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BDS2; CHHD > Rheumatology II > Flashcards

Rheumatology II Flashcards

1. Identify and recognise signs and symptoms of common non-autoimmune rheumatological conditions 2. Understand the role of imaging and blood investigations at arriving at a diagnosis 3. Explain dental relevance of non-autoimmune rheumatological conditions and their clinical management

1
Q

List inherited non-autoimmune bone disorders

A
  1. Osteogenesis imperfecta (brittle bone syndrome)
  2. Cleidocranial dysplasia
  3. Osteoporosis (marble bone disease)
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2
Q

List acquired non-autoimmune bone disorders

A
  1. Osteomalacia and rickets
  2. Osteoporosis
  3. Osteomyelitis
  4. Paget’s disease of bone
  5. Osteoarthritis
  6. Fibrous dysplasia
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3
Q

What is osteogenesis imperfecta

A

A rare autosomal dominant inherited condition closely related to the gene for dentinogenesis imperfecta, and it is characterised by brittle bones susceptible to fracture due to defective type I collagen formation and small osteoblasts - this means mainly woven bone is formed (this is more fibrous than cortico-lamellar bone which is stronger)

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4
Q

Outline the clinical features of osteogenesis imperfecta

A
  1. Multiple fractures on minimal impact (less post puberty)
  2. Gross deformity and dwarfism due to bone distortion on healing from fractures
  3. Parietal bossing causing eversion of upper ear
  4. Deafness, blue sclera, easy bruising
  5. Loose/weak tendons and ligaments
  6. Hernias
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5
Q

How is osteogenesis imperfecta diagnosed

A
  • positive family history
  • clinical presentation (multiple fractures, ear eversion due to parietal bossing, deformed bone healing)
  • radiography
  • skin biopsy
  • DNA based sequencing
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6
Q

How is osteogenesis imperfecta managed

A
  • No cure
  • Supportive therapy to decrease fractures
  • Bisphosphonates to prevent bone loss
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7
Q

What is the dental relevance of osteogenesis imperfects

A
  1. Handle patients carefully due to bone fragility
  2. Do not confuse with physical abuse
  3. Minimal force, support jaws and ensure haemostasis
  4. Chest deformity can contraindicate surgery (kyphoidosis)
  5. Dentinogenesis imperfecta (so weak teeth due to dentine not being strong - this predisposes to caries)
  6. Bisphosphonates can cause MRONJ
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8
Q

What is cleidocranial dysplasia

A

A rare autosomal dominant trait on chromosome 6 causing defects of membrane bone formation (bone formed directly from CT not from cartilage) e.g. skull and clavicles

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9
Q

Describe the clinical features of cleidocranial dysplasia and how is it diagnosed

A
  • Absent/ defective clavicle
  • Prognathic mandible due to maxillary hypoplasia (looks like mandible protrudes out and causes a reverse overbite)
  • Depressed nasal bridge
  • Frontal, parietal and occipital bossing
  • Kyphoscoliosis and pelvic abnormalities

Diagnosis is based on these clinical features and radiography

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10
Q

What is the dental relevance of cleidocranial dysplasia

A
  1. Facial abnormalities
  2. Deciduous teeth retention causing delayed/failure of eruption of permanent dentition
  3. Hyperdontia, supernumerary teeth
  4. Twisted roots (complicate extractions)
  5. Malformed crowns
  6. Dentigerous cysts (form when teeth are retained in the bone as they cannot erupt)
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11
Q

What is osteopetrosis

A

Marble bone disease = rare genetic disorder characterised by excessive bone density, defective osteoclastic activity and remodelling to give dense but weak fragile bone which can heal normally

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12
Q

What are the clinical features of osteopetrosis and the findings on investigation

A
  • Bone pain, fractures, osteomyelitis
  • Infection and anaemia
  • Cranial neuropathies (XS bone can compress nerves)
  • Epilepsy and learning disabilities (rare)
  • Dense appearance on radiographs

Normal Ca2+ and PO43- on testing as there is no issue with osteoclastic activity

Radiographs show dense marble-like bone appearance

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13
Q

What is the dental relevance of osteopetrosis

A
  1. Frontal bossing and hypertelorism (increased distance e.g. between orbit and eye)
  2. Trigeminal/ facial neuropathies can be a complication
  3. Jaw fractures
  4. Anaemia
  5. Delayed tooth eruption
  6. Osteomyelitis is a complication of osteopetrosis
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14
Q

