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Dental Considerations for Patients withLupus Erythematosus
Dr. Ph
Roll No.
Dip.D.Sc. can
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Lupus Erythematosus
Immunologically mediated condition
so called collagen vascular or connective tissue diseases
Several clinicopathologic forms
1. Systemic lupus erythematosus ( SLE )
2. Discoid lupus erythematosus ( DLE ) or
Chronic cutaneous lupus erythematosus ( CCLE )
3. Subacute cutaneous lupus erythematosus
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Systemic Lupus Erythematosus ( SLE )
Is the prototypic multisystem autoimmune disorder with a broadspectrum of clinical presentations encompassing almost all orga
tissues Hallmark feature chronic inflammation
Can affect
Skin
Joints
Kidneys
Lungs
Nervous system
Serous membrane such as pleura and pericardium
Mucous membrane
Other organs of the body
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Women ( age between 30 40 years ) are affected morfrequently than Man
Average ratio ~ 10 : 1
Worldwide prevalence between 12 and 50 per 100,
Clinical course episodes of recurrent acute or chroniinflammation, and intervening periods of
remission
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Lupus flare
Flare can be considered as a reappearance of clinical features wwere earlier quiescent
Certainly easily identifiable and avoidable triggers for lupus flar
1. Exposure to sunlight
2. Physical and mental stress
3. Intercurrent infections
4. Pregnancy
5. Non compliance with treatment or sudden withdrawal of dru
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Clinical features which can be considered as a warning oimpending flare:
Increasing fatigue
Arthralgias and myalgias
New or worsening rash
Persistent headache
Fever
Abdominal pain
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Aetiology
Genetic factors and specific gene loci
Environmental factors
- exposure to sunlight ( photosensitivity )
- drugs ( pharmacogenetics )
- infections ( Epstein-Barr virus )
These factors lead to an irreversible break in immunolotolerance manifested by immune responses againstendogenous nuclear antigens
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Pathogenesis
Type III Hypersensitivity reaction
may be generalized or organ specific
Appropriate antigen (+)formation of soluble immune complexes
(endogeneous nuclear (mainly composed of IgG and IgM
antigen/autoantigen)
Inflammatory response & tissue damage
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Type IIIHypersensitivit
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Aberrant apoptosis or insufficient clearance of apoptotic
Apoptotic blebs and nucleosomes
These taken up by immature myeloid dendtritic cells (m
Mature mDCs produces proinflammatory cytokines such
Activation of Helper T cells (Th-1, Th-2) and Inhibition of Regul(Tregs)
Activated B cells
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Autoreactive B cells produce autoantibodies
Autoantibodies + Apoptotic material
Immune complexes
These were taken up by Plasmacytoid dendritic cells (pDCs)
INF- which enchances autoantibodies production and isotyp
Result in increasing concentrations of immune compl
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EAC early a
M macrop
ACB apopt
mDC myeloTh helper T
IL interleuk
Treg regula
pDC plasmcell
IFN tumour
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Clinical Presentation
Constitutional symptoms
complaint of
- fatigue
- malaise
- arthralgia
- myalgia
- mucocutaneous lesisons
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1. Musculoskeletal features
Artharalgia
- earliest manifestation
- asymmetric and migratory
- joints of hands are mostly affected
Arthritis
- small joints of hands, wrists and knees
Tendon involvement deformities
Myositis
- generalized myalgia and muscle tenderness involving pmuscles
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2. Mucocutaneous features
Skin lesions
Classic malar or butterfly rash
-presents acutely as an erythematous, elevated lesionor
painful in malar distribution
-may last from days to weeks
-that spares the nasolabial crease
Photosensitivity development of rash after exposure toUVA radiation from sunlight or fluorescent lights
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Malar or Butterrash
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Oral lesions
25 45 % of SLE patientsIrregularly shaped raised white plaques
areas of erythema
silvery white scarred lesions, and
Ulcers with surrounding erythema
Soft or hard palate and buccal mucosa
Usually painless
Advance cases may have features of Sjgrens Synd
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Histopathology of Oral lesions
Microscopic features are quite similar to those of lichenand erythema multiforme
