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4th yr- CMS- Bones, Skeleton and trauma > Bone, none disorders and arthritis > Flashcards

Bone, none disorders and arthritis Flashcards

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Introductory Sommelier Exam (CMS) flashcards
1
Q

What is bone

A

A form of specialised connective tissue with a calcified extracellular matrix

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2
Q

Describe the composition of bone

A

Mainly inorganic ions deposited in an organic proteinaecous matrix

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3
Q

Name the different cells that make up bone

A
  1. Osteocytes
  2. Osteoclasts
  3. Osteoprogenitor
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4
Q

What do osteoblasts do

A

They produce new bone by secreting collagen matrix AND calcium salts

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5
Q

What is the collagen matrix also referred to as

A

Osteoid

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6
Q

What happens to the osteoblasts as new bone is laid down

A

Osteoblasts get trapped in their own lacunae and their structure and functions change into that of osteocytes

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7
Q

What is the new layer of bone formed called

A

Lamellar bone

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8
Q

Where are osteoprogenitor cells found

A

Inside the bone marrow

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9
Q

What do osteoprogenitor cells do

A

They are where osteoblasts and osteocytes come from

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10
Q

Why are osteoprogenitor cells so important

A

As osteoblasts and osteocytes can’t divide do new one needs to come from stem cells

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11
Q

What is the turnover rate for healthy bone

A

10%

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12
Q

What do osteoclasts do

A

They are responsible fro bone resorption

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13
Q

Describe osteoclasts

A

Large, multinucleate cells

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14
Q

How do osteoclasts resorb bone

A

they secrete hydrochloric acid and proteolytic enzymes which metabolise bone

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15
Q

Where are osteoclasts derived from

A

White blood cell lineage mostly monocytes and macrophages

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16
Q

What are osteocytes formed from

A

Trapped osteoblasts

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17
Q

Why are osteocytes important

A

They secrete enzymes into the matrix to help maintain mature bone

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18
Q

How is the balance of bone secretion and absorption managed

A

Chemical messengers such as hormones

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19
Q

Which hormones are associated with bone resorption

A
  1. Vitamin D
  2. Parathyroid hormone
  3. Thyroid hormone
  4. Growth hormone
  5. High levels of circulatory calcium ions
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20
Q

Which hormones are associated with bone formation

A
  1. Oestrogen
  2. Calcitonin
  3. Androgens
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21
Q

What is the very first type of bone laid down referred to as

A

Woven or immature bone

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22
Q

What does woven (immature) bone get remodelled into

A

Secondary bone

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23
Q

What is secondary bone divided into

A
  1. Cortical or lamellar bone

2. Cancellous or trabecular bone (spongy bone)

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24
Q

What percentage of secondary bone is made up of cortical (lamellar) bone

A

80%

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25
Q

What percentage of secondary bone is made up of Cancellous or trabecular bone (spongy bone)

A

20%

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26
Q

What is cortical (lamellar) bone made up of

A

Concentric layers o bone

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27
Q

Describe cortical (lamellar) bone

A

Dense and compact

Has a central bone marrow

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28
Q

Where is cortical (lamellar) bone found

A

In long bones

It is the outermost layer or codec of many bones of the skeleton

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29
Q

Describe the appearance of Cancellous or trabecular bone (spongy bone)

A

appearance of a sponge

The voids are islands of marrow and the main structure is low density sheets of bone

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30
Q

How is lamellar bone arranged

A

In the Haversian canal system

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31
Q

What is another term for vitamin D

A

calcitriol

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32
Q

What is vitamin D a key component of

A

Bone metabolism

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33
Q

What does vitamin D do

A

Its presence increases the amount of calcium and phosphate circulating in the body

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34
Q

What is vitamin D synthesised from

A

Cholesterol in the skin upon exposure to sunlight (UVB)
OR
Obtained from the diet in o

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35
Q

What in your diet can contain vitamin D

A
  1. Oily fish
  2. Red meat
  3. Liver
  4. Egg yolk
  5. Fortified cereals
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36
Q

