Jaw disease Flashcards

1
Q

What is a cyst?

A

A cyst is a pathological cavity filled with fluid, semi-fluid or gaseous contents and which is not created by the accumulation of pus. It is usually but not always lined by epithelium. A cyst has a wall, lumen and lining.

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2
Q

How are cysts classified?

A
  • Epithelial cysts
    • Odontogenic cysts
      • Inflammatory
      • Developmental
    • Non-odontogenic
      - Nasopalatine duct cyst
      - Nasolabial cyst
  • Cyst like lesions
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3
Q

What are the types of odontogenic cyst?

A
Inflammatory:
- Radicular cyst
- Residual cyst 
- Paradental/collateral cyst 
Developmental:
- Follicular
     - Dentigerous cyst
     - Eruption cyst
- Odontogenic keratocyst
- Gingival cyst
- Lateral periodontal cyst/Botryoid odontogenic cyst
- Calcifying odontogenic cyst
- Glandular odontogenic cyst
- Orthokeratinised odontogenic cyst
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4
Q

What is the frequency of the different cyst types?

A
  • Radicular 65%
  • Follicular 20%
  • Keratocyst 5%
  • Nasopalatine 5%
  • Others 5%
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5
Q

What do cysts need in order to form?

A
  • A source of epithelium
  • A stimulus for proliferation
  • Growth and bone resorption
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6
Q

What are the sources of epithelium for the different cyst types.

A

Radicular cysts develop from remnants of Hertwigs Root sheath (periodontal ligament contains epithelial remnants called rest cells of Malassez). Follicular cysts develop from the reduced enamel epithelium. Odontogenic keratocysts and gingival cysts develop from remnants of the dental lamina (enamel organ develops from this)

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7
Q

What is the stimulus for proliferation for cysts?

A

Inflammation and an apical granuloma for radicular cysts. Periodontitis for inferior lateral periodontal cysts and pericoronitis for paradental cysts. For developmental cysts the factors are largely unknown. For a dentigerous cyst it may be eruptive force, proliferation and hydrostatic pressure. For a keratocyst it may be epithelial proliferation, hydrostatic pressure and tumour.

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8
Q

How do cysts grow and expand (three ways)?

A

Osmosis and hydrostatic pressure:

  • Cytokines cause cyst to grow
  • Ball of cells exceeds capacity of blood supply to keep alive so cells in the centre break down forming a rim of viable cells and hypertonic centre
  • Hypertonic centre wants to bring water in to make it isotonic so water drawn in by osmosis
  • Hydrostatic pressure increases so cyst expands - unicentric expansion
  • E.g. radicular and dentigerous cyst

Proliferation of the lining:

  • Enlargement of the cyst at the peripheries due to active division of the cells of the epithelium of the lining of the cyst
  • Finger like projections are zones of active cell division or proliferation
  • e.g. Odontogenic keratocyst

Bone resorption:

  • IL1 and IL6 (cytokines)
  • Prostaglandins
  • Endotoxins
  • Stimulation and activation of osteoclasts
  • All incorporate methods whereby they stimulate bone to be resorbed
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9
Q

What is a radicular cyst?

A

They arise in the periodontal ligament from the epithelial cell rests of malassez as a result of inflammation following death of the pulp. It is always associated with a non-vital tooth. It can be apical at the apex of a tooth associated with the opening of a root canal. It can be lateral at the side of a tooth associated with a lateral branch of the root canal. It can be residual which is a radicular cyst which has persisted after extraction of the associated tooth. Radicular cysts are mostly in younger patients, in the maxilla and mostly affect incisors. It always develops in a periapical granuloma. Proliferating odontogenic epithelium leads to a cyst.

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10
Q

What features are seen in the histology of a radicular cyst?

A

Mucous metaplasia is seen in 15%. Cholesterol is a bi-product of the cells breaking down and it tends to gather as crystals. Cholesterol crystals are seen in 30%. Mucous cells are seen in 15%, hyaline bodies in 10%, cilia in 10% and keratin in 2%.
Non-keratinised stratified squamous epithelium is seen.

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11
Q

How can you tell the difference between cysts and granulomas?

