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Growth Pathologies of the Vertebral Column Flashcards

1
Q

Where is the most common location for MSK TB?

A

Vertebral column

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2
Q

What is Pott’s disease?

A

Vertebral column TB

2 or more vertebrae affected

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3
Q

What is the average number of vertebrae affected in Pott’s disease? (Reference?)

A

2.6 vertebrae

Hugar et al., 2013

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4
Q

When and by who was spinal TB first reported?

A

5000 years ago

Ancient Egyptians

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5
Q

How much of the world population was affected by TB according to WHO in 1997?

A

More than 1/3

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6
Q

What percentage of TB cases are spinal in HIV- individuals?

A

3-5%

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7
Q

What percentage of TB cases are spinal in HIV+ individuals?

A

60%

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8
Q

Why are more TB cases spinal in HIV+ individuals?

A

Lower CD4+ count

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9
Q

Is spinal TB usually primary TB or secondary to extraspinal TB?

A

Secondary to extraspinal TB

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10
Q

What can spinal TB result in in children?

A

Severe kyphosis due to vertebral body destruction

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11
Q

What is the most common pattern of spinal TB?

A

Spondylodiscitis:

  • > =2 vertebrae
  • Infection spreads anteriorly across disc space
  • Relative sparing of disc space
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12
Q

What are the risk factors for spinal TB?

A 
Poverty
Overcrowding
Malnutrition
Alcoholism
Diabetes
HIV infection
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13
Q

What did Zhang et al., (2010) suggest predisposes an individual to spinal TB?

A

Polymorphism in Vit. D receptor gene:

- Investigated by PCR

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14
Q

What are the sequelae of spinal TB?

A
  1. Destruction of vertebral bodies and IV discs
  2. Formation of abscesses/lesions
  3. Anterior wedging
  4. Functional disability
  5. Spinal cord compression
  6. Back pain
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15
Q

What cells are involved in the pre-pus inflammatory reaction in the spread of TB?

A

Langerhans giant cells
Epitheloid cells
Lymphocytes

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16
Q

What causes a paraspinal abscess in the spread of TB?

A

Tissue necrosis and inflammatory cell breakdown

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17
Q

What are the steps of TB spread to the spine?

A
  1. Haematogenous spread from primary Po./GU infection
  2. Pre-pus inflammatory reaction
  3. Granulation tissue proliferates and vessel thrombosis
  4. TIssue necrosis and inflammatory cell breakdown
  5. Continued necrosis = Kyphosis
  6. Spread to other VBs by longitudinal ligaments
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18
Q

What treatments may be prescribed if spinal TB is confused for other pathologies?

A

Anti-inflammatory drugs
Physical therapy
Posture-correcting corsets

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19
Q

What imaging techniques are used to diagnose spinal TB?

A

CT for guidance
MRI:
- High sensitivity for early diagnosis
- Good for measuring extent of disease and soft tissue involvement

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20
Q

What diagnostic technique is essential for diagnosing spinal TB?

A

Histopathological diagnosis

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21
Q

How are the IV discs involved in spinal TB in children?

A

IV discs are vascularised:

- Infection can spread and start there

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22
Q

How are the IV discs involved in spinal TB in adults?

A

Disc involvement is secondary:

- Via spread from adjacent vertebral body

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23
Q

How can MRI affect prognosis of spinal TB?

A

May aid in early diagnosis and reduce risk of neurological deficits due to compression of surrounding neural structures

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24
Q

When should anti-TB treatment be started for spinal TB?

