bone pathology Flashcards
what 3 types of lamellae are in an osteon-Haversian system?
circumferential
interstitial
concentric
where are blood vessels located in a Haversian system?
central (Haversian) canal
perforating (Volkman’s) canal
what overlies the surface of bone?
periosteum
where are osteocytes located?
in lacunae
what does the periosteum contain?
pain receptors and blood vessels
how is bone laid?
around Haversian canal
where do osteoblasts sit?
on periphery of trabeculae
once become enclosed in osteoid - osteocytes
what type of tissue is bone?
vital, dynamic tissue
appears static
mature and immature bone
mature cortical lamellar bone
immature woven bone
stimuli for bone remodelling
mechanical - muscle loading
systemic hormones - direct/indirect effects
- PTH, vit D3, oestrogen, others
cytokines
complex interactions promote growth of cells and bone matrix
what is the normal blood Ca?
2.2-2.6 mmol/L
how to test osteoblast activity - bone formation
serum alkaline phosphatase
osteocalcin (vit K dependent)
normal serum alkaline phosphatase
30-130 U/L
normal osteocalcin (vit K dependent)
<15ug/L
how to test osteoclast activity - bone resorption
collagen degradation urine and blood
normal PTH levels
1.6-7.5 pmol/L
normal vitamin D assays
> 50nmol/l adequate
developmental abnormalities
torus osteogenesis imperfecta achondroplasia osteopetrosis fibrous dysplasia rarefying osteitis sclerosing osteitis idiopathic osteosclerosis
torus
developmental exostosis - outgrowth of bone
when can torus be a problem?
with fitting dentures
torus palatinus
midline of palate
often single
torus/tori mandibularis
usually multiple
bilateral on lingual aspect of mandible (usually premolar region)
if unilateral may xray
if bilateral can usually just diagnose clinically
what are tori usually composed of?
dense cortical bone
osteogenesis imperfecta genetics
type 1 collagen defect
inheritance varied - 4 main types
OI clinical
weak bones, multiple fractures
sometimes associated with type 1 dentinogenesis imperfecta
achondroplasia inheritance
autosomal dominant
achondroplasia clinical features
poor endochondral ossification - limbs - dwarfism
frontal bossing - can use distraction osteogenesis
osteopetrosis
lack of osteoclast activity - failure of resorption
bone becomes v hard - increased density
marrow obliteration - can affect blood cell production
cause of fibrous dysplasia
uncommon - gene defect
clinical presentation of fibrous dysplasia
slow growing, asymptomatic bony swelling
- bone replaced by fibrous tissue
at what age is fibrous dysplasia active?
under 20yrs
stops growing after active growth period (usually)
what are the clinical phenotypes of fibrous dysplasia determined by?
the timing of the gene mutation
clinical phenotypes of fibrous dysplasia
monostotic
polyostotic
monostotic fibrous dysplasia
single bone (more common)
monostotic fibrous dysplasia in the jaws - where is it most commonly located?
maxilla>mandible
usually maxilla and unilateral
consequence of monostotic fibrous dysplasia in the jaws
facial asymmetry
polyostotic fibrous dysplasia
many bones
Albrights syndrome
Polyostotic fibrous dysplasia
melanin pigment
early puberty
consequence of fibrous dysplasia in maxilla
expansion of maxilla - early occlusion
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
if teeth are involved in fibrous dysplasia what can the effects be?
narrowing of PDL
loss of LD
v rarely external RR
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
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
sclerosing osteitis
localised increase in bone density in response to low-grade inflammation
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
idiopathic osteosclerosis
localised increase in bone density of unknown cause
- aka dense bone island
where is idiopathic osteosclerosis most common?
in premolar-molar region of mandible
if in maxilla would tend to be more anterior
is idiopathic osteosclerosis symptomatic?
no it is always asymptomatic
idiopathic osteosclerosis effect on adjacent structures
no bony expansion and no effect on adjacent teeth/structures
- IDC not displaced
how to distinguish between idiopathic osteosclerosis and sclerosing osteitis
carry out sensibility testing on tooth involved
inflammatory diseases
alveolar osteitis
osteomyelitis
Garre’s sclerosing osteomyelitis (periostitis productive)
bone necrosis
risk factors of alveolar osteitis (varied aetiology)
rinsing too early smoking female OCP mandible posterior tooth
symptoms of alveolar osteitis
severe pain
loss of clot
bone sequestra
delays healing process
osteomyelitis
rare endogenous infection
acute or chronic - suppuration is rare
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)
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
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
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)
osteonecrosis and bisphosphonates
mandible>maxilla
60% associated with a dental procedure
- poor healing after any trauma - ext/denture rubbing/spontaneous
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
metabolic bone disease
osteoporosis
rickets (children) and osteomalacia (adults)
hyperparathyroidism
mechanism of osteoporosis
bone atrophy - resorption exceeds formation endosteal net bone loss quantitative deficiency (bone formed is normal)
clinical features of osteoporosis
symptomless (no pain)
weak bone (hip and spinal fractures)
antrum enlarged
radiographic features of osteoporosis
loss of normal bone markings
radiolucent trabecular pattern
thinning of cortical bone
IDC and MF disappear
aetiology of osteoporosis
sex hormone status - oestrogen age Ca status physical activity secondary osteoporosis
secondary osteoporosis
reduced bone density as a result of other conditions/meds e.g.
