Bone and Joints 1 Flashcards

1
Q

What are the bone types?

A

Types depending on maturity of bone:
1. Woven bone:
Immature bone as the osteoid collagen is irregular, random & not organised due to It’s laid down quickly and early in sites that need rapid bone production or turnover. But over time, it can be remodelled into lamellar bone (organised & mature)

  1. Lamellar bone (L):
    Mature bone as the osteiod collagen is organised in Parallel bands (sheets “lamellae”) due to it’s laid down normally in normal healthy adults.

Types depending on location of bone:
1. Compact “Cortical”:
Concentric rings that are highly organised and is laid down in the hard outer layer of flat and long bones, maintaining the shape of bone and withstand the strain of pressure. And it has Haversian system that is formed by osteons

  1. Cancellous “Trabecular”:
    Spongy & Non-structural “filler” that is laid down in the middle regions “inside” flat bones and at the end region of long bones, containing the bone marrow and inter-connected network of rods and plates of bones, being one of the main sites of turnover of mineral homeostasis and helping in the resistance of compressive loads
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2
Q

What Collagen and Minerals found in bones?

A
  1. Type 1 collagen (Osteoid): Protein forms the parallel lamella of different densities
  2. Non-collagen proteins (Osteo-pontin and Osteo-calcin)

Bone minerals (Calcium phosphate ‘Calcium hydroxyapatite’)

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3
Q

Why is collagen mineralisation critical/important?

A

If the osteoid (collagen) is not mineralised, it would be soft and “bendy”, leading to bone disorders

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4
Q

Identify Bone cells and their functions:

A

1) Osteoblast (Ob):
Mesenchymal-origin cell (By osteogenic stem cell to produce new Ob) that has many functions:

  • Secretory function (secretes collagen “Osteoid”)
  • Mineralisation function and regulation (the mineralisation of the secreted osteiod), forming the bone matrix, building up the bone
  • Bone resorption regulation as Ob are rich in AOB (Active Ob)
  • Express receptors for (Parathyroid hormone “PTH”, oestrogen, glucocorticoids, vitamin D, inflammatory cytokines and TGF beta) which influence bone modelling

2) Osteoclast (O):
Macrophage lineage (macrophagic-origin) that has Bone resorption & remodelling function, removing the bone

3) Osteocyte (Oc):
Inactive osteoblast (Ob- derivatives) which activate bone formation and has a role in bone resorption. They are entrapped inside the bone after the secretion & mineralisation of osteiod

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5
Q

Once new bone is formed, what will happen to Osteoblasts?

A

Most of Ob either die off (apoptosis) or incorporated within the new bone as Osteocytes (Entrapped and inactive Obs)

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6
Q

How does blood Ca level affect on the activity of Parathyroid hormone?

A

Decreased Ca in blood will stimulate parathyroid gland to secrete PTH (increased), leading to:

1) ↑ Osteoclast bone resorption (taking Ca from bone)

2) ↑ Synthesis of 1,25- dihydroxyvitamin D3 (active D3 to absorb Ca and PO4 from intestines)

3) ↑ Intestinal Ca absorption (taking Ca from intestines)

4) ↑ Renal tubular resorption Ca (taking Ca from kidneys)

So increasing Ca in the blood

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7
Q

How does a damage to liver and kidneys lead to Vitamin D deficiency

A

as Vitamin D is converted into the most active form by the liver and kidneys as a result of parathyroid hormone and low Ca and PO4 levels

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8
Q

Function of the active Vitamin D?

A

↑ absorption of Ca & PO4 (from bone or intestines) & ↑ bone mineralisation depending on Ca level in serum.

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9
Q

Calcitonin opposes the action of PTH. HOW?

A

PTH increases Ca levels in blood. Whereas Calcitonin decreases Ca levels in blood by stimulating the deposition and mineralisation of Ca in the bones

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10
Q

What are the Stages of Fracture healing?

A

1) Inflammatory Cellular stage:
- When the bone is fractured, the blood will rush into the area, forming Haematoma (source of hemopoietic cells & Growth Factors which are useful for repairing). Then, inflammatory cells (Macrophages, neutrophils and platelets) will migrate to the fractured area secreting Cytokines which attract more cells (Fibroblasts & mesenchymal cells) into the fractured site, producing Granulation tissue (vascular tissue) around the fracture ends to stabilise it.

