bone pathology Flashcards
(124 cards)
1
Q
what 3 types of lamellae are in an osteon-Haversian system?
A
circumferential
interstitial
concentric
2
Q
where are blood vessels located in a Haversian system?
A
central (Haversian) canal
perforating (Volkman’s) canal
3
Q
what overlies the surface of bone?
A
periosteum
4
Q
where are osteocytes located?
A
in lacunae
5
Q
what does the periosteum contain?
A
pain receptors and blood vessels
6
Q
how is bone laid?
A
around Haversian canal
7
Q
where do osteoblasts sit?
A
on periphery of trabeculae
once become enclosed in osteoid - osteocytes
8
Q
what type of tissue is bone?
A
vital, dynamic tissue
appears static
9
Q
mature and immature bone
A
mature cortical lamellar bone
immature woven bone
10
Q
stimuli for bone remodelling
A
mechanical - muscle loading
systemic hormones - direct/indirect effects
- PTH, vit D3, oestrogen, others
cytokines
complex interactions promote growth of cells and bone matrix
11
Q
what is the normal blood Ca?
A
2.2-2.6 mmol/L
12
Q
how to test osteoblast activity - bone formation
A
serum alkaline phosphatase
osteocalcin (vit K dependent)
13
Q
normal serum alkaline phosphatase
A
30-130 U/L
14
Q
normal osteocalcin (vit K dependent)
A
<15ug/L
15
Q
how to test osteoclast activity - bone resorption
A
collagen degradation urine and blood
16
Q
normal PTH levels
A
1.6-7.5 pmol/L
17
Q
normal vitamin D assays
A
> 50nmol/l adequate
18
Q
developmental abnormalities
A
torus osteogenesis imperfecta achondroplasia osteopetrosis fibrous dysplasia rarefying osteitis sclerosing osteitis idiopathic osteosclerosis
19
Q
torus
A
developmental exostosis - outgrowth of bone
20
Q
when can torus be a problem?
A
with fitting dentures
21
Q
torus palatinus
A
midline of palate
often single
22
Q
torus/tori mandibularis
A
usually multiple
bilateral on lingual aspect of mandible (usually premolar region)
if unilateral may xray
if bilateral can usually just diagnose clinically
23
Q
what are tori usually composed of?
A
dense cortical bone
24
Q
osteogenesis imperfecta genetics
A
type 1 collagen defect
inheritance varied - 4 main types
25
OI clinical
weak bones, multiple fractures
| sometimes associated with type 1 dentinogenesis imperfecta
26
achondroplasia inheritance
autosomal dominant
27
achondroplasia clinical features
poor endochondral ossification - limbs - dwarfism
| frontal bossing - can use distraction osteogenesis
28
osteopetrosis
lack of osteoclast activity - failure of resorption
bone becomes v hard - increased density
marrow obliteration - can affect blood cell production
29
cause of fibrous dysplasia
uncommon - gene defect
30
clinical presentation of fibrous dysplasia
slow growing, asymptomatic bony swelling
| - bone replaced by fibrous tissue
31
at what age is fibrous dysplasia active?
under 20yrs
| stops growing after active growth period (usually)
32
what are the clinical phenotypes of fibrous dysplasia determined by?
the timing of the gene mutation
33
clinical phenotypes of fibrous dysplasia
monostotic
| polyostotic
34
monostotic fibrous dysplasia
single bone (more common)
35
monostotic fibrous dysplasia in the jaws - where is it most commonly located?
maxilla>mandible
| usually maxilla and unilateral
36
consequence of monostotic fibrous dysplasia in the jaws
facial asymmetry
37
polyostotic fibrous dysplasia
many bones
38
Albrights syndrome
Polyostotic fibrous dysplasia
melanin pigment
early puberty
39
consequence of fibrous dysplasia in maxilla
expansion of maxilla - early occlusion
40
radiographic appearance of fibrous dysplasia
variable
- ground glass (frosty, transparent)
- orange peel
- finger print whorl
- cotton wool
- amorphous
margins often blend into adjacent normal bone - no evident capsule/demarcation. wide zone of transition
bone maintains approximate shape (initially)
becomes more radiopaque as lesion matures
41
if teeth are involved in fibrous dysplasia what can the effects be?
narrowing of PDL
loss of LD
v rarely external RR
42
histology of active fibrous dysplasia
"fibro-osseous"
fibrous replacement of bone
- cellular fibrous tissue
- bone - metaplastic or woven, but will remodel and increase in density
43
rarefying osteitis
localised loss of bone in response to inflammation
always occurring secondary to another form of pathology
if at apex of tooth consider periapical periodontitis/granuloma/abscess
44
sclerosing osteitis
localised increase in bone density in response to low-grade inflammation
45
most common area of sclerosing osteitis
around apex of tooth with a necrotic pulp
- periapical radiopacity, often poorly defined
- may eventually lead to external root resorption if chronic
can also get due to chronic pericoronitis
46
idiopathic osteosclerosis
localised increase in bone density of unknown cause
| - aka dense bone island
47
where is idiopathic osteosclerosis most common?