A

Cysts tend to be larger, more radiolucent, well-defined, corticated and painless. But only 50% are diagnosed correctly pre-operatively. The larger the lesion the more likely it is to be a radicular cyst. At 1-1.4cm 50% are cysts, at 1.5-1.9cm 65% are cysts and at 2cm+ 90% are cysts.

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12
Q

What is a collateral/paradental cyst?

A

It is a cyst which arises on the lateral aspect of a tooth as a result of inflammation in a periodontal pocket. It arises from pocket epithelium. A particular type of paradental cyst arises at the buccal aspect of partially erupted molars. The histology is similar to the radicular cyst.

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13
Q

What is a follicular cyst?

A

They surround the crowns of unerupted teeth and arise from the reduced enamel epithelium. Dentigerous cysts are associated with an impacted tooth and eruption cysts are associated with an erupting tooth. It forms due to the follicular epithelium proliferating. An eruption cyst lies just beneath the oral mucosa and attaches at the ACJ.

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14
Q

What is an odontogenic keratocyst?

A

It is a cyst arising in the tooth bearing area from remnants of the dental lamina. It is characterised by a thin lining of parakeratinised stratified squamous epithelium. It may replace a tooth. There is epithelial proliferation which may be due to genetics or trauma. There is often little or no bucco-lingual expansion of the jaw. The recurrence varies between studies. Daughter cysts can form in the connective tissue and these can be left behind which can lead to recurrence. There is fragility of the lining.

  • 62% occur in males
  • 75% in the mandible
  • 50% in the lower third molar area
  • 50% associated with an unerupted tooth
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15
Q

What syndrome is associated with odontogenic keratocysts?

A

Gorlin Goltz/basal cell naevus syndrome.

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16
Q

What is basal cell naevus syndrome?

Don’t confuse with Gardner’s - multiple osteomas

A

It is autosomal dominant, chromosome 9q, prevalence is 1:60000. The features are:

  • Multiple and recurrent odontogenic keratocysts (tend to occur before 25, recurrence common)
  • Basal cell carcinomas of the skin (not limited to sun exposed areas, scarring on face and neck)
  • Frontal bossing (frontal region of skull is wide) and hypertelorism (eyes are wide set)
  • Skeletal abnormalities e.g. bifid ribs - like a wishbone
  • Cervical rib - rib coming off cervical vertebrae, compresses nerves passing to arms so there will be problems with sensation and motor function of arms
  • Cranial abnormalities e.g. calcification of falx cerebri (between right and left hemisphere of brain, if calcified there will be greater conduction leading to epilepsy
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17
Q

What is the evidence that an odontogenic keratocyst may be a benign neoplasm?

A
  • High proliferation rate in the epithelial lining
  • High rate of recurrence
  • Aggressive and infiltrative growth
  • Association with basal cell carcinoma in Gorlin Goltz
    - Molecular changes similar to basal cell carcinoma
    - PTCH (chromosome 9q) mutation in BCC and Gorlins
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18
Q

How have odontogenic keratocysts been classified and reclassified?

A

WHO classification 2005 renamed keratocyst as keratocystic odontogenic tumour. It was not widely accepted. In 2017 WHO classification reverted to odontogenic keratocyst.

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19
Q

What is a lateral periodontal cyst?

A

They occur on the lateral aspect or between the roots of vital teeth. It is developmental in origin from the rests of Serres. Occasionally it is multilocular and is called botryoid odontogenic cyst. Localised thickening of the lining is common.

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20
Q

What are gingival cysts?

A

In infants they arise from the dental lamina rests in the alveolar mucosa of infants (alveolar cysts) and are lined by thin parakeratinised epithelium.
In adults they arise from the dental lamina rests in the attached gingiva. They are lined by non-keratinised epithelium.

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21
Q

What is a glandular odontogenic cyst?

A

A cyst characterised by cuboidal or columnar epithelium with mucous production. Forms duct-like or glandular structures.

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22
Q

What is a calcifying odontogenic cyst?

A

There was a change in the 2017 classification and it is no longer a tumour. It is most common in aged 10-30 in the mandible and maxilla. Radiolucencies but may have calcifications. The histology shows a cyst lined by ameloblastoma like epithelium with ghost cells and dentine in the wall. It may be solid - odontogenic ghost cell tumour.

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23
Q

What is a nasopalatine duct cyst?