How is PTH involved in calcium metabolism

A

It is released from the parathyroid gland when there is low serum calcium levels and this acts on the bone and kidneys

In bone this causes the release of calcium to increase serum calcium levels

In kidney this increases calcitriol formation (active vitamin D3) and decreases the excretion of calcium

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15
Q

How is vitamin D involved in calcium metabolism

A

Vitamin D is hydroxylated in the liver to calcidiol and then in the kidneys to calcitriol - this increases the absorption of dietary calcium in the small intestine and acts on the bone to release calcium - In turn both of these increase the serum calcium levels

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16
Q

What is osteomalacia and rickets

A

Osteomalacia (adults) = failure of mineralisation of replacement bone
Rickets (children) = inadequate mineralisation of bone framework

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17
Q

What are the risk factors for osteomalacia and rickets

A
  • Vit D deficiency
  • Pigmented skin, sunscreen, elderly, institutionalised
  • Calcium malabsorption
  • Renal diseases
  • Drugs
  • Pregnancy and lactation (increased demands for calcium)
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18
Q

What are the clinical features of osteomalacia and rickets

A
  1. Weak, hypotonic muscles due to low Ca2+
  2. Bone pain
  3. Fractures as bone is weak (not mineralised)
  4. Bone deformity and impaired growth in children
  5. Hypocalcemia, tetany and seizures
  6. Swelling at costochondral joints ‘Rachitic rosary’
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19
Q

How is osteomalacia and rickets diagnosed

A
  • radiographically
  • low/normal PO43- and Ca2+
  • high ALP
  • high PTH
  • low vitamin D
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20
Q

How is osteomalacia and rickets managed

A

Treating underlying causes thus vitamin D and calcium supplements

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21
Q

What is the dental relevance of osteomalacia and rickets

A
  1. Delayed eruption in severe cases

2. If associated with malabsorption can cause vitamin K deficiency and secondary hyperparathyroidism

22
Q

What is osteoporosis

A

When the bone mass is diminished leading to fragility and increased risk of fracture affecting the spine, forearms and hips (increase in porosity)

23
Q

What are the modifiable risk factors for osteoporosis

A

Smoking, alcohol abuse, low dietary calcium intake, vitamin D deficiency, lack of physical activity, immobility, drugs (steroids, anticoagulants, anticonvulsants)

24
Q

What are the non-modifiable risk factors for osetoporosis

A
  • old age
  • sex: female
  • race: caucasian and asian
  • family history
25
Q

What are the clinical features of osteoporosis

A
  1. Fractures at - thoracic and lumbar vertebrae, head of femur, distal radius (Colles fracture)
  2. Kyphosis
  3. Height shrinkage (widow’s stoop)
26
Q

What investigations are done for osteoporosis

A
  • Bone density DEXA scan (
27
Q

Why is calcium, phosphate and alkaline phosphate are normal in patients with osteoporosis

A

Because it is to do with the bone density and matrix

28
Q

How is osteoporosis managed

A
  • Avoid modifiable risk factors
  • Increase dietary calcium and vitamin D
  • Bisphosphonates prevent fractures and slow the reduction in density
29
Q

What is the dental relevance of osteoporosis

A
  1. GA can be contraindicated in deformed chest and vertebral collapse
  2. Jaw osteoporosis can cause XS alveolar loss (esp. women)
  3. Bisphosphonates - MRONJ
30
Q

What is osteomyelitis

A

Infection of the bone mainly by staphylococcus (can be haemophilia influenza, salmonella in sickle cell anaemia) And the source can be haematogenous or direct/contiguous spread

31
Q

What are characteristics of the haematogenous source of osteomyelitis

A
  • Bacteria seeding from the blood
  • Involves a single specie of bacteria
  • Occurs in children
  • Common site is rapidly growing and highly vascular metaphysic of growing bones
32
Q

What are characteristics of the direct/contiguous source of osteomyelitis

A
  • Usually due to local infection caused by trauma/ surgery

- Tends to involve multiple bacterium

33
Q

What are the clinical features of osteomyelitis

A

Fever, localised pain and erythema

If in jaw:

  • deep seated boring pain with swelling, truisms and regional lymphadenopathy
  • lower lip paraesthesia
  • teeth are tender and may be mobile
  • pus discharges from gingival crevices/ several sinuses if cortical plate is penetrated
34
Q