2) Inflammatory Vascular stage:
- Neovascularisation occurs (new blood vessels formation), leading to Hyperaemia (increased blood flow). Then, Osteoclasts will absorb the fractured margins

3) Inflammatory Primary callus “Lump” stage:
- Osteoblasts (bone-production), chondrocytes (cartilage-production), fibroblasts (CT-production) will proliferate and start to produce their products (bone, cartilage and connective tissue), forming Callus (primary soft fibrous scar “cartilage” which is not visible radiographically)

4) Reparative Bony callus stage:
- The primary soft Callus (cartilage) is being produced quickly, stabilising the fracture temporarily. Then, Endochondral ossification converts soft Callus (cartilage “Osteoid”) to hard Callus (woven bone), stabilising the fracture

5) Remodelling stage (months & years):
- The hard Bony callus (woven bone) will be resorbed (by Osteoclast) & remodelled (by Osteoblast) into hard lamellar bone (bone’s original cortex structure) and the bone marrow cavity will be restored

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11
Q

what are the Genetic bone diseases?

A

Osteogenesis imperfecta
Cleidocranial dysplasia
Osteopetrosis (Albers-Schonberg Disease)

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12
Q

Osteogenesis imperfecta:
what is it?
symptoms?
dental relevance?

A

Autosomal dominant impaired osteoid (collagen type 1 defect) due to Gene mutations (COL1A1, COL1A2) in type I collagen (osteoid), leading to increased fractures (which starts in utero and can be diagnosed in utero too)

Symptoms:
1) Pt will have short bones
2) Pt might have multiple fractures
3) Blue sclera
4) Deafness (Hearing impairment)
5) Bruising easily
6) Loose joints and tendons

Dental relevance:
- Dentition with osteogenesis imperfecta, having Brown, purple, wear and soft dentine

  • Cardiac complications & chest deformities (not always) but be careful with General Anaesthesia

-Be carful with extractions as they have risk of fracture

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13
Q

Cleidocranial dysplasia:
what is it?
symptoms?
dental relevance?

A

Autosomal dominant involving skull and clavicle defects

Symptoms:
1) Clavicles absent or defective so the shoulder will be forward (characteristic look)
2) Brachycephalic (broad short skull)
3) Hypoplastic midface (Maxilla reduced and Mandibular protrusion “Class3”)
4) Clefts (not always)
5) Other skeletal defects

Dental relevance:
- Hyper-dontia and Super-numeraies (many teeth to grow in the mouth)
- Retained deciduous dentition
- Abnormalities with dentition (abnormal root and cysts formation)

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14
Q

Osteopetrosis (Albers-Schonberg Disease):
what is it?
symptoms?
dental relevance?

A

Defect in osteoclastic activity and bone remodelling, leading to excessive bone density. Although bones are more ‘dense’, there is a risk of fracture but normal healing

Symptoms:
1) Often no symptoms (so can be incidental finding radiographically)
2) Bone pain, fractures, osteomyelitis
3) Anaemia (not always)
4) Susceptibility to infections (due to the defective macrophages and neutrophils)

Dental relevance:
- Jaw fracture and osteomyelitis “Bone inflammation” (Be careful in extraction)
- When infection confirmed difficult to irradicate (If pt has any dental infection due to the defective macrophages and neutrophils, the patient is maybe at risk of sepsis)
- Atraumatic surgery
- Consider antibiotics for surgery

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15
Q

what are the acquired bone diseases?

A

Rickets (Osteomalacia)
Osteoporosis
Fibrous Dysplasia
Paget’s Disease
Hyper-parathyroidism

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16
Q

Rickets (Osteomalacia):
what is it?
symptoms?
dental relevance?
treatment?

A

Childhood disease due to inadequate skeletal bone mineralisation (osteoid “collagen 1” will not be mineralised) due to lack of vitamin D and calcium (Lack of sunlight exposure and supplemented food). And it worsens in dark skin ppl and premature children

Symptoms:
1) If Malabsorption diagnosis (Radiolucencies and hyper-parathyroidism and vit K deficiency)

Dental symptoms: Rare to see dental effects

Treatment: Vitamin supplements and dietary advice

17
Q

Osteoporosis:
what is it?
causes/factors affecting?
symptoms?
dental relevance?
diagnosis and investigation?
treatment?