in premolar-molar region of mandible
| if in maxilla would tend to be more anterior
48
is idiopathic osteosclerosis symptomatic?
no it is always asymptomatic
49
idiopathic osteosclerosis effect on adjacent structures
no bony expansion and no effect on adjacent teeth/structures
| - IDC not displaced
50
how to distinguish between idiopathic osteosclerosis and sclerosing osteitis
carry out sensibility testing on tooth involved
51
inflammatory diseases
alveolar osteitis
osteomyelitis
Garre's sclerosing osteomyelitis (periostitis productive)
bone necrosis
52
risk factors of alveolar osteitis (varied aetiology)
```
rinsing too early
smoking
female
OCP
mandible
posterior tooth
```
53
symptoms of alveolar osteitis
severe pain
loss of clot
bone sequestra
delays healing process
54
osteomyelitis
rare endogenous infection
| acute or chronic - suppuration is rare
55
osteomyelitis - other focal lesions
sequestrum - bone necrotic - body thinks it is foreign
actinomycosis - rare, after ext, need long-term ABs
chronic diffuse sclerosing osteomyelitis
periostitis (productive)
56
Garre's sclerosis osteomyelitis (periostitis productive)
generally children due to caries (/perio)
mandible growing and expands
periosteum lays down layers of bone in response to chronic inflammation
often get sclerosis
57
aetiology of bone necrosis
if blood supply affected in some way - mandible more prone
osteomyelitis - acute or chronic
avascular necrosis
- age related ischaemia: blood supply decreases as age
- anti-resorptive meds
irradiation
- ORN - endarteritis obliterans
- prone to infections
- also pharyngeal cancer - beware if you extract molars
58
mechanism of action and uses of bisphosphonates
osteoclast inhibitors
| used in osteoporosis, Pagets, bone metastases (prostate and breast cancer have tendency to metastasise to bone)
59
osteonecrosis and bisphosphonates
mandible>maxilla
60% associated with a dental procedure
- poor healing after any trauma - ext/denture rubbing/spontaneous
60
management of bisphosphonates related osteonecrosis
conservative - extraction as a last resort
if established - supportive
manage any (super)infections - antibiotics
don't tend to excise necrotic bone as causes further insult to healthy bone - chain
61
metabolic bone disease
osteoporosis
rickets (children) and osteomalacia (adults)
hyperparathyroidism
62
mechanism of osteoporosis
```
bone atrophy - resorption exceeds formation
endosteal net bone loss
quantitative deficiency (bone formed is normal)
```
63
clinical features of osteoporosis
symptomless (no pain)
weak bone (hip and spinal fractures)
antrum enlarged
64
radiographic features of osteoporosis
loss of normal bone markings
radiolucent trabecular pattern
thinning of cortical bone
IDC and MF disappear
65
aetiology of osteoporosis
```
sex hormone status - oestrogen
age
Ca status
physical activity
secondary osteoporosis
```
66
secondary osteoporosis
reduced bone density as a result of other conditions/meds e.g.
- hyperparathyroidism
- Cushing's syndrome
- thyrotoxicosis
- diabetes mellitus
- many other causes
67
what are the causes of rickets and osteomalacia?
vit D deficiency
- lack of sunlight - daylight hours
- diet
- malabsorption
- renal causes - kidney involved in activating vit D
68
mechanism of rickets and osteomalacia
osteoid forms but fails to calcify
| defect within bone rather than lack of bone
69
presentation of rickets
poor endochondral bone (may have short limbs)
low Ca
raised alkaline phosphatase
- generic marker so can't use on its own to diagnose
70
PTH
release Ca from bones
71
effect of hyperparathyroidism
Ca mobilised from bones
- generalised osteoporosis
- osteitis fibrosa cystica (Brown tumours)
- metastatic calcification (kidney)
72
primary hyperparathyroidism
problem with parathyroid gland - neoplasm/hyperplasia
73
secondary hyperparathyroidism
hypocalcemia e.g. due to vit D deficiency
74
tertiary hyperparathyroidism
prolonged secondary results in hyperplasia
75
incidence pattern of primary hyperparathyroidism
1 in 1000 pop
mainly postmenopausal women
F:M 3:1
76
what are 90% of cases of primary hyperparathyroidism caused by?
parathyroid adenoma (increased PTH)
- hypercalcemia
- increased bone turnover
77
radiographic presentation of hyperparathyroidism
expansive ballooning out
v thin cortices, thin wispy septa
teeth displaced but rarely get resorption, can get pulp stones
radiolucent appearance of bone
78
what is osteitis fibrosa cystica?
characteristic cystic changes in bone due to prolonged unchecked hyperparathyroidism
79
presentation of osteitis fibrosa cystica
generalised osteoporosis
focal osteolytic lesions
giant cell lesion (brown tumour)
80
giant cell lesion (brown tumour)
area of significant resorption
granulation tissue fills spaces where bone was
lots of multinucleate giant cells
often bleeding into lesion - rbcs break down - haemosidrin - brown
81
giant cell lesions of the jaws
peripheral giant cell epulis
| central giant cell granuloma
82
central giant cell granuloma presentation
age 10-25
mandible>maxilla
may be multilocular
tends to grow in an AP direction along mandible so large before symptoms - can cause a lot of destruction
can sit on gingiva and resemble peripheral - radiograph
could have hard to explain mobility - radiograph before extraction
83
differential diagnoses of giant cell lesions
osteitis fibrosa cystica
aneurysmal bone cyst
giant cell tumours (v rare)
84
what may happen to central giant cell lesions?
