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Bone pathology
1. Bone Pathology
Dr. Arsalan Malik
Assistant Professor (Oral Pathology)
ِحَّالر ِمنْحَّالر ِهللا ِمْسِبِيم
1
2. Osteogenesis Imperfecta
It is a heterogeneous group of heritable diseases characterized by impairment of
collagen maturation.
Collagen forms a major portion of bone, dentine, sclerae, ligaments and skin
Osteogenesis imperfecta imparts problems in every structure made by collagen
Abnormal collagen maturation results in thin cortex, fine trabeculation and diffuse
osteoporosis
upon fracture, healing will occur but may be associated with excessive callus
formation
2
3. Clinical & Radiographic Features
Blue sclerae, altered teeth, hypoacusis, long bone, spine deformities and joint
hyperextensibility
Radiographs show deformation of the long bones, multiple fractures and
wormian bones in the skull.
3
8. Type I Osteogenisis Imperfecta
Most common and mildest form
Mild to moderate bone fragility
Most fractures occur during preschool time
Hearing loss develops before 30
Sclerae is blue and help in diagnosis
Hypermobile joints and easy bruising
8
9. Type II Osteogenesis Imperfecta
Most severe form
Exhibits extreme bone fragility and frequent fracture
many patients are still born and 90 % die before 4 week of age
Opalescent teeth may be present
9
10. Type III Osteogenisis Imperfecta
Moderately severe to sever bone fragility
Sclerae is pale yellow or blue and fades as the child grows
Hearing loss and ligament hyperextensibility present
Many have normal teeth and some have opalescent teeth
10
11. Type IV Osteogenisis Imperfecta
Mild to moderately severe bone fragility
Sclera may be blue but fades with age
In 50 % of patients fractures are present at birth
Many have normal teeth and some have opalescent teeth
Frequency of fracture decreases with age
11
12. Histopathological Features
Bone architecture remains immature
throughout life
Failure of woven bone to become
transferred to lamellar bone
Teeth show abnormalities of dentine
similar to dentinogenisis imperfecta
Teeth appear opalescent
12
13. Treatment
There is no cure for this, symptomatic treatment is the only choice
Management of fractures is a major problem
Mainstay of treatment is physiotherapy, rehabilitation and orthopaedic surgery
Medical treatment with Bisphosphonates provides relief from pain but its long term
use is not recommended
In patients with severe malocclusion, orthognathic surgery is recommended
13
14. Osteopetrosis (Marble Bone Disease)
It is a group of hereditary skeletal disorders characterized by marked
increase in bone density resulting from a defect in remodelling caused
by failure of normal osteoclast formation.
Number of osteoclasts is normal but function is defective
Continuous bone formation and defective resorption results in
thickening of bone.
14
15. Clinical & Radiographic Features
Infantile Osteopetrosis
Patients having disease at birth or early infancy usually have severe
disease called malignant osteopetrosis
Facial deformity, broad face, hypertelorism, snub nose, frontal bossing.
Narrowing of arches due to delayed eruption is common
In dental radiographs roots of teeth are often invisible due to increased
density of bone
15
16. Clinical & Radiographic Features
Adult Osteopetrosis
It is discovered later in life and exhibits less severe manifestations
Inherited as autosomal dominant trait and termed benign osteopetrosis
Approx 40 % of patients are symptom free and long bones are not
effected.
Often It is diagnosed by increased bone opacity in dental radiographs
Frequent fractures and cranial nerve compression are common
16
18. Histopathological Features
Tortuous lamellar trabeculae
replacing the cancellous bone
Globular amorphous bone
deposition in the marrow space
Osteophytic bone formation
18
19. Treatment & Prognosis
Adult Osteopetrosis is mild in severity and is associated with long term
survival as compared to infantile type where patients die during 1st decade of
life.
