be distinguished from the widespread
muscular pain associated with FM
– In both cases, the pain is often described as a “chronic
dull aching pain” and is central to the diagnosis of
both disorders
– When the muscle pain is primarily due to the FM, it
may not respond as well as the jaw pain from MFP
because FM is a systemic and not a local condition
and muscle pain is a typical presentation in FM

QUESTIONS TO ASK PATIENT WITH PSORIATIC
ARTHRITIS, GIANT CELL ARTERITIS, LYME
DISEASE, OR FIBROMYALGIA
• Psoriatic Arthritis
– What symptoms do you experience with PsA?
– What medications are you taking to treat PsA?
– Do you experience any fatigue or muscle weakness?
– Do you prefer to lay supine or semi-supine?
• Giant Cell Arteritis
– What symptoms are you currently having with GCA?
– What medications are you taking to treat GCA?
– Do you have frequent temporal headaches? Does it
hurt to open and close you jaw?
150

DISEASE, OR FIBROMYALGIA (CONT.)
• Lyme Disease
– When were you diagnosed?
– Have you been treated by a doctor?
– Are you suffering from any symptoms currently?
If patient is having symptoms of Lyme Disease in the
presence of a clear medical history and doesn’t have a
diagnosis you may ask:
• Have you noticed any tick bites?
• What symptoms are you experiencing?
• Do you have any rashes in the shape of a bull’s eye?
• Have you consulted with your primary care physician
and sought out testing? 151

DISEASE, OR FIBROMYALGIA (CONT.)
• Fibromyalgia
– When were you diagnosed?
– What symptoms do you have and what areas of your body
are in pain?
– What medications are you taking to treat FM?
– Do you have any pain or discomfort in any areas of your
head or neck region?
– Do you experience any pain opening and closing?
– Do you need any pillows or any certain chair position that
will help you be more comfortable?
152

PRODUCTS TO RECOMMEND TO PATIENT WITH
PSORIATIC ARTHRITIS, GIANT CELL ARTERITIS,
LYME DISEASE, OR FIBROMYALGIA
xerostomia.
• Floss reacher or other flossing aids such as a water flosser if
patient has limited movement in hands.
• Dry mouth rinses and products for patients with xerostomia.
153

Chapter 20 Rheumatologic Disorders

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