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Y3- I & W > pathology bone disorders > Flashcards

pathology bone disorders Flashcards

1
Q

what is bone

A

it is a rigid inflexible mineralised connective tissue

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2
Q

what is the ECM of bone mineralised by

A

ca/PO salts

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3
Q

why do we need bone

A

structural purposes

metabolic

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4
Q

what structural purposes do we need bone for

A

physical integrity
protection of squishy organs
insertion of muscles and tendons

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5
Q

what is haematopoiesis

A

The formation development and maturation of blood cells

Happens in the bone marrow (majority) and the liver for adults

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6
Q

where does haematopoesis occur in embryos

A

the yolk sac

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7
Q

what is bone made from

A

one is the non cellular mineralised matriculates

cellular component

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8
Q

what composes the non cellular mineralised material

A

type 1 collagen
calcium hydroxyapatite crystals
regulatory proteins and Growth factors

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9
Q

what is type 1 collagen called int he context of bone

A

osteoid

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10
Q

what is the cellular component of bone

A

osteoblasts
osteocytes
osteoclasts
stem cells which give rise to the osteoblasts

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11
Q

what do osteoblasts do

A

they form the bone matrix
mesenchymal in origin
secretory function and secrete the osteoid
involved in mineralisation

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12
Q

what do osteocytes do

A

entrapped osteoblasts which are inactive

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13
Q

what do osteoclasts do

A

from the macrophage lineage

sit at the surface of the bone and take place in bone resorption

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14
Q

how can we group different types of bone

A

by maturity

by location

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15
Q

what are the different types of bone which vary by maturity

A

woven bone

lamellar bone

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16
Q

describe woven bone

A

immature bone where the bone is laid down very quickly by osteoblasts
later remodelled to lamellar bone
more chance of fracturing

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17
Q

describe lamellar bone

A

bone is laid down in parallel bands

normal healthy bone

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18
Q

what are the 2 types of lamellar bone

A

compact bone

cancellous/trebecular bone

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19
Q

which type of bone is most immature

A

woven bone

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20
Q

what are the different types of bone which vary by location

A

cortical

cancellous

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21
Q

describe the bone remodelling cycle

A 
activation 
resorptions 
reversal 
formation
termination
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22
Q

what happens in the activation stage of bone remodelling

A

we need hormones or damage to activate the osteoblasts
OBs secrete cytokines
osteoclasts start to secret substances that break down the bone

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23
Q

what happens in the resorptions phase of bone remodelling

A

macrophage lineage osteoclasts secrete substances that resorp the bone
the the osteoclasts migrate

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24
Q

what happens in the removal phase of bone remodelling

A

monocytes clear debris for the bone formation

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25
Q

what happens in the formation phase of bone remodelling

A

the osteoblasts are recruited
they secrete a new matrix which is mineralised
OBs now sit on new bone and some incorporated as osteocytes

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26
Q

what is osteoarthritis

A

progressive erosion of articular cartilage

it is not just erosion but a complex impbalance of damage and repair

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27
Q

what can we see in osteoarthritis

A

the underlying bone becoming exposed and then leading to cysts and pain

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28
Q

what is the common symptom of osteoarthritis

A

joint space narrowing
Pain and functional limitation
Morning stiffness

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29
Q

what are the common signs of osteoarthritis

A

Crepitus( crunching)
Restricted movements
Bony enlargement
Instability

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30
Q

what are the primary causes of osteoarthritis

A

unknown causes

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31
Q

what is the secondary causes of osteoarthritis

A

pre existing joint disease eg RA, gout
metabolic disease eg acromegaly
systemic disease eg haemophilia

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32
Q

what are the investigations we can do for osteoarthritis

A

blood tests
erythrocyte sedimentation rate
CRP- c reactive protein
rheumatoid factor is NEGATIVE

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33
Q

what is the management of osteoarthritis

A

hydrotherapy, weight loss
NSAIDS
joint replacement

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34
Q

describe RA

A

It is an autoimmune disease

resulting in inflammation of the synovialm of the joints but can be systemic and affect the lungs

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35
Q

risk factors for RA

A

women more likely
strong association with the HLA antigen
assoc with epstein barr virus
can also occur due to contribution of the oral microbiome

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36
Q

how does RA cause damage in the body

A

occurs from a process called citrullination of self antigens- changes in self antigens and they are recognised as abnormal and the immune system attacks them

37
Q

what happens to the synovial cavity

A

becomes hyper cellular which leads to inflammation and damage

38
Q

what is pannus formations

A

inflammatory infiltrate forming a mass in the tissues

39
Q

what are some systemic manifestations of RA

A

carpal tunnel syndrome
pericarditis
lymphadenopathy
sjogrens syndrome

40
Q

investigations for RA

A

CRP
anti citrullinated peptide antibodies
rheumatoid factor +

41
Q

management for RA

A

no cure
NSAIDS
disease modifying anti rheumatic drugs

42
Q

what is ankylosis

A

abnormal stiffening in joints due to bony fusion

43
Q

describe pagets disease

A

It Is a disorder of bone turnover/remodelling
There is increased osteoclastic bone resorption and increase of new bone formation
Increased formation > resorption but it is woven bone

44
Q

what is the aetiology of pagets disease

A

unknown
but
can be viral/microbial
genetic history

45
Q

symptoms of pagets disease

A

bone and joint pain
cotton wool skull appearance
hypercementosis
high alkaline + phosphate levels