may "burst out"
85
cherubism genetics
rare, autosomal dominant inheritance
86
cherubism presentation
multi cystic/multilocular lesions in multiple quadrants
- resorption of bone and replacement by GC lesions
grow before about 7yrs and regress after puberty
87
histology of cherubism
vascular giant cell lesions
88
what can Paget's disease of bone be treated with?
anti-resorptive meds
89
incidence patterns of Paget's disease of bone
age >40
M>F
3% of routine autopsies
90
aetiology of Paget's disease of bone
unknown
genetic?
racial predilection?
viral?
91
types of Paget's disease of bone
monostotic
| polyostotic
92
serum biochemistry for Paget's disease of bone
raised alkaline phosphatase
93
clinical S and S of Paget's disease of bone
vary depending on which bones affected and which stage of disease (can often be subclinical)
bone swelling
pain
nerve compression - deafness/blindness/paralysis
dentures always getting tight - jaws increasing in size
94
cause of Paget's disease of bone
disordered bone turnover
95
stages of Paget's disease of bone
1 - lytic stage - bone resorption
2 - mixed stage - bone resorption and deposition
3 - sclerotic stage - bone deposition
initially bone soft and deformed then calcified
96
extractions and Paget's disease of bone
complications depend on which stage
- lytic - lots of bleeding
- sclerotic - barely any bleeding, risk of dry socket and even necrosis
97
general radiographic appearance of Paget's disease of bone
skull commonly affected (normally diploic): thickened and very irregular, cotton wool appearance
variable bone pattern
- changes as disease progresses
- osteoporotic/mixed/osteosclerotic
98
dental changes in Paget's disease of bone
loss of lamina dura
hypercementosis (PDL remains outside)
migration (due to bone enlargement)
99
histology of Paget's disease of bone
active - increased bone turnover
OC and OB activity
osteoclasts dark multinucleate giant cells - sit in Howship's lacunae
- bone forming and resorbing on same side of trabecular
will burn out
reversal line: recognise changes between deposition and resorption, in Paget's v dark
100
complications of Paget's disease of bone
infection of affected bone
osteosarcoma (tumour)
pathological fractures as abnormal bone
101
in which stage of Paget's disease of bone is the bone marrow often very vascular?
1st stages
102
what happens to the blood vessels in the sclerotic stage of Paget's disease of bone?
they decrease
103
bone tumours
```
osteoma
osteoblastoma
ossifying fibroma
cementoblastoma
(cemento)-osseous dysplasia
osteosarcoma
```
104
osteoma
small, benign
| solitary, mostly cortical
105
if multiple osteomas, what syndrome should be suspected?
Gardner syndrome
106
Gardener syndrome
colon polyps (polyposis coli)
osteomas
ST torso growths - dermoid cysts
GP referral, genetic testing/colonoscopy
107
osteoblastoma
rare, benign but more aggressive
may be a giant osteoid osteoma
often v active growth
anywhere inc jaws
108
which tumours have a nomenclature problem?
ossifying fibroma
| (cemento)-osseous dysplasias - probably not neoplastic - more likely reactive lesions, benign
109
clinical presentation of ossifying fibroma
```
slow growing (in children often fast growth)
wide age range
mainly mandible
```
110
radiographic appearance of ossifying fibroma
well-defined
| often fibrous tissue capsule or well-separated from surrounding bone
111
histology of ossifying fibroma
cellular fibrous tissue
immature bone
acellular calcifications
112
where is a cementoblastoma always found?
jaws
113
clinical presentation of cementoblastoma
neoplasm attached to root, often apex
| late stage bony expansion
114
histology of cementoblastoma
same as osteoblastoma
115
radiographic features of cementoblastoma
```
well-defined radiopacity with radiolucent margin
rim part of PDL space
lose definition of root, can get RR
often incidental finding
often posterior mandible
```
116
types of osseous dysplasias
periapical
focal
florid
117
periapical OD
starts as radiolucency, later calcification
| affects L anteriors, VITAL teeth (differentiates from PA cyst)
118
focal OD
one quadrant/area
119
florid OD
all 4 quadrants affected or growing v rapidly/large
120
which pts are usually affected by OD?
mostly adult females, Afro-Caribbean origin
121
symptoms of OD
none
dull pain
swelling
122
radiographic appearance of OD
radiolucent background with developing radiopacity, unusual shapes, apices of teeth
can still see PDL space between root and lesion
rarely RR
some resemble bone and cementum
123
potential risk of OD
increased risk of dry socket/infection post-extraction?
124
osteosarcoma
```
malignant
rare
usually younger adults - 30s
- if elderly likely Paget's related
mandible>maxilla
varied clinical and xray presentation
local destruction
recurrence and metastasis
```
