Bone Pathology Flashcards

1
Q

What is the bone structure

A

Cortex - compact bone consisting of a parallel arrangement of osteons

Cancellous medullary - bone composed of sponge like trabecular bone

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2
Q

What is osteomyelitis

A

It is an infection of the bone and the bone marrow, most often caused by the bacteria S. aureus

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3
Q

What is the Haematogenous Spread

A

The condition where bacteria enter the bone via the bloodstream, causing infection

The primary manifestation or complication is from other organs or is systemic

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4
Q

What is the mechanism of Haematogenous Spread

A

Bacteria enter the bloodstream from a distant site and these bacteria start to seed in the bone marrow, especially in areas with rich blood supply

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5
Q

Why the metaphysis site of the bone for Haematogenous Spread

A

The blood flow in metaphysis is slow and turbulent, allowing bacteria to settle.

In children, metaphyseal vessels form loops close to the growth plate, a site where immune surveillance is lower.

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6
Q

What are the clinical features of Haematogenous Spread

A

Fever, localized bone pain, swelling.

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7
Q

What are the complications associated with Haematogenous spread

A

Abscess formation (Brodie’s abscess).

Spread into the joint space

Sequestrum (dead bone) and involucrum (new bone around sequestrum).

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8
Q

What is the Contiguous Spread of osteomyelitis

A

The spread of infection or disease from an adjacent area or source to another area that is in close proximity

  • More common with adults in association with Diabetic foot ulcers, Post-surgical wounds, and pressure sores
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9
Q

What is the mechanism of Contiguous spread

A

From adjacent soft tissue or skin, directly to the underlying bone

The pathogen/inflammatory reaction permeates the periosteum or erods the articular surface and extends to cortex/medulla

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10
Q

What are the risk factors of Contiguous spread

A
  • Diabetes mellitus
  • Peripheral vascular disease
  • Immunosuppression
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11
Q

What are the clinical symptoms of Contiguous spread

A

Local signs of infection (redness, warmth, discharge).

Chronic draining sinus can develop.

Systemic signs may be minimal.

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12
Q

How does direct implantation contribute to osetomyelitis

A

When organisms are introduced directly into bone

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13
Q

What is the mechanism of direct implantation

A

Trauma, Orthopaedic surgery, Penetrating wounds

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14
Q

What is the histopathology and imaging of osteomyelitis

A
  • Acute osteomyelitis: Neutrophilic infiltrates, necrosis of bone (sequestrum), possible abscess
  • Chronic osteomyelitis:
    Fibrosis, lymphocytes, plasma cells, granulation tissue, and involucrum formation
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15
Q

What is the pathophysiology of bacterial osteomyelitis

A

The pathogen adheres to the collagen matrix and forms actively reproducing colonies; compromised blood flow by compression and thrombosis

This altered perfusion increases the chances of proliferation

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16
Q

What is the immune response to bacterial osteomyelitis

A

There is formation of abscess and granulation tissue (Suppurative inflammation) leading to intraosseous pressure, further hampering the perfusion

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17
Q

How would the bacterial osteomyelitis spread

A

1) Spread through the medulla

2) Spread along the Haversian Canals

3) Through the Cortex

4) To the Periosteum

5) Extension to the Soft Tissue or joints

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18
Q

What happens as the bacteria spreads through the Medulla

A

The medulla is the central cavity of the bone (where bone marrow is found)

The infection would begin here and the bacteria would multiply to provoke an inflammatory response that causes pus to accumulate

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19
Q

What happens as the infection spreads to the Haversian Canals

A

The Haversian Canals are the microscopic structure of the compact bone that carry blood vessels and nerves

The bacteria and pus use these canals as ‘highways’ to move through the dense bone matrix

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20
Q

What happens as it spreads through the cortex

A

The cortex is the hard outer layer of the bone

The infection travels from the medulla and Haversian canals outward through the cortex

The inflammation, pressure from pus, and enzymatic destruction from immune cells would lead to cortical bone necrosis - this sets the stage for sequestrum formation

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21
Q

What happens at the periosteum stage

A

The periosteum is the outer fibrous layer that covers bones, it contains blood vessels and nerves

As the pus accumulates under pressure, it may lift and separate the periosteum from the cortex

This disrupts blood supply even more, worsening necrosis

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22
Q

What happens as the infection spreads to soft tissue or joints

A

If the infection breaks through the periosteum, it can:

  • Spread into the soft tissue, leading to abscesses
  • Enter adjacent joints (especially if the bone is intra-articular) leading to septic arthritis
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23
Q

What is osteomalacia and rickets and what is the difference between the two

A

These are both metabolic bone diseases characterised by defective mineralization of the bone matrix, primarily due to vitamin D deficiency

Osteomalacia = Affects adults (mature skeleton)

Rickets = affects children (growing skeleton)

24
Q

What are the two main components bone

A

1) Organic matrix (mainly collagen)

2) Mineral component (mainly calcium and phosphate)