Bone marrow transplant is the only hope for treatment
Supportive measures include transfusion, antibiotics, drainage and surgical
debridement
19
20. Cleidocranial Dysplasia
It is best known for its dental &
clevicular abnormalities
It is caused by the mutation in gene
that is responsible for osteoblastic
differentiation and bone formation
20
21. Clinical & Radiographic Features
Mainly the clevicles and skull are effected however other bones may be
involves.
Clevicles show varying degree of hypoplasia and malformation
In 1 % of patients, clevicles are absent
Patient’s appearance is diagnostic (Large head and frontal bossing)
skull radiographs show delayed suture closure or wide open throughout life
21
23. Histopathological Features
Insufficient bone resorption is the
reason for impaired tooth eruption
Some theories suggested impaired
cementum formation as a main
factor but it is not proved
23
24. Clinical & Radiographic Features
Patients often have a narrow high arched palate and increased chances of
cleft palate
Abnormal spacing in the lower incisors and delayed eruption of teeth
Supernumerary teeth are present
increased density of mandible and narrow maxillary arch
24
26. Treatment & Prognosis
No specific treatment exists for skull, clevicles and bone abnormalities
Regarding dental problems, full mouth extraction with denture
construction, auto-transplantation of impacted teeth with prosthetic
restoration
removal of the primary and supernumerary teeth followed by
exposure of permanent teeth
26
27. Focal Osteoporotic Marrow Defect
An area of hematopoitic marrow that is sufficient in size to produce
an area of radiolucency which is confused with an intraosseous
neoplasm.
It does not represent a pathological process
Reasons may be
Aberrant bone regeneration after tooth extraction
Persistence of fetal marrow
Marrow hyperplasia in response to increased demand for erythrocytes
27
28. Clinical & Radiographic Features
Asymptomatic and purely an
incidental finding
It appears a radiolucent area varying
in size
Defect have ill defined borders and
fine central trabeculae
No expansion of jaw is observed
28
29. Histopathological Features
The defects contain cellular hematopoitic
or fatty marrow
Lymphoid aggregates may be present
No abnormal osteoblastic / osteoclastic
activity
29
30. Treatment & Prognosis
Incisional biopsy often is necessary to establish diagnosis
No treatment is necessary as it is not a pathological condition
30
31. Paget’s Disease of Bone
It is characterized by abnormal and anarchic resorption &
deposition of bone resulting in weakening and distortion of
affected bones
Inflammatory, genetic and environmental factors may play a role
in this disease
31
32. Clinical Features
Men > Women
Whites > Blacks
Older > younger
Asymptomatic disease is usually diagnosed in radiographs taken for
other reasons or serum alkaline phosphatase levels.
Its frequency increases with age
32
33. Clinical Features
Disease may be monostotic (limited to one bone) or polyostotic (multiple
bones involved)
Bone pain is a frequent complaint
Pegetic bone often forms near joints and promotes osteoarthritic changes with
associated joint pain and limited mobility
33
34. Clinical Features
Jaw involvement is present in almost 17 % of cases
Maxillary involvement results in mid face enlargement
Nasal obliteration, enlarged turbinates, obliterated sinuses and
deviated septum
Alveolar ridges become enlarged and create problems for denture
wearers
34
35. Radiographic Features
Initial stages show decreased radiodensity of bone and alteration of the trabecular pattern.
During bone formation patchy areas of sclerotic bones formed giving a cotton wool
appearance in radiographs
Teeth often exhibit hypercementosis
35
36. Histopathological Features
Apparent uncontrolled alternating resorbtion and
deposition of bone.
In active resorptive stage numerous osteoclasts
surround the trabeculae
‘’Reversal lines’’ mark the junction between
alternating resorptive and formative phase
A highly vascular fibrous connective tissue replaces
the bone
36
37. Diagnosis
Patients show raised levels of serum alkaline phosphatase but
normal levels of calcium and phosphate
Serum alkaline phosphatase is considered the most specific marker
of bone formation
Urinary hydroxyproline levels often are markedly elevated
Lab parameters and clinical examination is sufficient for diagnosis
37
38. Treatment & Prognosis
Asymptomatic patients usually do not need treatment
In symptomatic cases, bone pain is controlled by acetaminophen or
NSAIDs
Neurological complications are due to pressure of bony structures on
cranial nerves. Use of Parathormone (PTH) antagonists can reduce bone
turnover and improve the biochemical parameters.