How is vitamin D metabolised

A

first by the liver then by the kidney to the metabolically active 1,25- dihydroxycholecalciferol

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37
Q

What action does vitamin D carry out

A

Increases the amount of free calcium in the circulation

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38
Q

How does vitamin D increased the amount of free calcium in the circulation

A

promotes uptake in the small intestines and postman osteoclastic activity to release calcium from the skeleton

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39
Q

What effect on bone will their be if there is a vitamin D deficiency

A

There will be a failure of osteoid to mineralise

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40
Q

What can vitamin D deficiency in children lead to

A

Rickets

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41
Q

What does childhood rickets cause

A

Bowing of the long bones

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42
Q

What can vitamin D deficiency in adults lead to

A

Osteomalacia

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43
Q

What does osteomalacia cause

A

Softening of the bone

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44
Q

How does osteomalacia present

A

With vague bone pains and aches
OR
Pathological fractures

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45
Q

What are pathological fractures

A

Break in the bone as a result of an underlying disease process not due to accident

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46
Q

What is found on the posterior surface of the thyroid

A

A oval shaped glans which contains 4 parathyroid glands

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47
Q

What do the parathyroid glands secrete

A

Parathyroid hormone

48
Q

What does the parathyroid hormone do

A

Acts to raise the circulation concentration of calcium in the blood

49
Q

How does the parathyroid hormone raise calcium circulation

A

Promotes the kidneys to make vitamin D and resorbs calcium in the renal tubules to minimise loss in the urine

50
Q

Other than calcium what else does the parathyroid hormone effect and how

A

Encourages lOSS of phosphate

51
Q

What can happen if phosphate concentration in the blood is too high

A

Can lead to pathological bone resorption

52
Q

What can a person with malfunctioning parathyroid gland have

A
  1. Primary hyperthyroidism

2. Secondary hyperparathyroidism

53
Q

What is primary hyperthyroidism due to

A

Often due to adenoma of one of the parathyroid glands

54
Q

What happens in patients with primary hyperthyroidism

A
  1. Increase in parathyroid hormone levels
  2. Hypercalcaemia results
  3. Bone resorptive state is promoted
55
Q

In whom is secondary hyperthyroidism seen in

A

In patients with chronic renal disease

56
Q

Why do some patients with chronic renal disease develop secondary hyperthyroidism

A

They have an inappropriate calciuria and to compensate the parathyroid glands secrete more parathyroid hormone

57
Q

What can happen in secondary hyperthyroidism

A
  1. Increased resorption of bone

2. Renal osteodystrophy

58
Q

What is renal osteodystrophy

A

Failure of the kidneys to maintain calcium and phosphate levels and decline in kidney function

59
Q

How can hyperparathyroidism present in the jaw

A

As a central giant cell granuloma

60
Q

If you find a patient has a central giant cell granuloma in their jaw what should do

A

Refer them to have bone profile blood s to confirm diagnosis

61
Q

Name the different stages of bone healing following fracture

A
  1. Early inflammatory stage
  2. Repair stage
  3. Remodelling stage
62
Q

What happens in the early inflammatory stage of bone healing

A
  1. Bleeding occurs at the fracture sire with formation of a haemotoma
  2. Inflammatory cells and fibroblasts infiltrate the clot
  3. Blood vessel ingress into the haemotoma and granulation tissue forms
63
Q

what can delay fracture healing in the early inflammatory stage

A

If the fracture site is not adequately immobilised during this period

64
Q

Name some inflammatory meditar present in the early inflammatory stage of bone healing

A
  1. PDGF
  2. TNF- alpha
  3. TGF- beta
  4. IL- 1, 6, 10, 12
65
Q

When does the early inflammatory stage of bone healing occur

A

in the first 2 weeks post fracture

66
Q

What happens in the repair stage of bone healing

A
  1. The granulation tissue turns to callus
  2. Primary callus turns into secondary callus
  3. Osteoid is secreted it not eh area forming new weak bone
  4. Proteases degrade the extra cellular matrix
  5. cartilaginous calcification takes place
  6. Collagen fibres ingress into the area
  7. Formal new woven bone is created at fracture site
67
Q