25
What is the pathophysiology osteomalacia
In osteomalacia, the organic matrix is produced normally but there is inadequate mineralisation due to low vitamin D, calcium, or phosphate. This results in soft and weak bones prone to microfractures
26
Why is Vitamin D is so important
It increases calcium and phosphate absorption from the gut It helps mineralise osteoid into hard bone - without it, bones become soft and deformable
27
What is the pathology of rickets
- In the growing skeleton, the epiphyseal plates are still open - Impaired mineralisation of growth plates - Accumulated unmineralised cartilage and osteoid at metaphysis - Disorganised endochondral ossification leading to structural weakness
28
what is disorganised endochondral ossification
A developmental abnormality where the process of bone formation, specifically the type where cartilage is replaced by bone, is disrupted or abnormal.
29
What are the clinical features of rickets
- Bowed legs or knock knees which become deformed under the influence of body weight - Harrison's sulcus (rib cage deformity) - Frontal bossing (prominent forehead) - Widened wrists/ankles due to cartilage overgrowth
30
What are the clinical features of osteomalacia
- Bone pain - Muscle weakness - Waddling gait - Increased risk of fractures (especially vertebrae, pelvis)
31
How would you diagnose both osteomalacia and rickets
- X-rays: Looser's zoner (pseudofractures) in osteomalacia and metaphyseal fraying in rickets - Bone biopsy: shows excess unmineralised osteoid - Lab panel: Vitamin D, Calcium, Phosphate, and ALP
32
What is the etiology of osteomalacia and rickets
- Intrinsic Vitamin D disturbance - Kidney Disease - Inborn errors metabolism
33
What are examples of Intrinsic Vitamin D disturbances
- Inadequate endogenous production - Dietary deficiency of vitamin D - Inadequate intestinal absorption of Vitamin D - Aberrant metabolism of vitamin D
34
What kidney disease can cause osteomalacia
- Chronic renal failure - Renal tubular disorders
35
Where can osteomalacia occur
In the mature skeleton it can only occur at sites of active bone turnover - Looser's zone
36
What is an osteoid
A thick layer of unmineralised organic matrix
37
What is a trabecular bone
Spongy bone, is a porous type of bone tissue found within the body's vertebrae and at the ends of long bones
38
What is Hyperparathyroidism
A condition where one or more of the parathyroid glands in the neck produce too much parathyroid hormone (PTH)
39
How does hyperparathyroidism affect the bone
The negative impact of excessive parathyroid hormone (PTH), leads to bone weakening, increased risk of fractures, and potential bone diseases
40
What is the normal function of PTH
- Regulates calcium and phosphate levels in the body 1) Stimulates osteoclast activity indirectly which increases bone resorption, releasing calcium and phosphate into the bloodstream
41
What is a parathyroid adenoma
- A benign tumour of the parathyroid gland - Leads to excessive secretion of parathyroid hormone
42
what happens in the bloodstream when PTH is chronically elevated
Calcium levels go up Phosphate levels go down PTH levels go up When there are abnormally high levels of Calcium and PTH in the blood, there is abnormal parathyroid function
43
What does the biopsy show in hyperthyroidism
- Giant cell rich lesion interpreted as a giant cell tumour of bone (primary bone tumour)
44
What is Paget's Disease of Bone
- It is a chronic disorder of bone remodeling - Characterised by excessive bone resorption followed by disorganized bone formation - Results in enlarged, deformed, and structurally weak bones
45
What is the pathophysiology of Paget's Disease of Bone
1) There is initial osteolytic phase - intense osteoclast activity 2) Mixed phase - osteoclast and osteoblast activity with chaotic bone formation 3) Sclerotic (burnt-out) phase - disorganised bone is laid down
46
What is the histology of Paget's Disease of Bone
- Mosaic pattern of lamellar bone: irregular cement lines due to disorganised remodeling - Numerous large osteoclasts with multiple nuclei - Bone marrow spaces are replaced fibrous stroma, blood vessels and sometimes haematopoietic tissue
47
What are the benign bone forming tumours
- Osteoid osteoma - Osteoblastoma
48
What are the malignant bone forming tumours
Osteosarcomas High grade intramedullary tumours Periosteal tumours Parosteal tumours
49
What is osteosarcomas
A high-grade malignant bone tumour in which cancerous cells produce osteoid or immature bone They arise from primitive bone-forming mesenchymal cells that are characterised by the production of malignant osteoid (immature bone) by tumour cells
50
What are the common sites of Osteosarcomas
Metaphysis of long bones: - Distal femur - Proximal tibia - Proximal humerus
51
What is the pathophysiology of Osteosarcomas
Genetic mutations in TSGs - Rb - TP53 Rapidly dividing malignant osteoblasts lay down osteoid in a disorganised way
52
What is the histology of Osteosarcomas
Malignant pleomorphic cells Direct production of osteoid by tumour cells May also have areas of chondroid or fibrous matrix
53
What is the conventional pattern of high-grade intramedullary osteosarcoma
Tumour arising in the medullary cavity of the bone, towards one end of the bone (the metaphysis) There is an admixture of bone destruction (lysis) and new bone formation on the X-ray - The new bone formation would be outside the cortex and beneath the elevated periosteum
54
What are the histological features of high-grade osteosarcoma
There are sheets of disorganised malignant osteoblasts that fill the space between the bony compartment There are also irregular islands of non-structural tumour bone
55
What are the different cartilage forming benign tumours
Enchondroma Osteochondroma Chondromyxoid fibroma Chondroblastoma
56
What are the chondrosarcomas
A type of bone cancer that develops from cartilage cells. It's a primary bone cancer, meaning it originates in the bone rather than spreading from another part of the body
57
How are chondrosarcomas classified
They are classified according to site (intramedullary or peripheral) and histological features (conventional - hyaline or myxoid - clear or dedifferentiated)