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imed3003 > Fracture Healing, Osteonecrosis & Arthritis > Flashcards

Fracture Healing, Osteonecrosis & Arthritis Flashcards

1
Q

What is a fracture defined as?

A

Discontinuity in the bone with disruptions in cortex, trabecular bone, or both.

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2
Q

How is a bone frature-classified?

A

Categorised according to:

Anatomical location

Direction of fracture

Whether linear or comminuted (shattered into fragments)

Whether impacted (jammed together)

Whether open or closed

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3
Q

What causes stress fractures?

A

Repeated stress to a bone may result in an incomplete stress or fatigue fracture which is an accumulation of microfractures leading to a true fracture of the cortex.

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4
Q

How is a stress fracture different to an insufficiency fracture?

A

Insufficiency fracture is caused by normal stress on abnormal bone whereas a fatigue fracture is abnormal stress on a normal bone

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5
Q

What is a pathological fracture? How is it different to insufficiency fractures?

A

A fracture caused by primary or secondary neoplasms. This is as opposed to insufficiency fractures which are fractures in bone affected by non-neoplastic disease.

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6
Q

What are the stages of fracture healing?

A

Inflammatory phase: Disruption to bone, periosteal and soft tissues, haematoma encases bone and fragments, neovascularisation.

Reparative phase: Fibro (soft) to bony (hard) callus formation, cutting cones formed by osteoclasts

Remodelling phase: Restoration of cortex organisation (blood and nerve supply as well as osteoblasts and clasts)

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7
Q

How long does each phase of fracture healing last?

A

Inflammatory phase: Days

Reparative phase (weeks - months)

Remodelling phase (weeks - years)

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8
Q

What are the 4 most important factors that affect healing of bone fractures?

A

Wound immobilisation

Vascular supply

Presence of infection

Physical stress

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9
Q

What causes non-union of fractures? What occurs as a result of this?

A

Can result from soft tissues coming in between the bone fragments, excessive motion or gaps, infection, poor blood supply, malignancy,

Pseudoarthrosis forms (joint-like tissues)

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10
Q

What is osteonecrosis?

A

All encompassing term for death of bone and marrow in the absence of infections.

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11
Q

What are the features of osteonecrosis?

A

Caused by changes in the structural integrity and shape of the bone head.

Arthritis:
Similar presentation to osteoarthritis but with a more sudden onset, and in younger populations; AVN is increasingly recognised as a cause of degenerative arthritis.

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12
Q

What is the most common type of osteonecrosis? And what part of the bone is typically affected?

A

Avascular necrosis, it most commonly affects the end of a long bone and is increasingly recognized as a cause of arthritis.

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13
Q

What causes avascular necrosis?

A

Vast majority of cases are secondary to trauma

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14
Q

What are the non-traumatic causes of avascular necrosis?

A

Alcohol consumption

Corticosteroids

Emboli

Infection

Systemic diseases

Thrombosis

Legg-Calve-Perthes

Idiopathic

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15
Q

How can osteonecrosis be diagnosed?

A

Bone scan (Skeletal scintigraphy)

MRI

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16
Q

What is Legg-Calvé-Perthes disease?

A

A paediatric condition which causes osteonecrosis of the hip

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17
Q

How is Legg-Calvé-Perthes disease managed?

A

Management depends on age and severity:

Osteotomy

Conservative containment using brace, slings and springs, broomstick plasters

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18
Q

What cells are found more abundantly in osteonecrosis?

A

Osteoclasts

Necrosis of bone and growth cartilage

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19
Q

How does necrotic bone heal?

A

Necrotic bone heals differently in trabecular and cortical bone

Trabecular bone heals by ‘creeping substitution’ which means necrotic marrow is replaced by invading neovascular tissue. (Bone remodelling and intramembranous ossification)

Cortical bone heals by “cutting cones” where osteoclasts bore holes into the necrotic cortex via vascular channels with osteoblasts trailing forming new lamellar bone

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20
Q

Who gets osteonecrosis of the jaw?

A

Exposed bone of the mandilble/maxilla that fails to heal 8-weeks after a patient has received systemic bisphosphonates and who has not undergone local radiation therapy to the jaw.

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21
Q

What is arthritis?

A

Clinical arthritis is the consequence of loss of the joint’s normal function.

22
Q

What are the types of arthritis? How are they distinguished?

A

Based on characteristic presentations and pathology there are several types of arthritis:

Non-inflammatory “osteoarthritis” (degenerative joint disease)

Rheumatic/inflammatory syndromes

Infectious arthritis

Metabolic / crystal associated arthritis

23
Q

What are the signs and symptoms of arthritis?

A

Symptoms:

Pain

Stiffness

Deformity

Loss of function

Systemic illness

Signs:

Heat

Redness

Swelling

Loss of movement

Deformity

Tenderness

Abnormal movement

Crepitus

Functional abnormality

24
Q

What is the most common joint disorder? How is it different to other joint disorders?

A

Osteoarthritis, It is characterized by altered joint anatomy and especially loss of articular cartilage and primarily seen in weight bearing joints and fingers. It is essentially non-inflammatory in nature.

25
Q

How does osteoarthritis progress?

A

Begins as disorder of articular cartilage

Leads to abnormality in joint mechanics

Progressive loss of cartilage and subchondral bone changes

26
Q

What are the predisposing factors to osteoarthritis?

A

Infection

Inflammatory arthropathy

Trauma

Metablic Joint Disease

Avascular bone necrosis

Altered loading through the joint

Genetic

Most cases are idiopathic

27
Q

Who gets osteoarthritis most commonly?