Dental patients may require new dentures due to increased size of
alveolar ridges.
38
39. Central Giant Cell Granuloma
It is considered to be a non neoplastic lesion
60 % cases arise before 30 years
Females > males
70 % cases arise in mandible
Anterior portion > posterior
39
40. Clinical Features
Some cases are asymptotic and diagnosed in routine radiographs
Symptomatic cases represent pain, paraesthesia or perforation of cortical
plate resulting in ulceration of overlying mucosa
Nonaggressive lesion
Exhibit few or no symptoms, slow growth, no cortical perforation / root resorption
Aggressive lesions
Pain. Rapid growth, cortical perforation, tendency to recur
40
41. Radiographic Features
Radiolucent defects which may be unilocular / multilocular
Range from 5 mm to 10 cm in diameter
D/D of unilocular lesions
Perioapical granuloma
Periapical cyst
D/D of multilocular lesions
ameloblastoma
41
42. Histopathological Features
Multinucleated giant cells in back ground of ovoid mesenchymal cells &
round monocyte-macrophages
Stroma is loosely arranged and edematous
Areas of erythrocyte extravasation and hemosiderin deposition are
prominent
Foci of osteoid and newly formed bone are occasionally present in lesion
42
44. Treatment & Prognosis
Usually treated by thorough curettage
Aggressive lesion show more tendency to recur
They require radical surgery for cure
Three alternatives to surgery are
Corticosteroids
Calcitonin
Interferon alfa-2a
44
46. Cherubism
It occurs due to spontaneous mutation in gene that codes for
protein responsible for activity of osteoblasts & osteoclasts during
bone formation
The term Cherubism is used because of pulmp-cheeked little angles
depicted in some paintings
46
47. Clinical Features
Usually occur between 2-5 years of age
Clinical alterations progress till puberty then stabilize and slowly regress
Bilateral involvement of the posterior mandible that gives chubby cheeks
‘’Eye upturned to heaven’’ appearance due to wide rim of sclera noted
below the iris
Marked cervical lymphadenopathy
47
48. Clinical Features
Mandibular lesions typically appear as painless, bilateral expansion of
the posterior mandible
Bilateral expansion is symmetrical
Maxillary tuberosity area may be involved
Widening and distortion of alveolar arches
Failure of eruption, impair mastication, speech difficulties, loss of
normal vision
48
49. Radiographic Features
Multilocular, expansile radiolucencies
Appearance is virtually diagnostic because of bilateral location
It typically involves the jaws but ribs & humerus may be involved
49
50. Histopathological Features
Lesional tissue consist of vascular fibrous tissue
containing variable number of multinucleated
giant cells
Giant cells are small and arranged focally
Foci of extravasated blood is common
Stroma tends to be loosely arranged
In older resolving lesions, tissues become more
fibrous, the number of giant cells decreases and
new bone formation is seen.
50
51. Treatment
In many cases lesion is self limiting after puberty
In some patients the recovery is very slow and in some the deformity
may persist
In some cases surgical curettage may result in early recovery and in
some cases it worsens the situation
Radiation therapy is contraindicated because of risk of development
of postirradiation stroma
51
52. Fibro-Osseous Lesions of the Jaws
It is a diverse group of processes that are characterized by replacement of normal
bone by fibrous tissues containing a newly formed mineralized product.
