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Oral pathology > OP14 diseases of the facial bones and joints I > Flashcards

OP14 diseases of the facial bones and joints I Flashcards

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1
Q

What is the gross structure of bone?

A

Outer dense/compact bone
Trabecular/cancellous bone
Central medullary cavity
Periosteum - fibrous and cellular layer

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2
Q

What are Haversian systems?

A

Concentric lamellae with osteons in the centre and osteocytes inside, intercommunicating with small canals.
Circumferential lamellae around the tissues.

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3
Q

What is the composition of bone?

A

Osteoid (type I collagen)
Mineralised
Cells - osteoblasts/clasts, osteocytes

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4
Q

What are the genetic/congenital/developmental diseases of bone?

A

Osteogenesis imperfecta
Cleidocranial dysplasia
Osteopetrosis
Achondroplasia
Cherubism
Gardner’s syndrome
Fibrous dysplasia

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5
Q

What does osteogenesis imperfecta affect?

A

Type I collagen genes

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6
Q

What are the common types of osteogenesis imperfecta?

A
  • I. Common, mildest. AD. Bone fragility, blue-grey sclera, deafness, can be associated w/ Dentinogenesis Imperfecta
  • II. Multiple fractures in utero, fatal, AD
  • III. Rarest, progressing bone deformity, DI
  • IV. Dominant, white sclera. Otherwise as type I. Can be associated w/ Dentinogenesis Imperfecta
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7
Q

What is the clinical presentation of osteogenesis imperfecta?

A

Ligament laxity, deafness (ear ossicle deformation), short stature, blood vessel fragility, thin aortical wall and heart valves

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8
Q

What is the pathogenesis of osteogenesis imperfecta?

A

AA substitution in triple helix (glycine)

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9
Q

What does dentinogenesis imperfecta cause?

A

Normal contour
Opalescent amber-like
Attrition
Short roots/obliterated canals
Dec tubules/atubular

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10
Q

How does cleidocranial dysplasia present?

A

Aplasia of the clavicles
Delayed ossification of fontanelles
Prognatism, hypertelorism, short stature, anomalies in teeth number

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11
Q

What gene is affected in cleidocranial dysplasia?

A

RUNX2 gene - bone and cartilage development

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12
Q

What are the symptoms of osteopetrosis?

A

Frequent fractures in long bones which can fail to heal
Nerve compression pain - headaches, blindness, deafness
Haematological - anaemia, thrombocytopaenia, leukopenia, enlarged spleen, bleeding, stroke

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13
Q

What is the pathogenesis of osteopetrosis?

A

Mutations in CLCN7 - gene defect in osteoclastic function failed remodelling

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14
Q

What are the dental findings in osteopetrosis?

A

Delayed eruption, osteomyelitis (avascular necrosis) after extractions, root and bone fractures, unusual dentition including malformed short roots and unerupted teeth

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15
Q

What radiographical findings are there for osteopetrosis?

A

Abnormally dense bones, chalky white appearance, reduced marrow spaces

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16
Q

What is achondroplasia?

A

Dwarfism

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17
Q

What is the pathogenesis of achrondroplasia?

A

Mutated fibroblast growth factor receptor 3 gene leading to abnormal cartilage formation –> affects endochrondral ossification of bones

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18
Q

What are the symptoms of achondroplasia?

A

Normal sized drunk and head, protuberant abdomen
Short limbs, retrusive middle third of face (lack of development of base of skull)
Severe malocclusions

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19
Q

How does cherubism present?

A

‘Chubby’ face, rim of sclera visible under iris

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20
Q

How does cherubism change with age?

A

Normal at birth
2-4: painless symmetrical swelling of mandible and sometimes maxilla
7: lesions become statis or regress
Puberty onwards: improvement but cosmetic surgery sometimes necessary

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21
Q

What is seen on a radiograph of a pt with cherubism?

A

Multiocular radiolucencies, cortical thinning/perforation

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22
Q

What is histology of cherubism?

A

Cellular and vascular fibrous tissue + giant cells in focal collections, haemosiderin, metaplastic bone

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23
Q

What are the dental manifestations of cherubism?

A

Premature loss of deciduous teeth, displacement, abnormal unerupted permanent teeth.

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24
Q

What is the main manifestation of Gardener’s syndrome?

