bone pathology Flashcards
bone histology
Hard tissue but is vital
Compact bone made of osteons with haversian canal in the middle
* haversian canal has blood vessels – bone laid down in concentric lamellae bone rings (by osteoblasts)
Osteocytes sit in lacunae within the concentric lamellae
Interstitial lamellae between concentric lamellae
Circumferential lamellae – around outside
Lateral Volkman’s canals
* Allow osteocytes to communicate with each other and exchange info about environment.
Periosteum – where you find pain receptors and more vessels
Cellular, time goes get more lumbar
Osteoblasts – oval in shape, sit next each other
* Become surrounded by bone – osteocytes
* Multinucleated osteoclasts – sits on surface of bone, breaks down bone to release minerals into body if needed
bone remodelling cycles
factors
3 groups
mechanical stimuli
systemic hormones
* Parathyroid hormone (PTH)
* Vitamin D3 (hormone)
* Oestrogen
* others
cytokines – release them leads to osteoclast activation
complex interactions promote growth of cells and bone matrix
amount of bone recycled same as bone formed, net amount of bone in *skeleton is the same.
special test for bone
bone biochemistry
not easy to biopsy
bone biochemistry looks at
4
blood calcium (2.20 to 2.60 mmol/L)
osteoblast activity (bone formation)
* serum alkaline phosphatase (30 to 130 U/L)
* Osteocalcin (Vit K dependent) (< 15 ng/L)
osteoclast activity (bone resorption)
* collagen degradation urine & blood (collagen is found in bone)
parathyroid hormone (1.6 to 7.5 pmol/L)
vitamin D assays (>50 nmol/L adequate)
5 bone developmental abnormalities
torus
osteogenesis imperfecta
achondroplasia
osteopetrosis
fibrous dysplasia
torus
Developmental exostosis
Problem with fitting dentures
Torus palatinus - Midline of palate – horseshoe design, window relief
Torus/Tori mandibularis - Bilateral on lingual aspect of mandible (usually premolar region)
Benign
can be surgically reduced
not always symmetrical
CBCT scan
trabecullar bone is
cortical bone is
trabecullar bone is radiolucent
cortical bone is radiopaque
osteogenesis imperfecta
**Type 1 collagen defect **
* Inheritance varied - 4 main types (type 3 – has dentigerous imperfecta)
Clinical
* Weak bones, multiple fractures - Wheelchair bond eventually
* Sometimes associated with dentinogenesis imperfecta
achondroplasia
Autosomal dominant
Poor endochondral ossification (formation of long bones)
Dwarfism
osteopetrosis
Lack of osteoclast activity
* Failure of resorption
Marrow obliteration (due to dense cortical bone deposition)
* Anaemia and delayed healing
* Hard to extract teeth
opposite of osteoporosis
fibrous dysplasia
clincal appearance and occurence
Gene defect
Slow growing, asymptomatic bony swelling
**Bone replaced by fibrous tissue **
Active under 20years
Stops growing after active growth period – usually
Clinical phenotypes Determined by timing of gene mutation
Monostotic – single bone
* More common
* Maxilla > mandible
* Facial asymmetry
Polyostotic – many bones
* Albright’s syndrome - Melanin pigment (coffee spots on body); early puberty (under 5 for girls)
fibrous dysplasia
radiographic appearance
Variable appearances radiographically
* “Ground glass”, “orange peel”, “fingerprint whorl”, “cotton wool”, amorphous
* Abnormal trabecular bone – loss of pattern
* Margins often blend into adjacent bone
Bone maintains approximate shape (initially)
Becomes more radiopaque as lesion matures
what bone pathology is happening here
Compare to other side
Upper left quadrant – alveolar crest drops down - FIBROUS DYSPLASIA
Can get secondary lesions within – solitary bone cysts (radiolucencies within)
CBCT
axial view
look from above
CBCT
coronal view
look front on
CBCT
sagittal view
look side on
fibrous dysplasia histology
“fibro-osseous”
fibrous replacement of bone
* cellular fibrous tissue background with some bone in it
* bone – metaplastic or woven, but will remodel and increase in density (metaplastic - don’t have osteoplastic cells)
not separated – no capsule – blends into surrounding adjacent bone (both histopathologically and radiolucency)
Not exclusive to fibrous dysplasia – need clinical appearance, bone biochemistry to get clinical dx
clincal dx of fibrous dysplasia
clinical appearnce
bone biochemistry (osteoblast and osteoclast activity)
histological appearance
radiographs
should stop when pt stops growing
needs all for dx
clincal dx of fibrous dysplasia
clinical appearnce
bone biochemistry (osteoblast and osteoclast activity)
histological appearance
radiographs
should stop when pt stops growing
needs all for dx
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, periapical granuloma or periapical abscess
* Non-vital tooth
* Presents more radiographically rather than clinically ?