A

More common in women

Prevalence increases with age (>55 yoa)

28
Q

How does osteoarthritis present?

A

Usually with pain, stiffness, reduced mobility

On examination: reduced range of movement, no inflammatory signs, small effusions, crepitus

X-ray would show loss of hyaline cartilage with narrowing in joint space

29
Q

What is eburnation?

A

Complete loss of hyaline cartilage - exposed surface is “ivory-like”

30
Q

How are osteophytes formed?

A

Bone outgrowths from joint margin are broken off to form loose bodies in the joint

31
Q

What happens microscopically in osteoarthritis?

A

Loss of proteoglycan

Disruption of collagen network

Changes in superficial layers of articular cartilage (splits and fissures), bone changes, cysts and sclerosis

32
Q

How does osteoarthritis progress?

A

Normal joint gets some subchondral microdamage causing subchondral plate to lose thickness and become more porous and subchondral trabeculae deteriorate.

This progresses to late stage osteoarthritis where progressive cartilage destruction takes place. Calcified cartilage thickens with reduplicated tidemarks. Subchondral plate also thickens and suchondral bone cysts form as well as subchondral microdamage

33
Q

What are the features of end stage subchondral bone?

A

Bone cysts

Tide mark duplication

Microfractures

Bone sclerosis

34
Q

What are the differences between features of synovial fluid in normal joints and osteoarthritic joints?

A

Normal synovial fluid is clear, osteoarthritic joints are more yellow.

Osteoarthritic synovial fluid has more white blood cells/mm

In osteoarthritic joints there is a small fibrin clot which doesn’t exist in normal synovial fluid.

35
Q

What is rheumatoid arthritis?

A

Most common primary inflammatory arthropathy. It is a chronic autoimmune disease that primarily affects the lining of synovial joints. Often symmetrical, erosive polyarthropathy.

36
Q

What joints are primarily affected by rheumatoid arthritis?

A

Affects all joints, but predominantly small bones of hands and feet as well as cervical spine.

37
Q

What kind of disease is rheumatoid arthritis?

A

It is a systemic disease (extraarticular manifestations) with a highly variable presentation.

38
Q

What are the clinical symptoms of rheumatoid arthritis?

A

Very variable disease

Intermittent or persistent joint inflammation / destruction plus variable extra-articular manifestations.

General malaise

Pain and stiffness in the joints

Worse in the morning

Usually several joints in a symmetric pattern are affected particularly hands, wrists, knees, and feet

39
Q

What is the peak age of onset and who is more likely to get RA, males or females?

A

Females are three times more likely than males to get RA.

Peak age of onset is 40 to 70

40
Q

What are the criteria for diagnosing RA based on the ACR classification?

A

> 4 of the following symptoms must be present for at least 6 weeks::

  1. Morning stiffness (at least 1 hour)
  2. Arthritis in three or more joint areas
  3. Arthritis of hand joints (>1 swollen joints)
  4. Symmetric arthritis
  5. Rheumatoid nodules
  6. Serum RF
  7. Radiographic changes on X-ray of hands
41
Q

How effective is the ACR classification of RA?

A

Sensitivity of 79 - 80% and specificity of 90 - 93% for established RA

Sensitivity of 77%- 80% and specificity of 33%- 77% for early RA

42
Q

What is the cause of RA?

A

Cause is unknown

Thought to arise from a combination of genetic and environmental triggers

43
Q

What are the types of RA?

A

2 major subtypes classified by rheumatoid factor serotypes:

Anti citrullinated protein antibody positive (ACPAs) (~70%)

ACPA negative

44
Q

What is ACPA?

A

An abnormal antibody response to citrullinated proteins.

Citrullination is catalysed by peptidyl-arginine-deiminase (PAD)

45
Q

Which subtype of rheumatoid arthritis is more severe?

A

ACPA positive subset

46
Q

What are the 4 stages of rheumatoid arthritis formation?

A
  1. Triggering stage: ACPA production
  2. Maturation stage (More ACPA production due to citrullination of proteins in active T-cells and B-cells)
  3. Targeting stage (stage where joints are involved leading to inflammation and joint swelling and infiltration of WBCs and cytokines)
  4. Fulminant stage (hyperplasia of fibroblast-like synoviocytes, inflamed synovium ‘pannus’ encroaches on articular cartilage and proliferates over internal joint structures resulting in joint destruction and fusion (ankylosis))
47
Q

What causes the triggering stage of RA?

A

Genetic (HLA-DR:HLA-DR1, HLA-DR4 = share epitopes)

Environmental (Lung expsure to noxious agents eg smoke, silica, etc or periodontitis)

Infectious agents, Epstein-Barr virus, dietary factors influencing the gut

Combination leads to elevated ACPA production

48
Q

Where is the maturation stage of RA initiated?

A

At site of secondary lymphoid tissue or bone marrow

49
Q

What histological structure causes erosion of the cartilage at the joint margin?

A

The pannus which has destructive activity (the inflammatory synovial mass)

50
Q

What are the macroscopic features of RA?

A

Inflamed tendon

Erosion of bones

Hyperplastic synovium

Inflammatory cells

Thinning of cartilage

Joint instability

Subluxation

Damage to capsule

51
Q

What are the extra-articular manifestations seen in people with RA?

A

Subcutaneous rheumatoid nodules in approximately 1/3 of cases. These nodules are typically seen on extensor surfaces in relation to periarticular structures (eg olecranon bursa, proximal ulna, achilles and occiput.

Symptoms are usually related to traumatic disruption or secondary infection.

imed3003 (48 decks)

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