How is osteomyelitis diagnosed

A

From the history of clinical findings and radiographs show marked bony destruction in late stage

Blood tests show leukocytosis with neutrophilia and raised ESR

35
Q

How is osteomyelitis treated

A

Antibiotics: Flucloxacillin and fusidic acid for 4-6 weeks starting with IV route

36
Q

What is the dental relevance of osteomyelitis

A
  1. Can affect jaw (acute = adults, mandible/chronic = secondary to inadequate treatment of acute type or de novo from low virulent bacteria)
  2. Delay all dental treatment until complete resolution
37
Q

What is Paget disease of bone (osteitis deformans)

A

Progressive bone enlargement and deformity from osteoclastic and osteoblastic over activity - the increased abnormal bone resorption is followed by weaker new bone formation due to chaotic repair and renewal

There is increased local bone blood flow and fibrous tissue and the commonly affected sites are the pelvis, lumbar spine, femur, thoracic spine, skull and tibia

Incidence increases with age and is male dominating

38
Q

Describe the clinical features of Paget disease of bone (osteitis deformans)

A
  1. Asymptomatic in early stage, spared hands and feet
  2. Pain around hips, knees
  3. Deformities: skull enlargement, bowed tibia
  4. Pathological fractures (esp. in elderly)
  5. Cranial nerve compression
  6. High output cardiac failure due to bone hypervascularity (if disease is widespread)
  7. Osteosarcoma is a rare complication
39
Q

How can Paget disease of bone (osteitis deformans) be diagnosed

A
  • radiographs
  • radionuclide bone scans
  • raised alkaline phosphatase
  • normal calcium and phosphate
40
Q

How is Paget disease of bones (osteitis deformans) treated

A

Bisphosphonates

41
Q

What is the dental relevance of Paget disease of bone (osteitis deformans)

A
  • Patients can develop heart failure
  • Avoid GA
  • Hypercementosis can complicate extractions
  • Gross symmetrical widening of alveolar ridges
  • Poor blood supply may predispose to chronic osteomyelitis
  • Senses of hearing, sight and smell deteriorate
  • Osteosarcoma in the jaw
42
Q

What is osteoarthritis and what is it characterised by

A

This is the most common form of arthritis (>45 yrs) and is characterised by

  • degeneration of the articular cartilage
  • thickening of the exposed underlying bone
  • development of peri-articular cysts
  • joint deformation
43
Q

What are the risk factors of osteoarthritis

A

Age, gender, genetics, obesity, occupation, fracture through a joint, congenital joint dysplasia, Paget’s disease and gout

44
Q

Describe the clinical features of osteoarthritis

A
  1. Joint pain which is worse on movement and relieved by rest
  2. Stiff joints
  3. Deformity
  4. Loss of function
  5. Herberden’s nodes = hard bony lumps in the DIP joints of fingers
45
Q

How is osteoarthritis managed

A

Regular exercise, weight control, good footwear, using a walking stick, NSAIDs, antidepressants intra-articular injections and surgery

46
Q

Outline the dental relevance of osteoarthritis

A
  • Dental care access is complicated by age and motility
  • Bleeding tendency due to aspirin so ensure haemostasis
  • Reduced manual dexterity
  • TMJ involvement
47
Q

What is fibrous dysplasia

A

Replacement of an area of bone by fibrous tissue which causes localised swelling affecting a single bone (monostotic) or several bones (polyostotic): lesions start in childhood and stabilise

48
Q

What is mostotic fibrous dysplasia

A

This is the more common form and occurs more in females involving the jaw especially the maxilla

49
Q

What is polystotic fibrous dysplasia

A

Less common and can be unilateral and involve 50% of skeleton and cause abnormal skin hyperpigmentation Café-au-lait spots and Albright syndrome

50
Q

How is fibrous dysplasia diagnosed and mannaged

A

Ground glass appearance on radiograph with normal serum calcium, phosphate with raised alkaline phosphatase

  • It is self-limiting and stops progressing after adolescence
  • Bisphosphonate treatment can cause MRONJ
  • Surgery to correct cosmetic defects
  • Endocrine conditions can complicate treatment
51
Q

What is the dental relevance of fibrous dysplasia

A
  1. Facial bones are involved in monostotic type

2. Hyperthyroidism and diabetes may be associated with the polyostotic type

BDS2; CHHD (32 decks)

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