sclerosing osteitis
Localised increase in bone density in response to low-grade inflammation
Most common around apex of tooth with a necrotic pulp
* Periapical radiopacity, often poorly-defined
* May eventually lead to external root resorption if chronic
Dense trabeculation around grossly carious tooth
Indicates area of inflammation (non-vital tooth – XLA or RCT), its just dense bone – not radiopaque tumour.
Manage stimulus to resolve
*abnormal hardening *
idiopathic osteosclerosis
**Localised increase in bone density of unknown cause **
a.k.a. dense bone island
no inflammation
Most common in premolar-molar region of mandible
Always asymptomatic
No bony expansion & no effect on adjacent teeth/structures
E.g. teeth, or IDC (tumour would displace it)
what is the cause of these two bone pathologies?
RHS - 45m idiopathic osteosclerosis
LHS - 37 sclerosising ostetitis
heavily resotred – need to sensibility testing to see if tooth vital (more likely sclerosing then)
what to do is suspect sclerosis osteitis
carry out sensibility test to see if tooth involved is vital
what to do if suspect a benign bony pathology
reassure pt that not overly concerning (not likely malignant)
alveolar osteitis
dry socket
common
Complication of extraction
Severe pain, loss of clot, bone sequestra
* Pt often say more sore than tooth being taken out
Varied aetiology
* Female, smoke, OCP, lower and back, disturbing socket in first 24hrs post XLA
how to manage alveolar osteitis
Medicaments to calm the pain – don’t help the healing process but aid pain
Want to aid healing – LA, bleeding encourage (trauma), to restart process
osteomyelitis
Rare endogenous infection
Acute or chronic
* Suppuration is rare
Other focal lesions Changes within the bone due to infection
* Sequestrum
* Actinomycosis long standing infection spread to skin
* Chronic diffuse sclerosing osteomyelitis
* Periostitis (productive)
take out tooth create compound fracture, disturbing bone to air
case
F 39, C/O pain and swelling lower left jaw
36 extracted 18 months previously, swelling afterwards, incised, now increasing in size
Pain now for 5 weeks, swelling in gum
Swelling on lingual aspect and multiple draining sinuses from 33 to 36
Radiography: full panoramic (to allow comparison with right) and lower true occlusal
* discuss
LHS mandible more diffusely radiopaque – chronic inflammation causing sclerosing osteitis
Occlusal – breach of lingual cortical plate
CBCT – lingual plate, flaking away
Biopsy from the lingual surface of bone confirmed as osteomyelitis
Garre’s sclerosing osteomyelitis
Younger pts (teens), low grade source
Don’t tend to get pus or pain in area
Bony swelling in pt jaw
Here RHS – 85 carious RR, faint bulging of inferior border (not clear line like LHS)
Periosteal bone reaction – new bone being laid down to protect area – lump clinically
Manage source of infection
bone necrosis
aetiology
3
osteomyelitis
avascular necrosis
irradiation
avasular necrosis of bone due to
2
age related ischaemia (mandible reduces with age)
anti-resorpitive medication (MRONJ)
most common cause of bone necrosis
anti-resorptive medications
MRONJ management
Osteoclast inhibitors
* Used in Osteoporosis, Pagets, bone metastases
Osteonecrosis increasingly identified
* Mandible>maxilla
* 60% associated with a dental procedure
Management
* Conservative – extraction as a last resort
* If established – supportive
* Annoying from pt – not painful – sharp to tongue, adjacent tissue prone to infection (antibiotics)
metabolic bone disorders
3
Osteoporosis
Rickets and osteomalacia
Hyperparathyroidism
markers in blood to distinguish between them
osteoporosis
common
Bone atrophy: resorption exceeds formation
* Endosteal net bone loss
* Quantitative deficiency (bone formed is normal)
Clinical features
* Symptomless till traumatic event
* Weak bone
* Antrum enlarged