Common feature band like subepithelial inflammati
In SLE and EM, inflammatory infiltrate extends deeper underlying connective tissue and shows a perivascular
Lupus lesion will exhibit periodic acid-Schiff staining inbasement membrane zone
Direct immunofluorescent testing immunoglobulin ancomplement deposition along
basement membrane zone
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3. Renal features
30 % of patients Immune complex deposition intra-glomerular inflamm
Lupus nephritis Proteinuria
( grave complications of SLE )
To detect and monitor disease renal activity Urinalysis
Chronic renal failure influence the choice or dosage
medications
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4. Nervous System features
Headache Depression
Seizures
SLE affects both CNS and PNS
Dentists role to rule out odontogenic, TMJ and associamyofacial
sources of pain
Psychosis
Peripheral neuropath
Migraines
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5. Pleura and Lungs
Pleuritis most common manifestation Pleuritic pain ( generalized chest pain aggravated by d
inspiration)
Cough and rapid shallow breathing
Plueral effusion
Parenchymal damage
Hospitalized patient with SLE great risk of acqupneumonia
lead to
pneumonitis
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6. Cardiovascular features
Pericarditis Pericardial effusion may be asymptomatic
Myocardial involvement is rare
Patient may present with fever, dyspnea, tachycardia acongestive heart failure
Valvular heart disease ( most common abnormality is dthickening of mitral and aortic valves followed by vegevalvular regurgitation and stenosis )
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Endocarditisautoimmune basis resulting rheumatic valvular d
in a form of sterile vegetation
Libman-Sacks endocarditis/vegetation
Antibiotic prophylaxis is required to prevent infectiousendocarditis in SLE patients with valvular damage
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Advanced SLE-induced vasculitis can lead to multiorgadysfunction
Raynauds phenomenon cold- or stress-induced trcolor
changes of the hands and feet
Only 8 % of SLE patients have inflammation of retinal a
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Raynauds phenomeNailfold vasculitis
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7. Hematological features
Major clinical manifestations
Anaemia
due to autoimmune haemolysis
Leucopenia
WBC count < 4500/mm3Lymphocytopenia ( lymphocyte count < 1500/mm3 )
thrombocytopenia
usually mild ( platelet count 100000 150000 / mm3
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8. Lymphadenopathy and Splenomeg
lymphadenopathy- 40% of patients
- usually at onset of disease and during disease flares
- soft, non-tender, discrete in cervical, axillary and ingunodes
- rarely > 2cm
Splenomegaly
- 10 45 % of patients
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9. Liver and GI tract features
GI manifestations- presents in 25-40% of patients
- Dyspepsia
- Peptic ulcer
- Abdominal pain accompanied by nausea and vomitt
Hepatomegaly
- 12 25 % of patients
Frequency of various manifestations of SLE
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q y
Manifestations Onset (%) Anytime
Arthralgia 77 85
Constitutional 53 77Skin 53 78
Arthritis 44 63
Renal 38 74
Raynauds 33 60CNS 24 54
Vasculitis 23 56
Mucous membrane 21 52
Gastrointestinal 18 45
M if i O (%) A i (%
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Manifestations Onset (%) Anytime (%
Lymphadenopathy 16 32
Pleurisy 16 30
Pericarditis 13 23
Lung 7 14
Nephrotic syndrome 5 11
Azotaemia 3 8
Myositis 3 3
Thrombophlebitis 2 6
Myocarditis 1 3
Pancreatitis 1 2
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Chronic cutaneous ( discoid ) lupuserythematosus
Mild form of lupus
Skin lesion
discrete, erythematous, slightly infiltrated plaque covere
formed adherent scale that extends into dilated hair foll
(follicular plugging) Often seen on the face, neck, and scalp
leave depressed central scars, atrophy, telangiectasias, adyspigmentation
renal, cardiac, and cerebral disease are usually not presen
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Discoid lupuserythematosus
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Subacute cutaneous lupus erythemat
Intermediate form of lupus
Skin lesions are mild without discoid appearance, do n
common affected areasshoulders, forearms, neck antorso
With some degree of musculoskeletal involvement
renal, cardiac, and cerebral disease are usually not pre
S b t
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Subacutecutaneous luperythematosu
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Diagnosis
The diagnosis of lupus requires integration of patientssymptoms, physical examination findings, and the resudiagnostic tests or investigations.