Fibrous Dysplasia
Cemento-Osseous Dysplasia
Focal Cemento-Osseous Dysplasia
Periapical Cemento-Osseous Dysplasia
Florid Cemento-Osseous Dysplasia
Ossifying Fibroma
52
53. Fibrous Dysplasia
A developmental tumour like condition characterized by replacement
of normal bone by an excessive proliferation of cellular fibrous
connective tissue intermixed with irregular bony trabeculae
It may involve one bone, multiple bones with or without cutaneous &
endocrine manifestations
Degree of severity depends upon time of mutation
53
54. Clinical Features
Monostotic Fibrous Dysplasia
80 – 85 % of cases
Limited to single bone
Male = females
Jaws are most commonly effected
Maxilla > mandible
Painless swelling of jaws
54
55. Radiographic Features
Ground glass appearance due to poorly calcified bony trabeculae arranged in a
disorganized pattern
In mandible, superior displacement of inferior alveolar canal is observed
In maxilla, sinus floor shifts superiorly
55
56. Clinical Features
Polyostotic Fibrous Dysplasia
Relatively uncommon
Combined with café au lait pigmentation
is termed as jaffee-Lichtenstein
syndrome
Combined with café au lait pigmentation
and endocrinopathies is termed McCune-
Albright syndrome
56
57. Clinical Features
Polyostotic Fibrous Dysplasia
Pathological fractures are common
Pain and leg length discrepancy is common
In Mc-Cune-Albright Syndrome, sexual disturbances are
observed in females as endocrine manifestations
57
58. Histopathological Features
Irregularly shaped trabeculae of immature bone in
a cellular, loosely arranged fibrous stroma
Bony trabeculae are not connected to each other
and assume a Chinese Script writing appearance
Lesional bone directly fuse to normal bone
without any capsule
Jaw and skull lesions undergoes maturation with
time
58
59. Treatment
Smaller lesions are easily resected without difficulty
Larger lesions are difficult to resect completely
Some lesion tend to regress with time but cosmetic
problems are addressed through surgery
59
60. Cemento-Osseous Dysplasia
Occurs in tooth bearing areas of the jaws and most common fibro
osseous lesion in clinical practice
Some believe it arises from periodontal ligament and some believe it
arises from defect in extra-ligamentry bone remodelling.
Three types are observed
Focal
Periapical
Folrid
60
61. Focal Cemento-Osseous Dysplasia
Single site of involvement
3rd – 6th decade
90 % in females
Asymptomatic , smaller than 1.5 cm in
diameter
Occur in posterior mandible
Lesion varies from completely
radiolucent to dense radio-opaque
61
62. Periapical Cemento-Osseous Dysplasia
Periapical region of anterior mandible
Female > Males
3rd – 5th decade
Asymptomatic radiolucency covering the
roots of several teeth
Lesions tend to mature with time
Does not expand the jaws
62
63. Florid Cemento-Osseous Dysplasia
Multifocal involvement not limited to anterior mandible
Bilateral symmetrical involvement
May remain asymptomatic or manifest as dull pain and bony expansion
Both edentulous and dentulous areas are involved regardless of
presence of teeth
63
65. Histopathological Features
All three patterns of cemento osseous dysplasia demonstrate similar
histopathological features
Tissues consist of fragments of cellular mesenchymal tissues composed of
spindle shaped fibroblasts and collagen fibres
Free haemorrhage is typically noted interspersed throughout lesion
Within this fibrous connective tissue background is a mixture of woven bone,
lamellar bone and cementum like particles
As the lesion matures, the amount of mineralized material increases
65
67. Diagnosis
In most instances, the distinctive clinical & radiographic picture of periapical &
florid types allow a strong preseumptive diagnosis without need of biopsy
In case of focal type. Features are less specific and often require surgical
intervention
Findings from surgery are helpful in discrimination between focal cement-
osseous dysplasia and ossifying fibroma
67
68. Treatment
They are not neoplastic so they usually do not need treatment
The best management option for asymptomatic patient is regular follow
up & maintaining better oral hygiene to avoid periodontal disease.
In symptomatic patients, antibiotics are given but not effective because of
dead sclerotic bone.