Radiographs: loss of normal bone markings
osteoporosis
aetiology
Sex hormone status
Age
Calcium status and physical activity
Secondary osteoporosis
* Hyperparathyroidism
* Cushing’s syndrome
* Thyrotoxicosis
* Diabetes mellitus
* Others
osteoporosis management
preventative medications
MRONJ risk
rickets and osteomalacia
Vitamin D deficiency
* Lack of sunlight – daylight hours
* Diet
* Malabsorption
* Renal causes
**Osteoid forms but fails to calcify **
Rickets (children)
* Poor endochondral bone – bow shaped legs
* Low calcium
* Raised alkaline phosphatase
hyperparathryoidsim
**Calcium mobilised from bones **
* Generalised osteoporosis
* Osteitis fibrosa cystica (‘Brown Tumours’)
* Metastatic calcification - kidney
Primary – Neoplasia / hyperplasia
Secondary – Hypocalcemia e.g. due to Vit D Deficiency
Tertiary – prolonged secondary results in hyperplasia
overactive parathyroid
primary hyperparathyrodism
neoplasia/hyperplasia of parathryoid
1 in 1000 population
Mainly postmenopausal women
F:M 3:1
90% parathyroid adenoma (inc PTH)
* Hypercalcoaemia
* Increased bone turnover
Correct tumour – don’t necessary shrink in size but will slowly rectify
radiographic appearance of hyperparathyrodism
Bulging buccal cortex, thin cortices
Whispy septae within (mutliloculated) – ameloblastoma look similar
Displace teeth, loss lamina dura
Change in trabeculations
Pulp stones in teeth
Brown tumour only in 10%
osteitis fibrosa cystica a.k.a
Brown tumour
* haemorrhage into tissue giving brown colour*
Brown tumour (osteitis fibrosa cystica)
features
Generalised osteoporosis
Focal osteolytic lesions
Giant cell lesion (brown tumour)
* Get microfractures in bone – granulation tissue – giant cell
Red blood cells
giant cell lesions of the jaw
features
peripheral giant cell epulis
central giant cell granuloma
* age 10-25
* mandible>maxilla
* may be multilocular
central lesions may “burst out” erodes alveolar bone
* Grows in A-P direction like ameloblastoma
* Large before apparent clinically
common finding between osteitis fibrosa cystica, aneurysmal bone cyst, giant cell tumour?
all containe multinucleated giant cell
need to do special investigations to exclude
brown’s tumours in
hyperparathryoidism
ostitis fibrosa cystica
what to do when see peripheral outgrowth in dental papilla
take periapical to ensure it just a peripheral giant cell epulis lesion and not a central giant cell granuloma lesion (larger before present so more destruction)
cherubism
rare condition
autosomal dominant inheritance
**multicystic/multilocular lesions in multiple quadrants **
grow before about 7 years and regress after puberty
* painless swellings in jaw bone, stop and can regress at puberty
* orbits can be pushed up – looking up into heaven
histology: vascular giant cell lesions
Paget’s disease
presentation
age > 40
M>F
3% of routine autopsies
aetiology unknown
* racial predilection
* viral?
monostotic or polyostotic (1 or more bones involved)
disturbed turnover of bone
serum biochemistry
* raised alk phos (130 normal, 200-300 in Pagets)
clincal presentation of pagets
- asymptomatic
- bone swelling
- pain
- nerve compression- blindness, deafness, facial palsy
C/O – dentures getting small (unusual, normally looser with time)
Increase of maxilla bone
dental impact of pagets
Tx – osteolytic and osteosclerotic phases
* Osteolytic – bleed a lot after XLA
* Osteosclerotic - harder to XLA, more likely to get dry socket
Variable bone pattern
Changes as disease progresses
Osteoporotic/mixed/osteosclerotic – cotton wool appearance
Dental changes
* Loss of lamina dura
* Hypercemetosis – extra cementum deposited on root surface, complicated to XLA
* Migration (due to dental enlargement)
* dentures becoming ‘tight’
histology of pagets
active: increased bone turnover
osteoclastic & osteoblastic activity – occur simultaneously
* dark pink – osteoclast
* next to it is osteoblast??