A

Immediately

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25
What is the drug treatment protocol for TB?
``` Rifampicin Isoniazid Pyrazinamide Ethambutol All four for 2 months Then rifampicin and isoniazid for minimum of 4-8 months ```
26
What does early use of anti-TB drugs reduce the risk of?
Neurological deficits | Paraplegia
27
What happens in drug-resistant spinal TB?
Surgery is only option for cure
28
What surgical procedures can be used for spinal TB?
``` Screw insertion to correct deformity Bone grafts (spinal fusion) Abscess draining with needles ```
29
How is the correct area of spinal TB identified prior to surgery?
MRI
30
What surgical approaches can be used for spinal TB?
Anterior Posterior Combined
31
What are the risk of surgery for spinal TB?
Secondary post-op deformity if: - Incorrect fixation - Fusion of unsuitable segments - Poor balance
32
What are the potential positive outcomes of spinal TB?
Relieves spinal nerve compression Regaining spinal stability Correcting spinal deformity Eliminating sites of TB
33
What is a reference for surgery for spinal TB?
Long et al., 2015
34
Regarding anti-TB drugs and surgery for spinal TB, what did Rasouli et al., (2012) find?
6-9 months drug therapy plus surgery is equivalent to 18 months drug therapy 4-6 weeks of drug therapy = Pain and symptom improvement Combined approach (drugs and surgery) is best CT often used for needle guidance
35
What is Scheuermann's Disease characterised by?
Juvenile thoracic kyphosis
36
When does Scheuermann's Disease develop?
Prior to puberty
37
When does Scheuermann's Disease become more pronounced?
During adolescent growth spurt (aged 10-16 years)
38
What type of kyphosis does Scheuermann's Disease cause?
Primary kyphosis: - Concave anteriorly - Convex posteriorly
39
In what ages is Scheuermann's Disease most common?
12-15 years
40
What is the prevalence of Scheuermann's Disease?
0.4-8.3%
41
What are the typical locations of Scheuermann's Disease?
Mid-thoracic Lower thoracic Thoracolumbar junction
42
What is atypical Scheuermann's Disease?
Scheuermann's Disease in the lumbar spine
43
Are there variations in sex and geographical location for Scheuermann's Disease?
Sex - No | Geographical location - Yes
44
What is the most common presentation of Scheuermann's Disease?
Painless kyphotic deformity
45
How do more severe cases of Scheuermann's Disease present?
Painful kyphosis
46
What can worsen back pain in Scheuermann's Disease?
Physical effort
47
What compensatory features can be seen in Scheuermann's Disease?
Cervical and lumbar lordosis
48
Why can cutaneous pigmentation arise in Scheuermann's Disease?
Continual friction at apex of deformity
49
Where are flexion contractures present in Scheuermann's Disease?
Hip | Shoulder
50
What muscles can spasm in Scheuermann's Disease?
Hamstrings
51
How was Scheuermann's Disease described by Sachs et al., (1987)?
Kyphosis >45 degrees | At least 1 wedge-shaped vertebra - Minimum of 5 degrees
52
What are the six characteristics of Scheuermann's Disease according to Bezalel and Kalichman, (2015)?
1. Vertebral body wedging 2. Irregularity in vertebral end plate 3. Reduced anterior vertebral growth 4. Schmorl's nodes 5. Narrowing of IV disc space 6. Premature IV disc degeneration
53
What is vertebral body wedging?
When ventral height > dorsal height (or vice versa) Overall decrease in height ventrally Entire vertebral body can appear flattened
54
What is vertebral body wedging also a key feature of?
Scoliosis
55
What are the three broad categories of scoliosis?
1. Idiopathic 2. Congenital 3. Neuromuscular
56
What is the most common category of scoliosis?
Idiopathic (75-85%)
57
In regards to scoliosis, what is Scheuermann's Disease a common cause of?
Hyperkyphosis following idiopathic scoliosis
58
What is premature IV disc degeneration in Scheuermann's Disease linked to?
Slow loss of water in nucleus pulposus Reduced proteoglycan content Increased keratin sulfate to chondroitin sulfate ratio
59
In regards to IV disc degeneration in Scheuermann's Disease, what did Paajanin et al., (1989) find?
55%+ of IV discs were degenerate in 20 year old Scheuermann's Disease patients (5x more than the asymptomatic group) (MRI study)
60
What are the two components of the vertebral endplate?