A

Multiple polyposis of the large intestine

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25
What are the osseous anomalies in Gardener's syndrome?
Osteoma of the bones Dense bone islands of jaw bones Hazy sclerosis of jaw bones
26
What are the dental anomalies in Gardener's syndrome?
Odontomes Supernumerary teeth Impacted teeth
27
What type of lesion is fibrous dysplasia?
A fibro-osseous lesion
28
What is the pathology of fibrous dysplasia?
Somatic mutation of GSA gene, the G protein that regulated cAMP formation Overproduction of cAMP causes errors in regulating proliferation and differentiation of OBs and OCs
29
What are the 3 clinical types of fibrous dysplasia?
Monostotic Polyostotic McCune-Albright syndrome
30
What happens in McCune-Albright syndrome?
Polyostotic fibrous dysplasia, Endocryne abnormalities, Precocious puberty, increased pituitary hormones, large hands & feet, Cushing syndrome, thyroidal cysts, Cafe au lait spots in skin
31
What are the radiographical findings in fibrous dysplasia?
Radiolucent/mottled to opaque (depending on metaplastic bone formed) Typical 'orange peel' or 'ground glass' effect Expansile mass
32
What is histology of fibrous dysplasia?
Bone is replaced by cellular rich or collagenous fibrous tissue Metaplastic bone (woven or osteoid) arranged in irregular trabeculae Chinese characters
33
Is fibrous dysplasia radiosensitive?
No, so can turn into sarcoma if irradiated
34
When should surgery occur for fibrous dysplasia and why?
After growth phase, because lesions tend to expand during skeletal growth and then stop.
35
What are the inflammatory conditions of bone?
Alveolar osteitis Osteomyelitis Chronic periostitis with hyaline bodies
36
What is osteitis?
Localised inflammation without spread through marrow spaces
37
What are the 2 types of osteitis?
Alveolar osteitis Focal sclerosing osteitis
38
What is osteomyelitis?
More extensive inflammation with spread through marrow spaces
39
What is periostitis?
Inflammation of the periosteum May or may not be associated with osteomyelitis
40
What is alveolar osteitis more commonly known as?
Dry socket
41
How does alveolar osteitis occur?
Failure of blood clot formation Premature loss/disintegration of the blood clot The empty socket retains food debris and becomes infected Dead bone separated by osteoclasts (sequestra formation) Localised inflammation, slow healing, granulation tissue
42
What things can cause failure of the blood clot?
Poor blood supply: osteopetrosis, Paget's, radiotherapy, vasoconstrictors
43
What things can cause premature loss/disintegration of the blood clot?
Mouthwashes, proteolytic bacteria
44
What are the clinical features of dry socket?
Pain some days after extraction, foul taste and smell, denuded bone might become visible
45
What is Tx for alveolar osteitis?
Irrigate CHX Might require sequestrum removal Dressing with Alvogyl or similar
46
How does a normal socket heal?
Socket fills with blood Organisation - granulation tissue OC resorption of crestal alveolar bone Gingival epithelial migration across defect OB's after 10-14 days - granulation tissue - 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, decrease in height of alveolar bone.
47
When does focal sclerosing osteitis occur?
A sequelae of periapical inflammation - condensing osteitis
48
What is focal sclerosing osteitis?
A local response to a mild irritation, infection, or high tissue resistance. Body reacts by forming more bone around it. Must undergo RCT to remove even mild irritation.
49
How does focal sclerosing osteitis present on a radiograph?
Dense area at apex, but not attached to the tooth (asymptomatic so on routine x-ray finding)
50
What is the histology of focal sclerosing osteitis?
Increase in number and thickness of bone trabeculae, some lymphocytes and plasma cells and fibrous marrow tissue
51
What are the types of osteomyelitis?
Suppurative (acute or chronic) Sclerosing (chronic osteomyelitis with proliferative periostitis or diffuse sclerosing) Special types (radiation osteomyelitis)
52
What is the cause of suppurative osteomylitis?
Polymicrobial - dental abscess, fracture, penetrating wounds, extractions that havent healed well
53
How does suppurative osteomyelitis occur from the microorganisms?
Microorganisms proliferate in marrow spaces --> acute inflammation --> tissue necrosis --> suppuration Forms a sequestrum surrounded by pus and involucrum
54
What is a sequestrum and involucrum?
Sequestrum = mass of necrotic bone Involucrum = layer of new bone outside original/subperiosteal surrounding the infection
55
Is suppurative osteomyelitis more common in the mandible or maxilla and why?
Mandible due to better blood supply
56
How does suppurative osteomyelitis present clinically?
Pain, swelling, pyrexia, trismus, tooth mobility, intra- and extra-oral sinus formation
57
What is the histology of suppurative osteomyelitis?
Necrotic bone surrounded by inflammatory cells/pus
58
What is diffuse sclerosing osteomyelitis? (controversial)
Proliferative reaction due to low-grade infection
59
What is chronic osteomyelitis with proliferative periostitis (Garre's osteomyelitis)
Low grade apical inflammation reaching cortical bone
60
Where does Chronic osteomyelitis with proliferative periostitis (Garre’s osteomyelitis) occur?
Mandible of children/young adults
61
What does chronic osteomyelitis with proliferative periostitis (Garre’s osteomyelitis) cause?
Periosteal osteonecrosis (hard bone swelling on outer mandible surface) Seen as smooth subperiosteal overgrowth in occlusal radiographs
62
What is the histology of chronic osteomyelitis with proliferative periostitis (Garre’s osteomyelitis)?
Irregular trabeculae (woven bone), chronic inflammatory cells and fibrous marrow
63
What is chronic periostitis associated with hyaline bodies (pulse granuloma)?
Foreign body reaction with hyaline 'ring shaped' material and fibrous thickening of periosteum or pus
64
What possible foreign bodies could cause chronic periostitis associated with hyaline bodies?
Vegetable material (pulses) implanted through the tooth socket, root canal, surgical flap, traumatic ulceration etc.
65
What are the physical/chemical diseases of the facial bones?
Solitary bone cyst Osteoradionecrosis Phosphorus necrosis
66
What is phosphorus necrosis?
White phosphorus converts to bisphosphonates causing BRONJ. Epidemic in 1858.
67
What does radiation do?
Kills cells that proliferation, breaking chromosomes and distorting spindle formation so they die, eg thin skin, epithelium since skin proliferates lots
68
How does radiation obliterate blood vessel lumens?
Radiation induces proliferation of blood vessels intima causing endarteritis obliterans.
69
What does endarteritis obliterans cause?
Reduction in blood supply, thrombosis, especially in the mandible
70
What does post-radiotherapy leave patients susceptible to?
Tooth and perio infections Denture trauma ONJ
71
What should you do to prevent radiation ONJ?
Leave only sound teeth, removing others at least 2 weeks before treatment.

Oral pathology (27 decks)

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