Rheumatology Flashcards
What is the aetiopathogenesis of rheumatoid arthritis?
Unknown but it is recognised that it probably results from a combination of genetic and environmental factors leading to breakdown of immune tolerance.
What are the other autoimmune diseases as well as RA associated with in terms of aetiopathogenesis?
Associated with MHC:
* Rheumatoid Arthritis (RA): HLA-DR4 (more frequent in smokers)
* Systemic Lupus Erythematosus (SLE): HLA-DR3, complement components
* Progressive systemic sclerosis (PSS): HLA-DR3
- Immunological associations: serology often positive for a variety of autoantibodies
- Histology shows evidence of immune involvement
What are the auto-antibodies present in RA?
-RF (rheumatoid factor) present in RA, but non-specific
-95% specific to RA is the anti-CCP (anti-citrullinated protein antibodies)
What are auto-antibodies?
Antibodies produced by the immune system that mistakenly target and attack the body’s own tissues.
What are the auto-antibodies present in systemic lupus erythematosus (SLE)?
ANA (antinuclear antibodies), specifically dsDNA antibodies
What is the auto-antibody present in progressive systemic sclerosis (PSS)?
Scl 70
What are the auto-antibodies present in Sjogren’s syndrome?
ENA (extractable nuclear antigen) antibodies (Ro, La) as well as RF.
What are rheumatoid factors?
Auto-antibodies which target and attack IgG antibodies or IgM produced by the body itself.
This leads to inflammation, joint damage etc.
How prevalent is RA?
1% of population is affected with a female predisposition in the ratio F:M being 2.5:1.
What is RA?
-Symmetrical polyarthritis which often starts in hands and wrists.
-It’s a systemic disease which may have extra-articular movement.
-This means RA doesn’t only affect joints but also other organs and systems in the body.
What are the symptoms and signs of RA?
Symptoms:
-Pain
-Swelling
-Morning stiffness
-Malaise (fatigued)
-Non-articular symptoms
Signs:
-Swelling
-Warmth
-Tenderness
-Limited movement
-Deformity
What can advanced RA look like?
-Bountonniere deformity of thumb (z-shaped)
-Ulnar deviation of metacarpophalangeal joints
-Swan neck deformity of fingers
What does the anatomy of a RA joint look like compared to a healthy joint?
In the RA joint:
1.The synovial membrane is thickened
2.There’s an overgrowth of the synovia sites (pannus)
3.Marked influx of inflammatory cells; each of those producing cytokines which stimulates inflammation
4.Osteoclasts get activated to eat away at the bone
5.Cartilage overlying the bone is getting damaged and removed
6.Swelling of the overlying soft tissues is caused; there’s damage to the ligaments and structures supporting the joints
7.The joint itself also gets damaged
What does the pannus look like histologically?
slide 20
What are some of the complications of RA?
-rheumatoid nodules
-Tendon rupture
-Normochromic, normocytic anaemia
-Nerve entrapment e.g. median nerve
-Vasculitis - a group of conditions that cause inflammation of the blood vessels.
-Atlanto-axial subluxation
-Eye complications
How are patients with RA treated?
Analgesia (e.g. NSAIDs reduce pain and swelling)
DMARDs especially methotrexate, hydroxychloroquine for mild to moderate
TNFa blockade e.g. Infliximab, Etanercept
Anti-B cell monoclonal ab e.g. rituximab
What is the relevance of RA to dentistry?
Hand deformity - oral hygiene, blister packs
Carpal tunnel syndrome
Atlanto-axial subluxation during GA
TMJ dysfunction
Sjogren’s syndrome
Anaemia
Complications of systemic treatment
What is Sjogren’s syndrome?
An autoimmune disease which can cause oral and ocular dryness.
It can either be a primary disease (dry eyes, mouth, vagina, etc.) or it can be secondary to other autoimmune diseases (e.g. RA, PSS, SLE)
What is the incidence of Sjogren’s syndrome and who is most likely to get it?
It’s quite rare but it’s much more common in females (F>M 9:1) with 2 peaks of onset: mid 30s and then postmenopausal 45-60 due to reduction is oestrogen
What are the symptoms of Sjogren’s syndrome?
-Sicca symptoms (95%): dryness of mouth, eyes, skin, vagina
-Excessive fatigue (75%)
-Arthralgia - pain in joints without joint inflammation.
-Myalgia - muscle pain/aching
-Dental caries
-Loss of teeth
-Candida
-Swollen salivary glands and Lacrimal glands
If you have Sjogren’s syndrome, what is there also an increased risk of?
Lymphoma/maltoma
Have to look out for B cell lymphoma, mucosal associated lymphoid tissue
What investigations are required in order to diagnose Sjogren’s syndrome?
- Measure salivary flow, whether it’s stimulated or unstimulated:
-For stimulated parotid flow, normal is >0.4ml/min
-For unstimulated whole salivary flow, normal is >0.2ml/min
- Schirmer test
- Do bloods: FBC, inflammatory markers, auto-antibodies Ro and La, others as indicated
- Ultrasound (has largely replaced sialography & scintigraphy)
- Labial gland biopsy
What is the relevance of Sjogren’s syndrome to dentistry?