Cartilaginous | Bony
61
What do the vertebral endplates predispose to and why?
Mechanical failure: | - Weakest part of disc and vertebral body interface
62
What is the function of the vertebral endplate?
Physical shield between IV disc and adjacent VBs IV disc nutrient supply: - Capillaries from vertebral arteries through endplate
63
What are the sequelae of vertebral endplate irregularities?
Reduced nutrients reaching IV disc
64
What can end plate irregularities mimic?
Multiple compression fractures
65
How does reduced anterior vertebral growth occur in Scheuermann's Disease?
Increased stress on anterior part of growth plate Greater weight = Greater compressive force Uneven force distribution: - Faster growth in posterior column
66
How are mild cases of Scheuermann's Disease managed?
Left alone
67
What sports must be avoided in Scheuermann's Disease?
Those involving excessive spinal load bearing: - Rugby - Weightlifting
68
The first line treatment of Scheuermann's Disease is rehabilitation. What are the aims of this?
Relieve pain Improve sagittal balance: - Re-establish posture - Promote muscle balances
69
What are the gold standard methods of rehabilitation of Scheuermann's Disease?
Physiotherapy | Bracing
70
What are the purposes of exercise techniques in the treatment of Scheuermann's Disease?
Strengthen and stretch the trunk Postural control Musculotendinous stretching
71
The second line treatment of Scheuermann's Disease is orthopaedics. In what regions is it most effective?
Lower thoracic | Lumbar
72
What are the purposes of orthopaedics in Scheuermann's Disease?
Reduce pressure on anterior endplate Reduce pain Reduce coronal deviation Limit rotation
73
What does a static brace do?
Provides constant pressure | It is rigid
74
What does a dynamic brace do?
Movement opposes spinal movement using flexible bands
75
How often do braces need worn in Scheuermann's Disease?
Depends on severity Can be: - Full time - At intervals
76
What does the selection of a brace in Scheuermann's Disease depend on?
Location of curve Severity of curve Patient cooperation
77
What is surgery reserved for in Scheuermann's Disease?
Severe kyphosis (>70 degrees)
78
What is the surgical procedure for Scheuermann's Disease?
``` Spinal fusion (bony graft) WITH Instrumentation (metal implants or support) ```
79
In spinal fusion for Scheuermann's Disease, where is the fusion carried out?
Fusion extends just above and just below kyphosis
80
When is posterior spinal fusion carried out in Scheuermann's Disease?
Curvatures less than 55 degrees
81
What are the complications of surgery for Scheuermann's Disease?
Neurological injury | Infection
82
What diseases is ankylosing spondylitis related to?
``` Rheumatoid arthritis Other spondyloarthropathies: - Reactive arthritis - Enteropathic arthropathy - Psoriatic arthritis ```
83
What is the incidence of ankylosing spondylitis in caucasian populations?
0.2-0.8%
84
In what group is ankylosing spondylitis more common?
Males
85
What are the symptoms of ankylosing spondylitis?
``` Chronic pain: - Lower back - Buttocks Increased stiffening of spine As disease progresses: - Stooped/hunchback posture - Difficulty expanding chest ```
86
Why does ankylosing spondylitis cause stooped posture and difficult expanding the chest as it progresses?
Fusion affects: - Costovertebral joints - Costosternal joints
87
How else does ankylosing spondylitis manifest?
``` Hip/Shoulder arthritis (33.3%) Peripheral joint arthritis (50%) Acute anterior uveitis (25-40%) Aortic regurg (2-10%) Conducting system disturbances Secondary amyloidosis Nerve subluxation and cauda equina IBD ```
88
What HLA is ankylosing spondylitis associated with?
HLA-B27
89
What is HLA?
Proteins derived from HLA complex consisting of 200 genes on chromosome 6 3 classes: - Class 1 expresses HLA on surface of almost all cells
90
What percentage of ankylosing spondylitis are HLA-B27 negative?
15-20%
91
What percentage of HLA-B27 positive individuals develop ankylosing spondylitis?
5%
92
Using gene mapping, how many loci are associated with ankylosing spondylitis and what percentage of risk do these contribute?
114 | Contribute another 7% of risk
93
How can infection result in ankylosing spondylitis?