Mosaic appearance of bone – more prone to bleeding
will burn out
3 possible complications of Paget’s
infection
tumour – osteosarcoma (younger age group tends, so if older – think pagets)
bisphosphate meds
osteoma
benign bone tumour
solitary, mostly cortical
denture construction issue
Gardner syndrome
3 features
multiple osteomas
Polyposis coli – prone to malignant change
Freckles around mouth - Peutz-jegher syndrome
osteoblastoma
Rare
May be a Giant Osteoid Osteoma
Often very active growth
ossifying fibroma
appearance
nomenclature problem
fibrous tissue becomes calcify
clinical
* slow growing - in children can be more aggressive
* wide age range (young and old – fibrous dysplasia just young)
* mainly mandible
radiologically well defined – unlike fibrous dysplasia (differential)
* radiolucent initially then more radiopaque – but has a border
* mass like bulge growing out from centre
ossifying fibroma
histology
cellular fibrous tissue
immature bone
acellular calcifications
difference between ossifying fibroma and fibrous dysplasia
fibrous dysplasia will stop eventually – no need for tx, ossifying fibroma needs intervention
cemento-osseous dysplasia
characteristics
nomenclature problem, probably not neoplastic
periapical COD
* starts as well defined radiolucency
* later calcification, till fully calcified mass attached to tooth
* Lower incisors apical are but are vital
focal COD
* Areas in jaw not related to tooth, can be pinpointed
florid COD
* involve more than one region of jaw – excessive growth
* more in females 9:1, Afro-Caribbean origin
* usually present radiolucent (miss for a cyst) but then become mixed and then radiopaque
* symptomless enlargement of jaw bone
Sclerosing osteitis like – but teeth is still vital
Radiolucent margin
imp - separate to PDL
important radiographic features of cemento-ossifying dysplasia
Sclerosing osteitis like – but teeth is still vital
See pdl space by tooth – imp, separate to PDL
Radiolucent margin
3 types of cemento-ossifying dysplasia
periapical COD
focal COD
florid COD
periapical cemento-ossifying dysplasia
starts as well defined radiolucency
later calcification, till fully calcified mass attached to tooth
Lower incisors apical are but are vital
focal cemento-ossifying dysplasia
Areas in jaw not related to tooth, can be pinpointed
florid cemento-ossifying dysplasia
involve more than one region of jaw – excessive growth
more in females 9:1, Afro-Caribbean origin
usually present radiolucent (miss for a cyst) but then become mixed and then radiopaque
symptomless enlargement of jaw bone
case
39yo female of middle eastern origin
Bony swelling in anterior mandible detected by GDP at routine check-up
Swelling extending into floor of mouth,
present > 2 years but unsure if expanding, no other symptoms
describe OPT and course of investigations
mass in centre mandible – clumps radiopaque areas with radiolucent margins
RHS body of mandible – less mature, small radiopacity floating within
Sufficiently unusual presentation warranted CBCT and biopsy (concern osteosarcoma)
Masses resembles bone or cementum on biopsy
osteosarcoma
rare
age 30s
* if elderly, likely Paget’s related
mandible > maxilla
varied clinical and x-ray presentation (sunburst appearance)
local destruction
recurrence and metastasis poor prognosis
cementoblastoma
neoplasm attached to root histology
same histology as osteoblastoma
Rare, Teens-twenties
Radiolucent margin continuous with PDL – PDL doesn’t continue into lesion (cementum deep to PDL so pushes PDL out to edge of tumour)
Symptomatic – dull ache pain, expansion of bone in area
fibrous dysplasia histology
“fibro-osseous”
fibrous replacement of bone
* cellular fibrous tissue background with some bone in it
* bone – metaplastic or woven, but will remodel and increase in density (metaplastic - don’t have osteoplastic cells)
not separated – no capsule – blends into surrounding adjacent bone (both histopathologically and radiolucency)
Not exclusive to fibrous dysplasia – need clinical appearance, bone biochemistry to get clinical dx