Name the process that turns primary callus into secondary callus

A

endochondral ossification

68
Q

What can happen if the fracture site is not adequately immobilised during the repair stage of bone healing

A

A fibrous union may form in place of the solid bone formation

69
Q

How long does the repair stage take

A

Typically 4 weeks in adults but much less in children

70
Q

What does the remodellignstage allow fro

A

Redistribution of the proportion of compact and woven bone

71
Q

What co ordinate the remodelling phase

A

Organised osteoblastic and osteoclastic activity

72
Q

How long does the remodelling stage last

A

Many weeks of months

73
Q

What factors can impact fracture healing

A
  1. Blood supply to the fracture site
  2. Infections
  3. underlying bone pathologies
  4. Whether fracture is closed or compound
  5. Degree of tissue loss
  6. Comorbid conditions eg diabetes
  7. Use of NSAIDs
  8. Tobacco smoking and high alcohol intake
  9. Nutritional status of patient
  10. Risk of further falls
74
Q

Name some specific bone disease we should be aware of

A
  1. Osteogenesis imperfecta
  2. Osteopetrosis
  3. Osteopenia
  4. Osteoporosis
  5. Paget’s disease
  6. Osteoarthritis
  7. Rheumatoid arthritis
  8. Ankylosing spondylitis
75
Q

What is osteogenesis imperfecta

A

A collection of familial inherited defects of collagen

76
Q

What does osteogenesis imperfecta result in

A

Failure of normal biomineralisation of bone

77
Q

In dentistry we should be aware of osteogenesis imperfecta caused by what?

A

Type 1 collagen mutation

78
Q

What happens in osteogenesis imperfecta caused by type 1 collagen mutations

A

Can result in partial or complete absence of collagen giving a varying clinical phenotype

79
Q

What can patients with osteogenesis imperfecta caused by type 1 collagen mutations have an increased number

A

Patients sustain multiple fractures due to low impact trues as their bones are more brittle and easy to break

80
Q

What is osteogenesis imperfecta also referred to as

A

Brittle bone disease

81
Q

What can patients with osteogenesis imperfecta caused by type 1 collagen mutations present with

A
  1. Grey blue discolouration to the sclera
  2. Shortened or bowed long bone shapes
  3. hyper mobility of joints
  4. Varying degree of bone pain
  5. Deafness
  6. dentinogenesis imperfecta
82
Q

What are the oral features of osteogenesis imperfecta

A
  1. Skeletal class iii abnormality
  2. Anterior open bite
  3. Impacted first or seconds permanent molar teeth
  4. Thin greyish brown enamel
  5. Defective or premature eruption
  6. Defective dentinal development or opalescent dentine
83
Q

When does osteopetrosis occur

A

Where osteoclasts fail to resorb bone leading to increased bone formation

84
Q

Describe bones affected by osteopetrosis

A

They are harder, more marble like and have less ability to flex and elastically recoil

85
Q

How do bones affected by osteopetrosis look on radiograph

A

Denser so more opaque

86
Q

What can happen as a result of increased inorganic component in bone affected by osteopetrosis

A

Can lead to haematopoietic insufficiency by the bone marrow effectively being walled off by the pathologically thicker bone

87
Q

What can patients with osteopetrosis come in with

A
  1. Delayed tooth eruption
  2. Growth imaprimetns
  3. Nerve entrapment syndrome
88
Q

What is Osteopenia

A

Where bones have thinned to a mild degree (may not result in pathological fracture)

89
Q

How are patients with Osteopenia diagnosed

A

DEXA scan

90
Q

What does a DEXA scan of a patient with Osteopenia show

A

A T score between -1 and -2.5

91
Q

What does a T score of less than -2.5 indicate

A

Osteoporosis

92
Q

What does DEXA stand for

A

Dual Energy X-ray Absorptiometry

93
Q

What does a DEXA score measure

A

How dense your bones are in comparison to the average healthy adult of 30 years of age