Gut infection if genetically predisposed can cause ankylosing spondylitis
94
What is the molecular mimicry theory?
Different HLA-B27 subtypes have small differences in binding sites: - May allow bacterial protein binding (Chlamydia trachomatis or other arthritogenic bacteria)
95
What subtypes of HLA are affected by the molecular mimicry theory?
HLA-B27*05 HLA-B27*02 HLA-B27*04
96
What does insufficient peptide binding and interaction with chaperone protein of HLA-B27 result in?
Misfolding and accumulation in ER
97
What does HLA-B27 misfolding result in?
Acute ER stress: - Protein degradation and autophagy = Increased expression of XBP1 promotes autophagy in AS lesions - Cytokine production = Inflammation
98
What receptors, used by NK and T-cells, are used more in ankylosing spondylitis? What does this receptor do?
KIR3DL2: Binds HLA-B27: - Expression of RORy - Th17 proliferation
99
What do abnormal reactions at the KIR3DL2 receptor cause?
IL-17 production: | - Promotes inflammation in AS
100
What does inflammation in ankylosing spondylitis begin with?
Enthesitis: | - Inflammation of ligament insertion into bone
101
Where is inflammation found in ankylosing spondylitis?
IV disc surface SIJ Costovertebral joint Sternum
102
When the inflammation in ankylosing spondylitis moves to subchondral bone, what cells are responsible for the resulting osteitis?
Lymphocytes Plasma cells Macrophages Chondrocytes
103
What do the invading cells in ankylosing spondylitis cause?
Erosion of cartilage | Erosion of subchondral bone
104
What forms over areas of degradation in ankylosing spondylitis?
Fibrous tissue
105
What do remodelling and osteoproliferation result in in ankylosing spondylitis?
SIJ: - Obliteration - Fusion Entheses of ligaments to ossify = Hyperostosis
106
When does facet joint fusion in ankylosing spondylitis occur?
Before syndesmophyte formation
107
What are the stages of facet joint fusion in ankylosing spondylitis?
1. Reduced joint space (due to inflammation) 2. Articular cartilage fusion 3. Bone fusion
108
Where do fibroblasts and osteoblasts accumulate in the facet joints in ankylosing spondylitis?
At join borders
109
What causes facet joint articular cartilage degeneration in ankylosing spondylitis?
Increased chondrocyte apoptosis | Matrix degeneration
110
What happens once subchondral bone is thinned by osteoblasts in the facet joints in ankylosing spondylitis?
Allows fibrous tissue to invade bone marrow | Fibrous tissue replaces 20-30% of subchondral bone
111
What do chondrocytes lose from the matrix in ankylosing spondylitis?
Proteoglycan
112
How do syndesmophytes form in ankylosing spondylitis?
1. Inflammation 2. Build up of granulation tissue where annulus fibrosus meets VB 3. Remodelling and osteoproliferation 4. Bony bridge up sides of annulus fibrosus connecting adjacent vertebrae = Syndesmophytes
113
What do syndesmophytes cause?
Restrictions of spinal movements
114
What do physiotherapy and exercise improve in ankylosing spondylitis?
Posture Pain Chest expansion Lung capacity
115
What is the first line treatment for ankylosing spondylitis if physiotherapy doesn't work?
NSAIDs
116
What is the second line drug treatment for ankylosing spondylitis?
TNF antagonists
117
What effects do NSAIDs have in ankylosing spondylitis?
Reduce pain | Reduce inflammation
118
What are the side effects of NSAID therapy?
10-60% have GI issues | CVS and renal-relted hypertension
119
How do NSAIDs affect disease progression in ankylosing spondylitis?
Do not halt it
120
When are TNF antagonists used in ankylosing spondylitis?
If NSAIDs fail to relieve symptoms
121
What effect do TNF antagonists have in ankylosing spondylitis?
Improve pain and functionality
122
What effect do TNF antagonists have on disease progression of ankylosing spondylitis?
None
123
Give examples of TNF antagonists?
Etanercept | Infliximab
124
What are bisphosphonates used for in ankylosing spondylitis?
Osteoporosis
125
Give examples of bisphosphonates?
Pamidronate | Alendronic acid
126
What are DMARDs used for in ankylosing spondylitis?
To treat peripheral arthritides
127
Do DMARDs treat ankylosing spondylitis?
No
128
Give examples of DMARDs?
Methotrexate HCQ Sulfasalazine

Vertebral Column (14 decks)

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