A

Nasopalatine duct cysts arise in the nasopalatine (incisive) canal from epithelial residues of the nasopalatine duct. They are lined by respiratory epithelium or stratified squamous epithelium or often both. The hard palate forms by the fusion of three processes. The point where they meet is where the nasopalatine duct arises and this is shown by the inciisve papilla.

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24
Q

What is a nasolabial cyst?

A

It arises in the soft tissue overlying the alveolar process at the base of the nostril deep to the nasolabial fold. It probably arises from remnants of the nasolacrimal duct and is usually lined by pseudostratified columnar epithelium.

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25
Q

What are cystic lesions of the jaws?

A

They don’t have an epithelial lining. It can be a solitary (simple) bone cyst or Stafne’s bone cavity.

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26
Q

What are the ways of removing cysts?

A
  • Enucleation - removal of the cyst in its entirety without cutting, blunt dissecting it out
  • Curettage - Removal of tissue by scraping and scooping in portions
  • Resection - removal of part of an organ, takes pathology and margin of normal tissue
  • Marsupialisation - creation of a pouch by suturing the cyst lining to the external surface, the pouch can heal from the base upwards
    The approach for most cysts is enucleation.
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27
Q

When would you apicect a tooth?

A
  • Anterior tooth (mainly)
  • Acceptable orthograde RCT
  • Patient accepts risks e.g. recession
  • Consider implant first
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28
Q

What are the indications for apicectomy (need both)?

A
  • Persistent symptoms/pathology in a non-vital tooth
  • Re-RCT is unfeasible

Apicectomy more likely to work in short term than re-RCT but re-RCT more successful in longterm.

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29
Q

What may the persistent symptoms of a tooth requiring apicectomy be?

A
  • Apical cyst
  • Swelling
  • Discharge
  • Mobility
  • Pain
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30
Q

When is re-RCT unfeasible?

A
  • Adequate re-RCT has failed
  • Sclerotic canals, cannot instrument
  • Canal morphology e.g. curvature, accessory canals
  • Post-crown, cannot remove
  • Complex crown/bridge, perforation more likely than instrumentation
  • Root perforation
  • Fractured instrument, cannot retrieve
  • Fractured root
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31
Q

What are the relative and absolute contraindications to apicectomy?

A
Relative:
- Previous apicectomy 
- Poor OH
- Molars
- Active caries
- Advanced perio
- Implant 
- Unwilling to have LA
- High mobility index
- Sinus disease (recurrent sinusitis)
Absolute:
- Severe bleeding disorder
- Endocarditis risk
- Unrestorable tooth
- Post-crown retrievable
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32
Q

How is an apicectomy done?

A
  • Ideally enucleate, may have to curettage if friable
  • Apical 3mm of root removed (apical delta)
  • Don’t need to remove to base of bone cavity
  • 90 degrees to long axis of tooth
  • IRM vs MTA as retrograde RCT
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33
Q

What are the types of flap design?

A
  • Mucoperiosteal
  • Semi-lunar
  • Leubke-Oschenbein
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34
Q

What is a semi-lunar flap?

A

It is not used anymore. There is scarring and the potential to leave a margin of incision overlying the cystic cavity - void.
(See image in notes)

35
Q

What is a Leubke-Oschenbein flap design?

A

It is 4mm below the gingival margin but in the attached mucosa which is not possible in some people who don’t have enough attached mucosa. It can leave scarring. There are difficulties with the location of the gingival sulcus as you may expose the root surface rather than bone. Other questions you would need to ask:
- where is the crestal bone for a tooth that is non-vital and infected
- where do you stitch the flap
- blood supply to marginal gingivae is not healthy
(Image in notes)

36
Q

What are the benefits and a risk of a mucoperiosteal flap?

A

It provides the best access, minimal scarring and there will be some gingival recession. It can be modified with the reverse hatchet incision which improves the blood supply to the tissue not in the flap.
(Image in notes)

37
Q

What is the apical delta?

A

It tends to be 3mm and has lots of bacteria due to the structure. You make an incision at 90 degrees to remove it in its entirety. The historical method was 45 degrees but this would leave some apical delta behind leading to infection or it would remove too much root.

38
Q

What is MTA made of and what is the difference with portland cement?

