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Oral candidiasis > 14. Diseases of the facial bones and joints > Flashcards

14. Diseases of the facial bones and joints Flashcards

1
Q

What are the 4 layers in the structure of bone?

A

Outer, dense compact bone
Trabecular or cancellous bone
Central medullary cavity
Periosteum

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2
Q

Where is marrow found and what types can it be?

A

In the medullary cavity
Red or yellow marrow

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3
Q

What are the 2 layers of the periosteum?

A

Fibrous layer
Cellular layer

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4
Q

What does fibrous periosteum contain?

A

Sharpey’s fibres that anchor down into the bone and attach the periosteum to the bone

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5
Q

What is bone composed of?

A

Osteoid- Type 1 collagen that becomes mineralised.
Cells- osteoblasts, osteocytes, osteoclasts

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6
Q

What are the 2 types of bones?

A

Mature lamellar
Woven bone

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7
Q

What gene does osteogenesis imperfecta affect?

A

Type 1 collagen genes
COL1A1 COL1A2

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8
Q

What genes do the 4 rare types of osteogenesis imperfecta affect?

A

CRTAP
LEPRE1

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9
Q

What is the clinical presentation of osteogenesis imperfecta?

A

Brittle bones
Deafness- ear ossicles deformation
Ligament laxity
Thin aortic and heart valves
Blood vessel fragility
Short stature

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10
Q

What is the pathogenesis of osteogenesis imperfecta?

A

Amino acid substitution in the triple helix (glycine).

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11
Q

What are the types of osteogenesis imperfecta?

A

Type 1- common, mildest, AD, deafness, bone fragility, blue-grey sclera +-DI
Type 2- in utero fractures, respiratory dys, fatal, AD and AR
Type 3- rarers, progressive bone deformities, DI
Type 4- White sclera, same as type 1

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12
Q

What gene causes opalescent teeth in osteogenesis imperfecta?

A

COL1A

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13
Q

What gene causes dentinogenesis imperfecta?

A

DSPP

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14
Q

What are the features of dentinogenesis imperfecta?

A

Opalescent Amber teeth
Affects primary more than secondary
Normal colour
Short roots/obliterated canals
Decreased caries
Increased attrition
Decreased dentinal tubules or atubular

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15
Q

What is cleidocrania dysplasia due to?

A

Mutation in RUNX2 gene- controls osteoblast differentiation
Autosomal dominant

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16
Q

What are the symptoms of cleidocranial dysplasia?

A

Aplasia of clavicles
Frontal bossing- delayed ossification of fontanelles
Short stature
Hypertelorism
Delayed eruption of secondary teeth
Supernumerary teeth
Prognathism

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17
Q

What occurs in osteopetrosis?

A

Reduced bone resorption and diffuse symmetric skeletal sclerosis

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18
Q

What is the inheritance of osteopetrosis?

A

2 modes
Autosomal dominant more rare than autosomal recessive
Autosomal recessive is fatal if untreated

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19
Q

What is the pathogenesis of osteopetrosis?

A

Defect in carbonic anhydrase 2
Mutation in CLCN7- proton pump/gene defect
Causes defect in osteoclastic function and so failed remodelling

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20
Q

What are the general symptoms of osteopetrosis?

A

CN palsy- sclerosis of foramina at base of skull compresses nerves
Enlarged spleen
Anaemia
Increased fracture
Recurrent infection

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21
Q

What are the dental symptoms of osteopetrosis?

A

Malformed short roots and unerupted teeth
Osteomyeleitis after extractions
Delayed eruption
Root and bone fractures
Unusual dentition

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22
Q

What are the radiographic findings of osteopetrosis?

A

Abnormally dense bones
Chalky white appearance
Reduced marrow spaces

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23
Q

What is the treatment for osteopetrosis?

A

Bone marrow transplant

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24
Q

What is the genetic reason for achondroplasia?

A

Mutation in fibroblast growth factor receptor 3 gene
Abnormal cartilage formation which affects endochondral ossification

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25
Q

What disease is achondroplasia associated with?

A

Mutations of the FGRF3 also associated with Crouzon syndrome

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26
Q

Which type of achondroplasia is fatal?

