Bone lesions of jaw Flashcards
Ossifying fibroma
Benign neoplasm composed of fibrous tissue which froms spicules, island or cementicles of bone
Age - 20-50 ave 35
Children can be affected
F > M
Slow growing
Mandible most common
May be in craniofacial bones
Premolar or molar region
Well-defined, partially corticated. Well defined is what differentiates from fibrous dysplasia
Radiolucent to start but as lesions grown, can be radiopaque deposits
Resoprtion adj teeth, slight expansion
Mgt - conservative enucleation, resection, low occurence
Fibrous dysplasia
Developmental or reactive 25% H&N Age 15-20 Male = female Painless, smooth, large swellings Maxilla more common Poorly demarcated radiolucency - ground glass apperance of bone Can be monostotic or polystotic - single or multiple If multiple lesions, H&N involved in 50%, peak age <15, may be part of McCune Albright’s syndrome
Management:
Growth stabilises over time
Debulking and contouring ofbone
Recurrence during growth phase
Surgical removal - not common
Orthodontic and orthagnathic surgery
Low risk malignant transformation
Cemento osseous dysplasia COD
A clinicopathological spectrum of reactive lesions
Age 30-50
Often females
Multiple radiolucencies in tooth brearing areas of jaws
Composed of irregular trabeculae of woven bone and cementum in fibrous stroma
Classification - focal = single lesions
Periapical = multiple lesions at apex teeth
Florid = multiple lesions throughout jaws
Pagets Disease
Clinical features
Dental implications
Rare disorder affecting all bones
Bone turnover increased and no longer related to functional demands
In early stage - bone becomes v vascular, can cause hart failure
In later stage - bone becomes sclerotic and shows numerous resting and reversal lines
Clinical features:
Bowed legs
Enlargement of skull causing constriction of foramen - deafness, hats dont fit
Jaw becomes enlarged - spacing, dentures dont fit
More common in Western Europe, USA, Canada, australia,
Rare in Asia/Africa
Possible genetic/hereditary association
Cause generally unknown
Dental implications:
Bone sclerotic - difficult XLAs and prone to infections
Hypercementosis
Bisphosphonates
Reputed increase in incidence osteosarcoma and other bone malignancies
Rare
Giant cell lesions of jaws (3)
Characterised by replacement of bone by fibrous tissue containing numerous multi-nucleate giant cells
Reactive or hyperplastic lesions
Benign but may be locally destructive
Age 10-30
60% females
Usually mandible
Chcraterised by osteoclasts
Cherubism, CGCG, hyperparathyroidism
Cherubism
Developmental condition
AD
Bilateral expansion of posterior mandible
Radiograph - large, multilocular lesions
CGCG
Well demarcated radiolucency
Composed of giant cells - osteoclasts
Pt management: blood biochemistry, curettage, resection, 20% recurrence rate
Hyperparathyroidism
1^ parathyroid adenoma
2^ renal failure, malabsorption
Hereditary - AD
Blood biochemistry - ^^ alkaline phosphatase, PTC, calcium, phosphate
Radiolucent lesion
Brown tumour - identical to CGCG
Mgt - txt of hyperparathyroidism, surgery
Dry socket (alveolar osteitis)
Usually molars, particularly 3rd
Caused by loss or failure of blood clot in socket
May be due to: excessive rinsing, fibrinolysis of clot e.g. via smoking, poor blood supply due to radiotherapy/Pagets, excessive use of vasoconstrictors
Localised inflammatory reaction in bone adjacent to socket
Bone adjacent to socket becomes necrotic and removed by osteoclasts
Healing is v slow - irrigation, antiseptic dress
V rarely develops into osteomyelitis
Sclerosing osteitis
Also known as - focal sclerosing osteitis, condensing osteitis, bone scar
Diff dx - hypercementosis, cementoblastoma, osteoma
Focal bone reaction to low grade inflammation e.g. chronic pulpitis
Any age
Commonly mandibular molars
Radiograph - uniform opacity at apex of tooth, often with periapical lucency
Txt - cause of inflammation
Osteomyelitis
Inflammation within marrow cavities of bone
Any age
Acute or chronic type
Subtypes - sclerosing osteomyelitis, proliferative periostitis (Garre’s)
Can be due to problem with blood supply - osteoporosis, Pagets, radiotherapy
Or problem with host response - immunosupression, poor nutrition
Other causes - bisphosphonates
Acute osteomyelitis
Aetiology - most commonly infectious - staphylococcus, streptococci
Extension of PA abscess
Physical injury/fracture
Acute inflammatory response - pain, pyrexia, lymphadenopathy, malaise
Histology - acute inflammatory infiltrate, increased bone resoprtion, decreased bone formation
Chronic osteomyelitis
Aetiology - low grade inflammatory reaction, may be progression from acute osteomyelitis
Chronic inflammatory response associated with low grade infection - pain swelling bone loss sequestrae
Histology - chronic inflammatory infiltrate e.g. macrophages and lymphocytes, not neutrophils
Both osteoclastic and osteoblastic activity
Reversal lines
Mgt - remove source infection, remove infected bone, hyperbaric oxygen can help
Osteonecrosis
Osteoradionecrosis - complication of irradiation, H&N malignancies, compromised vasculature - endarteritis obliterans (ends of little arteries in mandible get blocked)
Bisphosphonate/medication relation osteonecrosis - BRONJ, MRONJ
Associated with - bisphosphonates, denosumab
Other associated factors - poor OH, smoking, diabetes, prolonged drug use, dental extractions
Pt management - dental assessment, OH, smoking cess, limiting alcohol
low risk - osteoporosis, atrumatic extractions
high risk - malignancy/Pagets/immunosupressed/history of MRONJ - refer to OS/OMFS
Osteoma
Localised bony nodule on maxilla or mandible
Shows continuous growth
Distinguished from tori
May be associated with syndromes
Histopath - composed of either compact bone or compact and cancellous bone