Saucerization of the dead bone may speed healing.
68
69. Ossifying Fibroma
It’s a true neoplasm with significant growth potential
Composed of fibrous tissue containing variable mixture of bony
trabeculae and cementutum like spherules.
The cementum like material in the lesion is variation of bone.
69
70. Clinical Features
Majority of cases are present in 3rd & 4th decade
Female predilection
Mandible > maxilla
Most common in peremolar & molar area
Smaller lesions are asymptomatic but large lesions cause painless swelling
of involved bone
Pain & paraesthesia are rarely present
70
71. Radiographic Features
Well defined and unilocular
May appear completely radiolucent because of calcified material
produced in tumour
True lesions are completely radio-opaque with thin radiolucent
border.
Root resorption or resorption may be seen
71
73. Histopathological Features
Lesion is well demarcated from
surrounding bone
Some are encapsulated others are not
Tumour is usually submitted in one large
or few small pieces
It consists of fibrous tissues of varying
cellularity and mineralized material hard
tissue portion consist of bone or
cementum like material
Intra-lesional haemorrhage is unusual
73
74. Treatment
Circumscribed nature of lesion allows enucleation of tumour with
ease
Large tumours may need surgical resection and bone grafting
Chances of recurrence are very rare
74
75. Osteoma
Benign tumours composed of mature compact or cancellous bone
These are strictly restricted to craniofacial region
Common palatal & mandibular tori are not considered as osteomas
75
76. Clinical Features
Osteoms of the jaws arise from surface of the bone or they may be present
in medullary bone
Asymptomatic and present in younger age
Body of the mandible, condyle are common locations
Condylar osteoms are considered to be true neoplasms
They disturb the occlusion by deviating the jaw to one side
Facial swelling, pain and limited mouth opening are other signs
76
77. Radiographic features
They appear as circumscribed sclerotic masses
Periosteal osteomas may exhibit uniform sclerotic pattern or sclerotic
margins with central trabeculae
Smaller osteomas are difficult to differentiate from foci of sclerotic
bone
The true mature osteomas can be confirmed by observing continued
growth
77
79. Histopathological Features
Compact osteomas are composed of
normal appearing dense bone showing
minimal marrow tissue
Cancellous osteomas are composed of
trabeculae of bone and fibrofatty
marrow.
Osteoblastic activity may be fairly
prominent
79
80. Treatment
Larger osteomas of the mandibular body causing symptoms or
cosmetic deformity are treated by surgical excision
Smaller asymptomatic osteomas present endosteally do not need
treatment but should be observed periodically
Condylar osteomas are surgically removed
Osteomas are completely benign and patients do not experience
malignant change
80
81. Gardner Syndrome
A rare disorder that is inherited as an autosomal dominant
trait. Approximately 1/3rd cases represent spontaneous
mutations
it is considered to be the part of a spectrum of diseases
characterized by colorectal polyposis
81
82. Clinical Features
The associated colonic polyps develop in 2nd decade of life.
They are adenomatous, they transform into adenocarcinomas.
Common skeletal abnormalities include osteomas
Skull, paranasal sinus and mandible are the commonly affected sites
Patients demonstrate 3 – 6 lesions
Osteomas appear as areas of increased radiodensity
Large osteomas will limit mandibular opening
82
84. Clinical Features
Dental abnormalities include multiple osteomas, multiple impacted teeth and
supernumerary teeth
Frequency of extra teeth is low as compared to cleidocrania dyaplasia
Patients show epidermoid cysts of skin
Increased prevalence of thyroid carcinomas is also noted
84
86. Treatment & Prognosis
The major problem is malignant transformation of colonic polyps
in adenocarcinoma
Prophylactic colectomy is recommended
Removal of jaw osteomas & epidermoid cysts are advised for
cosmetic reasons
86
87. Osteoblastoma & Oteoid Osteoma
These both are closely related tumours that represent identical
histopathological features but different clinical behaviours
Osteoid osteoma contain a concentration of peripheral nerves not seen in
osteoblastoma
It produces prostaglandins that results in pain which is relieved by
prostaglandin inhibitors like asprin.