A

Reduced bone mass and density leading to fragile bones

Factors affecting / causes:
1) Calcium deficiency
2) Reproductive hormones (Oestrogen) deficiency
3) Parathyroid gland damage
4) Lack of physical activity

Symptoms:
1) Often asymptomatic in early stages until they have unexpected fracture
2) Back pain
3) Reduced height (over time)
4) Stooped posture
5) 17.5% increase of hip fracture risk and 16% increase of former fracture risk

Diagnosis:
1) FRAX tool
2) DEXA scan to measure bone density

Treatment:
1) Exercise (weight bearing to increase bone density and reduce risk of fracture)
2) Ca, Vit D, Fluoride and Calcitonin supplements
3) Hormone replacement therapy (HRT) of PTH
Bisphosphonates (Before giving pt bisphosphonate, assess if they are dentally fit to avoid the risk of MRONJ)

18
Q

Fibrous Dysplasia:
what is it?
diagnosis and investigation?
treatment?

A

Chronic disorder of benign fibro-osseous lesion in the craniofacial region. The lesion can be Mono-stotic (affects a single bone) or Poly-stotic (affects multiple bones), looking like a Scar-like tissue grows in place of normal bone weakening the bone over time

Diagnosis:
1) Radiology: lesion will look like ground glass appearance with poorly-defined margins
2) Blood test: detect the raised serum ALP “Alkaline Phosphate” (Serum Ca and PO4 are normal)
3) Urinary test: detect hydroxyproline

Treatment:
If lesion is big, it can be surgically reduced but it can bleed under GA

19
Q

Paget’s Disease:
what is it?
causes/factors affecting?
symptoms?
dental relevance?
diagnosis and investigation?
treatment?

A

Disorder of bone turnover (remodelling), leading to abnormal increase in osteoclasts, so increasing abnormal bone resorption, so increasing abnormal new bone formation (fast & pathological, so woven bone is laid down not lamellar bone). And as woven bone is weak and disorganised, so increasing Deformity and Fracture risk

Causes: Unknown (could be genetic or viral)

Symptoms:
1) Often asymptomatic in early stages
2) Bone pain
3) Systemic effects:
- Arterial-venous fistulas causing high cardiac failure
- Osteosarcomas

Dental symptoms:
1) Enlargement of maxilla and rarely mandible
2) Bulging in the zygomatic area
3) Hyper-cementosis of teeth
4) Risks of surgery either:
- Highly vascularisation so bleeding a lot
- Poor vascularisation leading to osteomyelitis

Diagnosis:
1) Radiographs: detect Osteolysis and mixed areas of lysis and sclerosis.
2) Blood test: detect the raised serum ALP “Alkaline Phosphate” (Serum Ca and PO4 are normal)
3) Urinary test: detect hydroxyproline and pyridinoline excretion

Treatment:
1) Bisphosphonates
2) Calcitonin for pain relief

20
Q

Hyper-parathyroidism:
types?
symptoms and treatment of each type?

A

1) Primary:
Autonomous ↑PTH due to a tumor (adenoma), leading to very high Ca levels (asymptomatic hypercalcemia)

Symptoms:
1) 50% asymptomatic
2) Hyper-calcaemia
3) Renal stones (Nephrolithiasis)
4) Giant cell tumours
5) Hypertension
6) Peptic ulcers and Pancreatitis
7) Corneal calcification
8) Thinning bone trabeculae, Bone pain and Pathological fracture
9) Bone lesions in skull and jaw (Pepper pot skull radiographically)
10) Local swelling in mandible
11) Sub-periosteal resorption of finger tips
12) Osteitis fibrosa cystica (fibrous replacement of resorbed bone)

Treatment:
Surgery for removal of adenoma but will lead to Post-op issues with hypo-calcaemia, so they need to have calcium supplements

2) Secondary:
Parathyroid hyperplasia that is a compensatory hyper-secretion of PTH due to chronic decreased Ca that caused by Chronic Kidney Disease, renal failure, malabsorption, ↓active V.D & ↓PO4 filtration & excretion (hyper-phosphataemia)

Symptoms:
1) Bone lesions (Common)
2) Giant cell lesions (Uncommon and present late “middle aged”)
3) Brown Tumours
4) Systemic diseases (Renal disease)