A
The components of MTA are:
- Tricalcium silicate
- Dicalcium silicate 
- Tricalcium aluminate 
- Tetracalcium aluminoferrite
- Gypsum
- Bismuth oxide
The only difference with portland cement is the addition of bismuth oxide which is added for radiopacity.
39
Q

What are the recurrence rates for the different treatment options for an odontogenic keratocyst?

A
  • Curettage 19.2%
  • Enucleation alone 28.7%
  • Enucleation with carnoys 1.6%
  • Radical enucleation and cryotherapy 31.3%
  • Marsupialisation 24.4%
  • Resection 0%
40
Q

What is Carnoy’s solution?

A

It is a fixative so can damage the ID nerve. Vorschmidt’s technique was developed which involves accessing the cyst through the mandible by removal of bone, deroofing the cyst and removing the contents. You are left with a cyst wall which has a high tendency to recur. Place Carnoy’s fixative into the wall and the lined cavity limits where the fixative can pass. Leave this for 5 minutes and it will fix the wall of the cyst and then you scrape it out with the daughter cysts. You avoid the fixation of the ID nerve by fixating before enucleating. This results in a significantly reduced recurrence rate.

41
Q

What is the treatment for follicular cysts?

A

Dentigerous cysts are enucleated along with extraction of the tooth. An eruption cyst requires no treatment.

42
Q

What is a mucus extravasation cyst and the treatment?

A

It is a cyst without a true epithelial lining. If you bite a duct of a minor salivary gland this will damage it and saliva pools under the surface of the skin. It will be encased by a condensed connective tissue border. The management is blunt dissection/excision. There is difficulty with removing it as it is housed in soft tissue, scarring/fibrosis and not epithelially lined. Make an incision through the centre or around the cyst and you also need to remove the minor salivary gland so that it doesn’t recur.

43
Q

What is a sebaceous (epidermoid) cyst?

A

It contains keratin not sebum and is formed due to punctum where injury causes implantation of the skin and tethering. There is traumatic implantation of skin and a cyst forms from this. It is acquired. You create an elipse and blunt dissect the cyst away.

44
Q

What are the components of bone and the blood supply?

A

Bone has a gross structure which has two main components: compact/cortical bone around the outside and trabecular bone in the centre. In the marrow spaces there is haematopoietic marrow and fat. Osteons are where blood vessels are and these surround Haversian canals. There are holes in bone (lacunae) which contain cells (osteocytes) and this is a good indicator that the bone is alive.
Blood supply is from the periosteal blood supply which carries nutrients into the bone. There is some blood supply from vessels in the bone but most is from the periosteum. Every time you raise a periosteal flap you interrupt this and this can lead to devascularisation.

45
Q

What is mature and immature bone called?

A

There is lamellar bone which is mature and woven bone which is immature bone. Woven bone is very haphazard in how the collagen fibres are arranged. There will be lots of osteoblasts on the surface. Woven bone will fill a healing socket and will then be remodelled into lamellar bone.

46
Q

How does bone remodelling occur and why?

A

Bone is laid down on the surface of bone (some osteoblasts form osteocytes). It is removed by osteoclasts which are large multinucleate cells. Turnover occurs in response to forces on bone. It results in resting and reversal lines.
Bone remodelling is due to:
- Mechanical stimuli
- Systemic hormones
- Parathyroid hormone PTH comes from the parathyroid gland on the back surface of the thyroid gland, it stimulates resorption of bone so increases the level of serum calcium
- Vitamin D3 causes increased absorption of calcium from the diet so increased serum calcium
- Oestrogen controls function of osteoblasts
- Others e.g. calcitonin control osteoclast function
- Cytokines (inflammatory)
- Complex interactions promote growth of cells and bone matrix

47
Q

What special tests can be done for bone biochemistry?

A
  • Serum calcium
  • Osteoblast activity (bone formation)
    • Serum alkaline phosphatase
    • Osteocalcin
  • Osteoclast activity (bone resorption)
    • Collagen degradation urine and blood
  • Parathyroid hormone: regulates serum calcium
  • Vitamin D assays
48
Q

Name 4 developmental abnormalities of bone and explain each one?