- hyperparathyroidism
- Cushing’s syndrome
- thyrotoxicosis
- diabetes mellitus
- many other causes
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
mechanism of rickets and osteomalacia
osteoid forms but fails to calcify
defect within bone rather than lack of bone
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
PTH
release Ca from bones
effect of hyperparathyroidism
Ca mobilised from bones
- generalised osteoporosis
- osteitis fibrosa cystica (Brown tumours)
- metastatic calcification (kidney)
primary hyperparathyroidism
problem with parathyroid gland - neoplasm/hyperplasia
secondary hyperparathyroidism
hypocalcemia e.g. due to vit D deficiency
tertiary hyperparathyroidism
prolonged secondary results in hyperplasia
incidence pattern of primary hyperparathyroidism
1 in 1000 pop
mainly postmenopausal women
F:M 3:1
what are 90% of cases of primary hyperparathyroidism caused by?
parathyroid adenoma (increased PTH)
- hypercalcemia
- increased bone turnover
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
what is osteitis fibrosa cystica?
characteristic cystic changes in bone due to prolonged unchecked hyperparathyroidism
presentation of osteitis fibrosa cystica
generalised osteoporosis
focal osteolytic lesions
giant cell lesion (brown tumour)
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
giant cell lesions of the jaws
peripheral giant cell epulis
central giant cell granuloma
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
differential diagnoses of giant cell lesions
osteitis fibrosa cystica
aneurysmal bone cyst
giant cell tumours (v rare)
what may happen to central giant cell lesions?
may “burst out”
cherubism genetics
rare, autosomal dominant inheritance
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
histology of cherubism
vascular giant cell lesions
what can Paget’s disease of bone be treated with?
anti-resorptive meds
incidence patterns of Paget’s disease of bone
age >40
M>F
3% of routine autopsies
aetiology of Paget’s disease of bone
unknown
genetic?
racial predilection?
viral?
types of Paget’s disease of bone
monostotic
polyostotic
serum biochemistry for Paget’s disease of bone
raised alkaline phosphatase
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
cause of Paget’s disease of bone
disordered bone turnover
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
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
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
dental changes in Paget’s disease of bone
loss of lamina dura
hypercementosis (PDL remains outside)
migration (due to bone enlargement)
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
complications of Paget’s disease of bone
infection of affected bone
osteosarcoma (tumour)
pathological fractures as abnormal bone
in which stage of Paget’s disease of bone is the bone marrow often very vascular?
1st stages
what happens to the blood vessels in the sclerotic stage of Paget’s disease of bone?
they decrease
bone tumours
osteoma osteoblastoma ossifying fibroma cementoblastoma (cemento)-osseous dysplasia osteosarcoma
osteoma
small, benign
solitary, mostly cortical
if multiple osteomas, what syndrome should be suspected?
Gardner syndrome
Gardener syndrome
colon polyps (polyposis coli)
osteomas
ST torso growths - dermoid cysts
GP referral, genetic testing/colonoscopy
osteoblastoma
rare, benign but more aggressive
may be a giant osteoid osteoma
often v active growth
anywhere inc jaws
which tumours have a nomenclature problem?
ossifying fibroma
(cemento)-osseous dysplasias - probably not neoplastic - more likely reactive lesions, benign
clinical presentation of ossifying fibroma
slow growing (in children often fast growth) wide age range mainly mandible
radiographic appearance of ossifying fibroma
well-defined
often fibrous tissue capsule or well-separated from surrounding bone
histology of ossifying fibroma
cellular fibrous tissue
immature bone
acellular calcifications
where is a cementoblastoma always found?
jaws
clinical presentation of cementoblastoma
neoplasm attached to root, often apex
late stage bony expansion
histology of cementoblastoma
same as osteoblastoma
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
types of osseous dysplasias
periapical
focal
florid
periapical OD
starts as radiolucency, later calcification
affects L anteriors, VITAL teeth (differentiates from PA cyst)
focal OD
one quadrant/area
florid OD
all 4 quadrants affected or growing v rapidly/large
which pts are usually affected by OD?
mostly adult females, Afro-Caribbean origin
symptoms of OD
none
dull pain
swelling
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
potential risk of OD
increased risk of dry socket/infection post-extraction?
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