A

Homozygous form

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27
Q

What are the features of achondroplasia?

A

Normal sized head, trunk
Protuberant abdomen
Short limbs
Retrusive middle third of face- due to lack of development of the base of skull
Severe Malocclusions

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28
Q

What are the treatment for achondroplasia?

A

Surgery for cleft palate
Orthodontics

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29
Q

What are the symptoms of cherbusim?

A

Individuals appear normal at birth AD
2-4- painless symmetrical swelling of mandible, and sometimes maxilla
7- lesions become static or regress
Chubby face
Rim of sclera visible underneath iris
Puberty onwards see improvement but cosmetic surgery may be necessary

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30
Q

What gene does cherubism involve?

A

Mutation in SH3BP2- function unclear thought to be involved in cell signalling in bone remodelling

31
Q

What do you see in radiographs of cherbusim?

A

Multiocular radiolucencies
Thinning or perforation of cortical bone

32
Q

What are the dental anomalies of cherubism?

A

Early loss of deciduous teeth
Displacement
Abnormal unerupted permanent teeth

33
Q

What is the histology of cherubism?

A

Cellular and vascular fibrous tissue
Focal collections of multinucleated giant cells
Haemosiderin
Metaplastic bone

34
Q

How does Gardner’s syndrome occur?

A

Autosomal dominant- APC gene
Recessive form- MUTYH gene

35
Q

What are the symptoms of Gardners syndrome?

A
  1. Multiple polyposis of the large intestine- premalignant
  2. Osseous anomalies
  3. Dental anomalies- supernumerary, odontome, impacted
  4. Epidermoid cysts of skin- scalp and back
  5. Desmoid tumours
36
Q

What osseous anomalies are seen in Gardner’s syndrome?

A

Hazy sclerosis of jaw bones
Dense bone islands of jaw bones
Osteomas of the bones. Jaw and skull/long bones

37
Q

How does fibrous dysplasia occur?

A

Somatic mutation in GNAS1 gene- G protein that regulates cAMP formation
Overproduction of cAMP leads to overexpression of c-fos, a protooncogene responsible for regulating proliferation and differentiation of osteoblasts

38
Q

What are the clinical forms of fibrous dysplasia?

A

Monostotic- most common- frequent in jaws
Polyostotic
McCune-Albright Syndrome

39
Q

What is McCune-Albright syndrome?

A

Polyostotic fibrous dysplasia
Cafe au lait spots in skin
Endocrine abnormalities such as precocious puberty, thyroidal cysts, pituitary adenoma, large hands and feet, cushing syndrome

40
Q

What is the radiographic appearance of fibrous dysplasia?

A

Orange peel ground glass appearance
Blends
Goes from radiolucent to radiopaque
Expansile mass

41
Q

What is the histology of fibrous dysplasia?

A

Bone replaced by cellular or collagenous fibrous tissue
Metaplastic bone (woven or osteoid) arranged in irregular trabecular pattern forming chinese characters
Fuses with the surrounding bone unlike cemento-ossifying fibroma

42
Q

How does fibrous dysplasia present as?

A

Common in jaws
Swelling painless
Not well circumscribed
Lesions expand during skeletal growth then stop
Not radiosensitive- if irradiated can transform into sarcomas
Surgical treatment preferable after growth phase

43
Q

What is the definition of osteitis?

A

Localised inflammation that does not spread through marrow spaces

44
Q

What is the definition of osteomyelitis?

A

Extensive inflammation that does spread through marrow spaces.

45
Q

What is periostitis?

A

Inflammation of periosteum

46
Q

What is alveolar osteitis?

A

Localised inflammation that occurs in some extractions

47
Q

What can alveolar osteitis be due to?

A

Failure of blood clot formation
Disintegration of blood clot

48
Q

How can a blood clot fail to form in alveolar osteititis?

A

Osteopetrosis
Paget’s disease
Poor blood supply
Vasoconstrictor
Radiotherapy

49
Q

How can a clot become disintegrated in alveolar osteititis?

A

Mouthwashes
Protelytic bacteria
Empty socket retains food and debris and becomes infected
Osteoclasts separate dead bone forming sequestra
Localised inflammation, slow healing, granulation tissue

50
Q

What is the tx for alveolar osteititis?