A

A torus is a developmental exostosis and causes problems with fitting dentures as they rock and become unstable. Torus palatinus is in the midline of the palate and torus mandibularis is bilateral on the lingual aspect of the mandible (canine area). Histologically there will be layers of cortical bone laid down.

Osteogenesis imperfecta is a type I collagen defect and the inheritance is varied and there are 4 main types. Clinically the patient has weak bones and multiple fractures. It sometimes associates with dentinogenesis imperfecta.

Achondroplasia is autosomal dominant, is dwarfism and caused by poor endochondral ossification.

Osteopetrosis is inherited and is due to a lack of osteoclast activity. There is failure of resorption. The jaw is formed of just compact bone so it is brittle and has a tendency to fracture. There will be marrow obliteration due to a problem with production of white blood cells.

49
Q

What are the 4 infections of bone?

A
  • Dry socket (alveolar osteitis) - very common
  • Sclerosing osteitis - relatively common
  • Osteomyelitis - rare
  • Osteonecrosis - rare but increasingly more common
50
Q

What is a dry socket?

A

It is also called alveolar osteitis. It usually affects molars, particularly impacted 3rd molars. It is caused by loss or failure of the clot to develop in a socket. This may be due to excessive rinsing, fibrinolysis of clot, poor blood supply due to radiotherapy or Paget’s disease and excessive use of vasoconstrictors. It is a localised inflammatory reaction in bone adjacent to the socket. The bone adjacent to the socket becomes necrotic and is removed by osteoclasts. Healing is very slow so and it needs irrigation and an antiseptic dressing. It very rarely develops into osteomyelitis.

51
Q

What is sclerosing osteitis?

A

It is also called focal sclerosing osteitis, condensing osteitis or bone scar. The differential diagnosis may be hypercementosis, cementoblastoma and osteoma.
It is a focal bone reaction to low grade inflammation e.g. chronic pulpitis. It occurs at any age and commonly affects the mandibular molars. It is asymptomatic and an incidental finding. Radiographically there will be a uniform opacity at the apex of the tooth, often with a peripheral radiolucency. Treatment is for the inflammatory cause and it can be left behind when the tooth is extracted.

52
Q

What is osteomyelitis?

A

It is inflammation within marrow cavities of bone. It can affect any age and can be acute or chronic. The subtypes are sclerosing osteomyelitis and proliferative periostitis (Garre’s osteomyelitis). An inflammatory process irritates the periosteum and lays down new bone.

53
Q

What is osteomyelitis due to?

A
  • Blood supply (age related, Paget’s disease, radiotherapy)
  • Host response (immunosuppression, poor nutrition)
  • Other causes (bisphosphonates)
    It doesn’t tend to occur in normal healthy patients.
54
Q

What is the cause, symptoms and histology of acute osteomyelitis?

A

The aetiology is most commonly infectious (staphylococci, streptococci). It can be an extension of a periapical abscess or due to physical injury/fracture. It is an acute inflammatory response leading to pain, pyrexia, lymphadenopathy and malaise. The histology will show acute inflammatory infiltrate, increased bone resorption and decreased bone formation.

55
Q

What is the aetiology, symptoms and histology of chronic osteomyelitis?

A

The aetiology is a low grade inflammatory reaction and it may be a progression from acute osteomyelitis. There is a chronic inflammatory response associated with low grade infection which leads to pain, swelling, bone loss and sequestrae (piece of dead bone that has become separate from normal bone). The histology shows chronic inflammatory infiltrate, both osteoclastic and osteoblastic activity, reversal lines and osteonecrosis. Proliferative periostitis is chronic osteomyelitis with periosteal inflammation.

56
Q

How is osteomyelitis treated?

A

You need to resolve the source of the infection, remove the infected bone and use hyperbaric oxygen.

57
Q

What are the types of osteonecrosis of the jaws?

A

Osteoradionecrosis is a complication of irradiation of head and neck malignancies. There is compromised vasculature (endarteritis obliterans).
Bisphosphonate/medication related osteonecrosis of the jaws (MRONJ, BRONJ, DRONJ) is associated with certain medications such as bisphosphonates, denosumab.

58
Q

What are the other factors that increase the risk of osteonecrosis?

A
  • Smoking
  • Diabetes
  • Poor oral hygiene
  • Prolonged drug use
  • Dental extractions
    (all reduce blood supply)
59
Q

How can osteonecrosis be prevented?