The American College of Rheumatology has designatedcriteria for diagnosis of lupus
To receive the diagnosis of lupus, a person must have more of these criteria
American College of Rheumatology Diagnostic Criteria for SLE , 1997(revised Tan and others 1982)
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SLE criterion Definition or Examples
Malar ( butterfly ) rash Fixed erythema over the malar eminences
Discoid rash Erythematosus raised patches, may scar
Photosensitivity Skin rash as a result of unusual reaction to sunlight
Oral ulcers Often painless sores
Arthritis Nonerosive: Jaccouds arthropathy
Serositis Pleuritis pleuritic pain, pleural rub, pleural effusionPericarditis ECG changes, pericardial rub, pericardial effusion
Renal disorder Proteinuria ( with 3+ or more protein noted in urinalysis specimprotein/day )Cellular casts in urine
Neurological disorder Seizures
PsychosisHematological disorder Hemolytic anemia
LeukopeniaLymphopenia
Thrombocytopenia
Immunological disorder Anti-DNA antibodiesAnti-Sm antibodiesAntiphospholipid antibodies
Anti-nuclear antibibody Antibodies to nuclear constituents
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If diagnosis of SLE is suspected,
Serologic tests
Complete blood count with differential white blood cell
Disease-specific tests for autoantibodies
- antinuclear antibody
- antibody to double-stranded DNA
- anti-Smith antibody
- Anti-Ro antibody
- Antiphospholipid antibody
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Autoantibodies found in patients with SLE and their significance
Antibody Significance
Antinuclear antibody Indicative of rheumatic diseaNot specific for SLE
Antibody to double-strandedDNS
Suggestive of SLEPredictive for renal involvem
Anti-Smith antibody Predictive for renal involvem
Anti-Ro antibody Suggestive for secondary Sjsyndrome
Antiphospholipid antibody Increased risk of thromboem
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Treatment
Goals of SLE management are based on
Prevention
Reversal of inflammation
Maintaining states of remission and
Alleviation of symptoms
Avoidance of flare-up of lupus and skin lesions
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Medication used in SLE
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Cyclooxygenase-2 ( Cox-2 ) selective inhibitors
Anti-malarials ( such as hydroxycholoroquine )
Systemic corticosteroids ( such as prednisone )
for patients with mobid symptoms associated with sigorgan
involvement
Cytotoxic drugs
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Dental considerations
Oral lesions
Long-term corticosteroids therapy & Adrenal suppressi
Infection
Hematologic abnormalities
Cardiac diseases
Renal diseases
Drugs
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Considerations for oral lesions
Oral manifestations of LE may be difficult from lichen p Immunofluorescence test
PAS-positive thickening of vascular membranes and
broad PAS-positive subepithelial band (lupus band)
The drug of first choice is the antimalarial( Hydroxychloroquine )
Topical steroid creams
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Adrenal suppression
Patients with SLE may be taking adrenal suppressive dose of
corticosteroidssusceptible to shock
Glucocorticoid therapy will cause adrenal suppression for up tmonths
If previous systemic steroid usage was ceased > 14-30 days, for replacement therapy
Lasted >2 weeks and ceased
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Infection
Patient who are taking cytotoxic or immunosuppressiveare at an increased risk of infection.
Impaired immune functions in SLE may predispose to i
Patients with absolute neutrophil count of between 500cells/mm3 will need perioperative prophylactic antibiot
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Haematological abnormalities
Patient with SLE can frequently develop normochromicnormocytic anemia, hemolytic anemia, leukopenia, andthrombocytopenia.
Periodontal surgery or extraction of teeth in these condmay lead to abnormal bleeding.
Therefore, preoperative complete blood count, prothrotime and partial thromboplastin time measurement shoperformed prior to any extensive dental procedures.
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Cardiac involvement
Libman-Sacks vegetations may occur in SLE patients
These vegetations can lead to bacterial endocarditis
Therefore, SLE patients with valvular damage should hantibiotic prophylaxis
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Renal involvement
Prescriptions for certain antibiotics and analgesics can
adversely affect kidney function
Therefore, the dentist should be aware of patients renfunction
( i.e, creatinine clearance )
Patients who are undergoing hemodialysis should recedental treatment on nondialysis days
D ith d i tl kid d d t
dependent elimination
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Drugs with predominantly kidney-dependentelimination
Nonsteriodal anti-inflammatory drugs
Acetylsalicylic acid
Penicillins
Cephalosporins
Tetracycline
Antifungals
Suggested adjustments
Consider increasing dose intervals and decreasing
dosage
Consider contacting physician if renal function is
unknown
Suggested alternatives
Acetaminophen
Narcotics
Drugs
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Drugs
certain drugs may exacerbate underlying SLE or induce alike illness
Drug-induced lupus erythematosus ( DILE )
The development of lupus-like symptoms ( commonly fevemusculoskeletal involvement ) which resolves with cessatioffending drugs.
Procainamide (antiarrhythmics) and Hydralazine
(antihypertensive) SLE exacerbation (acute lupus flare) by drugs such as pen
sulfonamides and NSAIDs.
all of these drugs should be used judiciously
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Dental considerations
Oral lesions
Long-term corticosteroids therapy & Adrenal suppressi
Infection
Hematologic abnormalities
Cardiac diseases
Renal diseases
Drugs
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Thank Youso much