94
Q

What happens to bone density as we get older

A

Bone density declines

95
Q

How many people are affected by Osteoporosis

A

3 MILLION in the uK

96
Q

Name the most common fractures caused by Osteoporosis

A
  1. Neck of femur (NOF)
  2. Wrist (Colles fracture)
  3. Vertebral bodies (compression or wedge fractures)
97
Q

What is a fragility fracture

A

One occurring due to a fall from standing height or less

98
Q

List some lifestyle factors that can accelerate bone loss

A
  1. High caffeine intake
  2. High salt intake
  3. Low BMI
  4. High levels of alcohol consumption
  5. Smoking tobacco
  6. Long period of prolonged immobility
99
Q

What can we eat to help prevent bone loss

A
  1. Increased calcium
  2. Dairy
  3. Vitamins and minerals
  4. Tofu
  5. Nuts
  6. Whole fish
100
Q

List some genetic factors that can accelerate bone loss

A
  1. Female gender (due to menopause)

2. Family history of osteoporosis

101
Q

List some endocrine factors that can accelerate bone loss

A
  1. Early menopause
  2. Oophrectomy
  3. Postmenopausal hormonal changes
  4. Amenorrhoea (Loss of period for extended period of time)
102
Q

List some diseases that can accelerate bone loss

A
  1. Cushings syndrome
  2. Hyperthyroidism
  3. Hyperparathyroidism
103
Q

List some DRUGS that can accelerate bone loss

A
  1. Glucocorticoids (aka corticosteroids)
  2. Thyroxine
  3. Heparin
  4. Diuretics e.g. furosemide
  5. Cytotoxic drugs
104
Q

How do we manage a patent with osteoporosis

A
  1. Patent education and lifestyle modifications
  2. Pain relief
  3. Physiotherapy
  4. Occupational therapy
  5. Physical aids eg walking stick
  6. Medication to prevent further loss of bone mass
  7. Active fall prevention
  8. Surgery
105
Q

What medications can be prescribed to prevent further loss of bone

A
  1. Vitamin D or calcium supplements
  2. Bisphosphonates
  3. Selective Oestrogen receptor modulators (SERMs)
  4. Parathyroid replacement Treatment
  5. Hormone replacement therapy (HRT)
  6. Testosterone Treatment
106
Q

What happens in Pagets disease

A

Increased resorption by overactive osteoclasts leading to overactivity and destruction of bone

107
Q

How does the body try to counteract the increased resorption by osteoclasts in pagets disease

A

Osteoblasts come highly active however the bone they secrete is larger and weaker than healthy bone

108
Q

What can happen to bone in pagets disease

A

Bone becomes weakened, tends to deform and fracture in some cases

109
Q

Name some of the commonly affected sites in pagets disease

A

Pelvis and spine

110
Q

What does pagets disease lead to

A

Constant dull bone pain

Sometimes cranial nerve deficits

111
Q

What are the oral presentations of pagets disease

A
  1. Enlargement of the maxillae/ mandible

2. Hypercementosis which can make dental extraction more difficult

112
Q

How can we treat pagets disease

A
  1. Bisphosphonates to regulate abnormal bone turnover
  2. Analgesia
  3. Physiotherapy
  4. Surgery
113
Q

What is osteoarthritis

A

A wear and tear degeneration of the joints accompanied with low levels of chronic inflammation of the joints

114
Q

Which sites are most affected by osteoarthritis

A

Affects large weight bearing joints eg the hip and knee

115
Q

What does primary osteoarthritis result in

A
  1. Synovial softening
  2. Tearing of articular cartilage
  3. Development of subchondral bone cysts
  4. Development of bony spurs or osteophytes in the joints
116
Q

What does secondary osteoarthritis occur following

A

Following trauma

117
Q

How do we manage osteoarthritis

A
  1. patent education and self management programmes
  2. Weight loss fro obese patients
  3. Physiotherapy and occupational therapy plus any required walking aides
  4. Analgesia
  5. Intra articular corticosteroid injections f
  6. Intramuscular corticosteroids infections
  7. Supplements with glucosamine and/or chondroitin sulphate
  8. Surgery

4th yr- CMS- Bones, Skeleton and trauma (3 decks)

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