A
  • Dental assessment
  • Oral hygiene
  • Smoking cessation
  • Limiting alcohol
60
Q

What is the management for low and high risk patients of osteonecrosis?

A

A low risk example is osteoporosis and there should be atraumatic extractions. A high risk example is malignancy, paget’s, immunosuppressed, history of MRONJ and you should refer to OS/OMFS.

61
Q

What are the types of benign and malignant bone neoplasms?

A

Benign includes osteoma and osteoblastoma.

Malignant includes osteosarcoma, chondrosarcoma.

62
Q

What is an osteoma?

A

It is a localised or bony nodule in the maxilla or mandible which shows continued growth. It is different from a torus and may be associated with syndromes e.g. Gardners. Radiographically it is radiopaque. Histologically it is composed of compact bone or compact and cancellous bone.

63
Q

What is osteosarcoma?

A

It is a malignant tumour which produces bone, mostly seen in long bones. It is very rare (120 cases per year in all sites) and there are about 10 jaw lesions per year in the UK (2-10% in jaws). It is seen in young adults.

64
Q

What are the features of osteosarcoma of the jaws?

A

It is mostly seen in age 20-40 and males are slightly more common. It is more common in the mandible than the maxilla. Early diagnosis is essential as it is a rapidly growing swelling, painful and there is nerve involvement. The radiographic features are radiolucency with bone formation (sunray) and loss of lamina dura is an important sign also.

65
Q

How is a patient with osteosarcoma managed?

A
  • Neo-adjuvant chemotherapy
  • Wide local excision +/- radiotherapy
  • 5 year survival - about 50%
66
Q

What are fibro-osseous lesions and how do they present radiographically?

A

They are lesions where normal bone is replaced by fibrous tissue in which abnormal bone is laid down. Radiographically there is initially a radiolucency because of bone loss and later there is a more mixed radiodensity lesion as the abnormal bone is laid down. The extent of this varies with the lesion and some lesions are almost always radio-opaque or radiolucent.

67
Q

What are the types of fibro-osseous lesion?

A
  • Neoplastic - (cemento) ossifying fibroma
  • Developmental - fibrous dysplasia
  • Reactive - (cemento) osseous dysplasia
  • Osteodystrophy idiopathic - Paget’s disease
68
Q

What is ossifying fibroma?

A

It is a benign neoplasm composed of fibrous tissue which forms spicules, islands of cementicles of bone. The most common age range is 20-50 and the average is 35 years, but children can be affected. Females are more common than males (3:1) and the mandible is overall the most common site (65%) in the premolar or molar region. It may be in the craniofacial bones. You may see some bone expansion and a well defined mixed radiopacity lesion radiographically.
Histologically the lesion has a well defined margin and is separated from the cortical bone. It is a fibrous lesion with trabecular bone laid down which does not resemble normal bone – bluer and more like cementum (basophilic) – why it is sometimes referred to as cemento ossifying fibroma. Some bone may resemble bone and some may resemble cementum (no osteocytes within it). The bone is randomly arranged with abnormal shapes. The fibrous tissue is more cellular (modified fibroblasts) than fibrous dysplasia. You need to consult the imaging to make a diagnosis.

69
Q

How is a patient with ossifying fibroma managed?

A
  • Conservative enucleation
  • Resection
  • Low recurrence rate
70
Q

What is fibrous dysplasia?

A

It is a developmental disorder of bone with mutations in GNAS1 and it is not inherited. 25% affect the head and neck and the maxilla is the most frequent site when it does affect the head and neck. It is most common in ages 15-30 and males and females are equal. It presents as a painless, smooth, enlargement/swelling and radiographically there is a poorly demarcated radiolucency with a stippled orange peel effect which merges with the surrounding bone. Histologically there is fibrous tissue and irregular trabeculae of bone laid down in this. It is less cellular (modified fibroblasts) than ossifying fibroma and the cells are more scattered. We often see retraction artefacts (result of processing – white spaces around bone) around trabecular bone. In fibrous dysplasia islands of bone often resemble bone and have osteocytes and are eosinophilic like normal bone. This is not exclusive (not always the case) so check the radiography). The margin of the lesion is poorly defined. There can be occasional blood vessels.

