dental considerations for patients with lupus erythematosus

7/28/2019 Dental Considerations for Patients With Lupus Erythematosus

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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

dental considerations for patients with lupus erythematosus

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