-Xerostomia: Dental caries, Loss of teeth, Candida
-Salivary gland enlargement
-Complications of systemic treatment
What are the variants of lupus erythematosus?
- Discoid lupus (DLE)– scarring skin lesions/oral (affects either just skin or just mouth)
- Subacute cutaneous (SCLE)- rash, systemic disease (predominantly affects skin but has some features of systemic disease)
- SLE (predominantly systemic but might include skin rash/oral lesion)
- Anti-phospholipid syndrome (sticky blood, prone to clots)
- Drug-induced lupus
What is the aetiology of SLE?
SLE is a multi-system disease
Pathology- widespread vasculitis (immune system mistakenly attacks blood vessels) of capillaries, arterioles and venules
Aetiology- genetic, complement deficiency
Triggers- UV light, infection, or even drugs
What investigations would we undertake in diagnosing lupus?
In the bloods, you’re looking for raised ESR, ANA, positive RF etc.
What are cerebral micro-infarcts?
Blood vessels in the brain affected.
White spots in the brain present
What is lupus nephritis?
Connective tissue disorder resulting from an abnormal immune system
how does lupus nephritis manifest as?
Foamy urine = increased protein in urine
Brownish urine due to blood present
Elevated creatine in the blood
High bp
odema of feet, lower legs and eyelids.
5% of patients with SLE will develop some degree of renal involvement
What can anti-phospholipid syndrome lead to?
Increased tendency to clotting
Venous thrombosis
Arterial thrombosis
Recurrent foetal loss
Thrombocytopenia - low platelet count
Livedo Reticularis - net-like pattern on skin due to change in blood flow affected small blood vessels in the skin.
What is the relevance of lupus erythematosus to dentistry?
Oral ulceration
Complications of systemic treatment
Candida
+/-Dry mouth (xerostomia)
Main differential is lichen planus (you might think the patient has lichen planus, but it’s actually an oral manifestation of their lupus)
What are the subtypes of scleroderma?
- Systemic fibrosis
- Limited systemic / CREST syndrome
- Localised to skin - morphoea
What can patients with diffuse systemic sclerosis have?
Scleroderma - thickening of skin
Skin induration - hardening/thickening of skin
Flexion Fingers: start to bend in and become claw-like and this starts distally & gradually works its way proximally
Digital gangrene may occur
Skin may look shiny
In terms of facial changes, the patient could develop microstomia and struggle to open their mouth wide
Can also have pulmonary fibrosis, diverticula (malabsorption), intimal arterial proliferation (kidney)
What is the relevance of scleroderma to dentistry?
Microstomia - abnormally Small mouth
Widened periodontal membrane
Severe sclerodactyly- difficulty with oral hygiene
Immunosuppression
What is affected in the more limited systemic disease variations of lupus?
CREST:
Calcinosis - calcium deposit in fingertips/soft tissues
Raynaud’s phenomenon - episodes of reduced blood flow to fingers and toes = turn white or blue
Esophagus (oesophagus) - difficulty swallowing
Sclerodactyly - thickening and tightening of the skin on the fingers and hands.
Telangiectasia - dilated blood vessels that appear as red spots on skin, particularly on face and hands
What treatments are there for these patients with lupus, systemic sclerosis, etc.?
Analgesics
Glucocorticoids
Immunosuppressive: cyclophosphamide, azathioprine, mycophenolate mofetil
Biologics
How is Raynaud’s treated?
Physical: gloves (heated)
Nifedipine: Ca channel antagonist
Losartan: angiotensin II antagonist
Who is most commonly affected by Osteoarthritis?
The general population >60yrs old
There is a 10% genetic predisposition though
What is osteoarthritis (OA)?
Non-autoimmune degenerative joint disease
What is the pathogenesis of OA?
Degenerative disease of cartilage
(may be genetic or mechanical insults, or biochemical abnormalities of cartilage)
What do Heberden’s nodes look like?
Heberden’s node on the distal interphalangeal joint is a characteristic joint to be affected in OA so it wouldn’t be seen in RA- key differentiating factor
Distal interphalangeal joint is the last joint (closest to nails) in the fingers
Compare and contrast primary OA with secondary OA.
Primary OA:
-Majority of cases
-Strong family history
-Onset around 50
Secondary OA:
-Congenital abnormality of joints
-Structural disorders in children which can lead to trauma causing OA
What are the clinical features of OA?
Symptoms:
-Pain– worse with use
-Morning stiffness <30 mins
-Disability
Signs:
-Swelling– hard and bony
-Crepitus - popping, clicking or crackling sound in a joint
-Muscle wasting
-Limited movement
-Joint deformity
-Monoarticular occasionally
-Bilat and symmetrical e.g. knees, hands, hips
What is the relevance of OA to dentistry?
-Reduced mobility
-Reduced manual dexterity
-TMJ dysfunction