71
Q

What are the clinical variants of fibrous dysplasia?

A
Monostotic (single bone involved):
- Single skeletal lesions
- Ribs and femur most common site
- 25% of lesions in head and neck
- Age 15-30 (average 25)
- Males = females
Polyostotic (multiple bones involved):
- Multiple lesions
- Head and neck involved in 50%
- Age <15
- 75% in females
- May be part of McCune Albright's syndrome
72
Q

How do you manage a patient with fibrous dysplasia?

A

The growth stabilises over time due to skeletal maturity. Treat by debulking and contouring the bone. There can be recurrence if it is treated during growth phase and it can reactivate in pregnancy. It can be surgically removed and there may need to be subsequent orthodontics/orthognathic surgery. There is a very low risk of malignant transformation.

73
Q

What are the differences between ossifying fibroma and fibrous dysplasia?

A

Fibrous dysplasia is a poorly defined lesion, which has no margin, males and females are equal and its often seen in the maxilla.
Ossifying fibroma is a well defined lesion with a clear margin. Females are more common than males and it is often seen in the mandible.

74
Q

What is (cemento) osseous dysplasia?

A

It is a clinicopathological spectrum of reactive lesions. It is seen in age 30-50 and often in females. There are often multiple radiopacities in the tooth bearing areas of the jaws. It is composed of irregular trabeculae of woven bone and cementum in a fibrous stroma.

75
Q

How is osseous dysplasia classified?

A
  • Focal is a single lesion in the jaw
  • Periapical is multiple lesions at the apex of teeth, often occurs on lower incisors, multiple mixed radiodensity lesions (radiolucent with radiopaque speckles within)
  • Florid - multiple lesions throughout the jaws
76
Q

What is familial gigantiform cementoma?

A

It is usually described as a variant of florid osseous dysplasia but it appears to be a different entity. It has an autosomal dominant inheritance pattern and is found in white patients. Male and female prevalence is equal.

77
Q

What is Paget’s disease?

A

It is a rare disorder affecting all bones. Bone turnover is increased and no longer related to functional demands. Early stage bone becomes very vascular (may result in heart failure) and later stage bone becomes sclerotic and shows numerous resting and reversal lines. It is more common in Western Europe, USA, Canada, Australia, New Zealand. It is rare in Asia and Africa. The cause is unknown and there may be a possible genetic/hereditary association or infective cause. The clinical features:

  • Legs become bowed
  • Enlargement of the skull causing constriction of foramen: deafness, hats do not fit etc
  • Jaws become enlarged: tooth spacing and dentures don’t fit
78
Q

What are the dental implications of Paget’s disease?

A
  • Bone sclerotic - difficulty with extractions and prone to infections
  • Hypercementosis - difficulty with extractions
  • Bisphosphonates may complicate matters
  • Increased incidence of osteosarcomas and other bone malignancy
79
Q

What are giant cell lesions of the jaws?

A

They are characterised by replacement of bone by fibrous tissue containing numerous multi-nucleate giant cells (osteoclasts). Examples are cherubism, central giant cell granuloma and hyperparathyroidism.

80
Q

What is cherubism?

A

It is a developmental condition with autosomal dominant inheritance. There is bilateral expansion of the posterior mandible which may regress after puberty. Histologically there are vascular multinucleated giant cell lesions.

81
Q

What are features of the other two giant cell lesions of the jaws?

A

They are reactive or hyperplastic lesions which are benign but may be locally destructive. They are seen in age 10-30 and 60% in females. It is usually seen in the mandible. They are characterised by osteoclasts.

82
Q

What is a central giant cell granuloma?

A

It is a well demarcated radiolucency composed of giant cells (osteoclasts). It may be destructive. The management is blood biochemistry (serum calcium initially - to check its not hyperparathyroidism), curettage, resection and there is a 20% recurrence rate.

83
Q

What is hyperparathyroidism?

A

It is also called a brown tumour and is identical to a central giant cell granuloma. It can be primary due to a parathyroid adenoma (90%) or secondary to renal failure or malabsorption. It is hereditary and autosomal dominant. There will be a radiolucent lesion. Blood biochemistry will show raised serum calcium, phosphate and PTH. The management is treatment of hyperparathyroidism, surgery.