A

Remove debris
Alveogyl
Irrigate with CHX
Sequestrum removal

51
Q

What are the symptoms of alveolar osteitis?

A

Severe pain
Foul taste
Foul smell
Denuded bone may be visible

52
Q

How does the socket heal after extraction?

A

Socket fills with blood
Formation of granulation tissue
Osteoclasts cause resorption of crestal alveolar bone
Gingival epithelium migrates across defect
10-14 days- formation of granulation tissue, and osteoblasts form woven bone
4-6 weeks- socket healed by repair, contains woven bone, outline of socket visible on rads
20-30 weeks- woven bone remodelled, formation of cortical cancellous bone, socket obliterated, alveolar bone reduces in height

53
Q

What is focal sclerosing osteititis?

A

Sequelae of periapical inflammation
Mild irritation
Infection
High tissue resistance

54
Q

What does focal sclerosing osteitits look like on radiograph?

A

Asymptomatic
Dense area at apex, but not attached to the tooth

55
Q

What is the differential for focal sclerosing osteitis?

A

Sclerotic bone islands

56
Q

What is the histology of focal sclerosing osteitits?

A

Plasma cells
Lymphocytes
Fibrous marrow tissue
Increase in thickness and number of bony trabaculae

57
Q

What types of suppurative osteomyelitis are there?

A

Acute or chronic
Chronic lasts more than 1 month

58
Q

Where does suppurative osteomyelitis occur most?

A

Mandible more common- occurs in areas with high blood supply

59
Q

What are the causes for suppurative osteomyelitis?

A

Abscess
Fracture
Local trauma
Penetrating wounds
Extraction

60
Q

What is the pathology of suppurative ostemyelitiis?

A

Microorganisms proliferative in bone marrow spaces
Acute inflammation
Tissue necrosis
Accumulation of pus

61
Q

What happens after suppurative osteoymyeleitis?

A

Sequesterum- formation of necrotic bone surrounded by pus
Involucrum- formation of new bone outside the original

62
Q

What are the clinical features of suppurative ostemyelitis?

A

Pain
Pyrexia
Paraesthesia of lip
Swelling
Trismus
Intra-oral and extra-oral sinus
Tooth mobility

63
Q

What is the histology of suppurative ostemyelitis?

A

Necrotic bone surrounded by inflammatory cells and pus
Involucrum

64
Q

What is the radiology finding of suppurative ostemyelitis?

A

Early stages- normal
10-14 days- irregular, moth-eaten radiolucency

65
Q

What is diffuse sclerosing osteomyelitis?

A

Similar to focal sclerosing, but more generalised
Proliferative reaction in response to low grade infection
Occurs in older age group

66
Q

What is chronic osteomyelitis with proliferative periostitis?

A

Occurs in mandible of children and young adults
Low grade apical inflammation reaching cortical bone
Periosteal reaction seen- thickening and swelling of bone- onion skin

67
Q

What are the histological features of chronic osteomyelitis with proliferative periostitis?

A

Fibrous marrow
Chronic inflammatory cells
Parallel layers of woven bone

68
Q

What is chronic periostitis associated with?

A

Hyaline bodies- pulse granulomas
Hyaline ring shaped material
Fibrous thickening of periosteum
Pus
May be due to vegetable material implanted through tooth socket, raised flap, traumatic ulceration, root canal

69
Q

What is phosphorus necrosis?

A

White phosphorus P4O10 converts to bisphosphonates
Causes MRONJ

70
Q

What is osteoradionecrosis?

A

Radiation causes proliferation of blood vessels intima- endarteritis obliterans
Reduction in blood supply, especially mandible, thrombosis

71
Q

When does osteoradionecrosis develop?

A

Months or years after radiotherapy

72
Q

What is osteoradionecrosis clinically similar to?

A

Osteomyelitis- pain swelling slow recovery, may be asymptomatic

73
Q

What should you do to head and neck radiotherapy patients to avoid osteoradionecrosis?

A

Leave only sound teeth and remove others at least 2 weeks before treatment

Oral candidiasis (18 decks)

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