46
Q

what are the phases of pagets disease

A

hot
mixed
cold

47
Q

what is the hot phase of pagets disease

A

high osteoclast activity

48
Q

what is the mixed phase of pagets disease

A

There is a little bit of osteoblast activity as well as osteoclast activity

49
Q

what is the cold phase of pagets disease

A

inactive burn out phase

50
Q

treatment for pagets disease and osteoporosis

A

bisphosphonates

51
Q

what do bisphosphonates do

A

inhibit osteoclast activity and recruitment

52
Q

what is the issue with bisphosphonates

A

need to be careful of BRONJ bisphosphonate related osteonecrosis of the jaw

53
Q

describe osteomyelitis

A

→ It is inflammation of the bone or bone marrow

→ Usually always due to infection

54
Q

how can we get osteomyelitis

A

through blood stream
extension from the adj site
direct implantation of the organisms

55
Q

what bacterium is the most common cause of osteomyelitis

A

S aureus

56
Q

what is the clinical presentation of osteomyelitis

A

○ Fever
○ Localised bone pain
○ Overlying tenderness/erythema
○ Hard to diagnose so we can use a bone biopsy

57
Q

treatment of osteomyelitis

A

immobilise
antibiotics
maybe drainage

58
Q

why might we get osteomyelitis of the jae

A

Polymicrobial

Odontogenic infection

59
Q

why might people get tuberculous osteomyelitis

A

Haematogenous spread from reactivated primary TB focus

60
Q

what are the subtypes of osteomyelitis

A

focal sclerosis
diffuse scleorising
proliferative periostitis

61
Q

what are the types of fracture

A 
simple 
compound
comminuted 
displaced 
stress 
greenstick 
pathologic
62
Q

what is the phases of fracture healing

A
  1. inflammatory phase
  2. reparative phase
  3. remodelling phase
63
Q

what happens in the inflammatory phase

A

1st week
Haematoma forms- source of hemopoietic cells and growth factor
Macrophages, neutrophils and platelets release Cytokines
Fibroblasts come to the fracture site
Granulation tissue forms around the fracture ends
Neovascularisation
Osteoblasts, chondrocytes( lay down cartilage) and fibroblasts leading to callus forming

64
Q

what happens in the endochondral phase

A

Cartilage provides provisional stabilisation

Endochondral ossification converts soft callus to hard callus woven bone

65
Q

what happens in the remodelling phase

A

The hard woven bone is remodelled into lamellar bone

66
Q

describe osteonecrosis

A

infarction of the bone marrow

67
Q

why does osteonecrosis occur

A

due to
alcohol
steroids
fracture

68
Q

what is the underlying cause of osteonecrosis

A

vascular insufficiency due to mechanical injury to the blood vessel eg thromboembolism

69
Q

presentations of osteonecrosis

A

→ Joint pain shoulder or hip
→ Can be asymptomatic–> collapse of articular bone
MRI shows bone marrow oedema

70
Q

management of osteonecrosis

A

→ Symptomatic
→ Surgical decompression
→ Grafts
joint replacement

71
Q

what happens if we have a drop in the calcium serum levels

A

PT glands to secrete PTH which increases calcium by
→ Increased osteoclast bone resorption
→ Increased calcium intestinal absorption
→ Increased synthesis of 1.25- dihydroxy vitamin D3
→ Increased renal tubular resorption Ca
→ Increased renal excretion PO4

72
Q

what happens when we have low calcium levels

A

bone resorption increases

73
Q

what is the other name for rickets

A

osteomalacia

74
Q

describe osteomalacia

A

The osteoid has not been mineralised and therefore defective mineralisation of the epiphyseal plate in children leading to weakened bones

75
Q

what is rickets

A

osteomalacia in children

76
Q

what is the aetiology of rickets

A

Aetiology is anything that interferes with bone mineralisation
Eg deficient intake or absorption of vitamin D( nutritional, malabsorption
Renal failure
Inhibitors of mineralisation
Defective vitamin D receptors

77
Q

what are the dental complications of vitamin D deficiency

A 
Familial hypophosphatemia 
Large pulp chamber 
Thin enamel 
Dentinal defects which is globular 
Prone to abscesses
78
Q

what is hyperparathyroidism

A

Anything pathological which causes increase in PTH

79
Q

what does an increase of PTH do

A 
→ Osteoclast bone resorption 
→ Intestinal Ca absorption 
→ synthesis of 1.25- dihydroxy vitamin D3 
→  renal tubular resorption Ca 
→  renal excretion PO4
80
Q

what are the different types of hyperthyroidism

A

primary hyperthyroidism
secondary
tertiary hyperthyroidism

81
Q

what is the most common cause of asymptomatic hypercalcaemia

A

primary hyperthyroidism

caused by adenoma, hyperplasia, malignancy

82
Q

what are the symptoms of hyperthyroidism

A

bones, stones, groans and moans
Bones- disease and pain
Stones- renal stones
Groans- GI groans including constipation nausea, gallstones and pancreatitis
Moans- CNS alterations, depression, lethargy

83
Q

describe osteogenesis imperfecta

A

brittle bone disease

84
Q

what are the gene mutations for osteogenesis imperfecta

A

COL1A1

COL1A2

85
Q

dental manifestations of osteogenesis imperfecta

A

Dentinogenesis imperfecta type II
In OI type IB
Blue discoloured teeth

86
Q

what is endochondral ossification

A

Cartilage is used as a template and is replaced by bone

87
Q

what is intramembranous ossification

A

In the skull, maxilla and mandible they are formed by the deposition of bone within primitive mesenchymal tissue

88
Q

what are the craniofacial issues with bone growth and achondroplasia

A 
→ Macrocephaly 
→ Flattened nasal bridge 
→ Hypoplasia of midfacial structures 
→ Maxillary hypoplasia 
→ Relative overgrowth of the mandible 
→ Narrowing of anterior plate 
Orthodontic intervention

Y3- I & W (21 decks)

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