osteomas are smaller than 2 cm & osteoblastoma is bigger than this
87
88. Clinical Features (Osteoblastoma)
Most commonly affected bone are vertebral column, sacrum,
calvarium, long bones & small bones of hand & foot
Occur before 30 years
Female predominance
Posterior region of mandible
2 – 10 cm
Pain, swelling & tenderness may lead to tooth mobility , root
resorbtion and tooth displacement
88
89. Radiographic Features (Osteoblastoma)
Well defined or ill defined radiolucent lesion often having a patchy areas of
mineralization.
Most osteoblastomas arise within the medulary bone however it may present as bony
projections from the periosteum of bone ( periosteal osteoblastomas)
89
90. Clinical Features (Osteoid Osteoma)
Occur in femur, tibia & phalanges
Very rare in jaws & pain is nocturnal &
relieved by salicylates
Mostly present out of the jaws
(extragnathic lesions)
90
91. Histopathological Features
Mineralized material that demonstrate reversal lines
At the periphery of large masses there are
multinucleated osteoclast like cells and numerous
osteoblasts
The supporting stoma consist of loose fibrous
connective tissues that contain loose vascular
channels
Aggressive osteoblastomas are marked by large
epitheliod cells with increased mitotic activity.
91
92. Treatment
Mostly cases of osteoblastoma & osteoid Osteomas are treated by
surgical excision or curettage
Prognosis is good and some lesions will regress even after
incomplete excision
92
93. Cementoblastoma
It is an odontogenic neoplasm of ameloblasts
No gender predilection
Mostly involves premolar & molar area of mandible
Signs of aggressive behaviour like bony expansion, cortical
erosion tooth displacement and infiltration into pulp chamber
may be observed
93
94. Radiographic Features
Radio-opaque mass fused to one or more roots and is surrounded by a thin radiolucent
rim
The outline and roots of the involved tooth is usually obscured as a result of root
resorption & fusion of tumour with tooth
94
95. Histopathological Features
It resemble osteoblastoma with the primary distinguishing feature of fusion
with the involved tooth.
Majority of the tumour consist of sheets and thick trabeculae of mineralized
material with irregularly placed lacunae & prominent basophilic reversal
lines.
Multinucleated giant cells are often present
Periphery of the lesion is composed of non calcified material which appears
as radiolucent rim on radiograph.
95
97. Treatment
Surgical Extraction of the tumour with involved tooth
Surgical excision of the mass with root amputation and
endodontic treatment may be considered.
Total removal of mass with tooth is closely related to chances of
recurrence.
97
98. Osteosarcoma
It is a malignancy of mesenchymal cells that have the ability to
produce osteoid or immature bone
Majority of osteosarcomas demonstrate intramedullary origin
but a small number may be justracortical
98
99. Clinical Features
It shows a bimodal age distribution 10 – 20 years and after 50 years
Initial peak occurs during the period of greatest bone growth and
involves proximal tibial metaphyses
In older age axial skeleton and flat bones are involved.
Peget’s disease & previous irradiation are associated with increased
prevalence
99
100. Clinical Features
Maxilla = Mandible
In mandible most tumours arise in posterior region
Maxillary tumours usually arise in inferior portion as compared to superior
portions
Swelling & pain are the most common symptoms.
Loosening of teeth, paresthesia and nasal obstruction can be seen
100
102. Radiographic Features
It varies from dense sclerosis to a mixed sclerotic and radiolucent lesion
to an entirely radiolucent process
Peripheral border of the lesion is ill defined and indistinct making it
difficult to distinguish the lesion
The classis sunburst appearance caused by osteophytic bone production
on the surface of the lesion is noted in about 25 % of jaw osteosarcomas
102