3. Classification
A). Based on Morphology:
Long
bones
e.g. upper
and lower
limbs;
Have
marrow
cavity filled
with yellow
marrow
Short
bones
e.g. carpels
and tarsals;
Have
marrow but
lack marrow
cavity
Flat
bones
e.g. skull
and facial
bones;
Spongy
bone is
present
between
upper &
lower
layer of
compact
bone
Irregular
bones
e.g. sphenoid
and ethmoid;
Spongy bone
covered with a
thin layer of
compact bone
and has
marrow
without any
marrow cavity
Sesamoid
bones
e.g. patella;
Develop in areas
of pressure or
tension
5. B). Based on Development:
Endochondral
Replacement of hyaline
cartilage with bony
tissue.
e.g. bones of trunk and
extremities
Intramembranous
Replacement of sheet
like connective tissue
with bony tissue
e.g. cranial & facial flat
bones of skull, mandible
and clavicle
6.
7. C). Based on Microscopic Structure:
Mature Bone Immature Bone
-first formed bone
-rarely seen after
birth
-seen in alveolar
bone & during
healing of fractures.
Compact/Lam
ellar/Cortical
Bone
-well formed
concentric
lamellae around
haversian canal
Cancellous/Spongy/Trab
ecular Bone:
-irregular bony spikules
called âTrabeculaeâ around
marrow spaces.
10. Composition
⢠Mineral Content
⢠Hydroxyapatite crystals with
carbonate content & low Ca/P
ratio.
⢠Bone crystals as âleaf likeâ
structures aligned parallel to
collagen fibres.
⢠Narrow gaps between crystals
is associated with water and
organic macromolecules.
⢠Organic Content
⢠Mainly type I collagen
⢠Also type V
⢠Alveolar bone = type I + type
III + type V + type XII
collagen
⢠Sharpeys fibres contain type
III with type I collagen
⢠Type III & type XII are
produced by fibroblasts during
production of periodontal
ligament.
⢠Type I, V and XII are
expressed by osteoclasts.
11. Non Collagenous Proteins
1). Osteocalcin:
-Has amino acid â gamma carboxy glutamic acid
-Demonstrated in alveolar bone
-Carboxy terminal is chemo-attractant to osteoclasts precursors.
2). Osteopontin:
-Present in alveolar bone
-Heavily glycosylated & phosphorylated
-Aspartate is predominant
-Inhibits hydroxyapatite crystal growth
3). Bone Sialoprotein:
-Glutamic acid is predominant
-Initiation of mineral crystal formation
4).Osteonectin:
-Calcium binding glycoprotein
12. Bone Histology
⢠Periosteum
⢠Endosteum
⢠Circumferential lamellae
⢠Concentric lamellae
⢠Haversian canal
⢠Haversian canal + Concentric Lamellae = OSTEON
⢠Reversal Line: sharply delineated by cement lines which is highly
basophilic(due to rich content of glycoproteins & proteoglycans) and marks
the limit of bone erosion prior to osteon formation.
⢠Resting Line
⢠Volksmann canal connects the osteons and the periosteum.
⢠Lacunae containing osteocytes at the junction of lamellae
⢠Canaliculi radiating from lacunae; helps in exchange of nutrients and
wastes between lacunae (osteocytes).
⢠Interstitial lamellae: present between osteons; remnants of osteon, left
behind during remodelling.
Fibrocollagenous layer
(outer)
Inner layer with bone cells with rich
vascular supply
15. ⢠Non heridetary disorder of unknown cause.
⢠Can occur in any part of the skeleton but the
bones of skull, thigh, ribs, upper arms and pelvis
are most commonly involved.
⢠It is not a form of cancer.
⢠Most lesions are monostotic, asymptomatic &
identified incidentally & can be treated with
clinical observation.
16. Etiology
⢠Post zygotic mutation in GNAS 1 gene(20q.13.2)
⢠GNAS 1(Guanine Nucleotide Binding Protein- alpha
stimulating activity polypeptide)gene encodes a G-
protein that stimulates the production of cAMP.
⢠Continuous activation of G-protein leading to over
production cAMP in the affected tissues.
⢠Hyperfunctioning of the affected endocrine organs.
⢠Leading to
i. Precocious puberty
ii. Hyperthyroidism
iii. GH & cortisol overproduction
iv. Increased proliferation of melanocytes resulting in
large Cafe-au-lait spots with irregular margins.
v. cAMP affects the differentiation of osteoblasts leading
to fibrous dysplasia
17. Pathophysiology
⢠Medullary bone is replaced by fibrous tissue which
appears radiolucent on radiographs-âGround Glass
Appearance â.
⢠Trabeculae of woven bone contains fluid filled cysts that
are embedded largely in collagenous fibrous matrix.
⢠Bony trabeculae are abnormally thin & irregular & often
described as âChinese Charactersâ
.
⢠Fibrous Dyspalsia is characterised by âShepherdâs
Crookâ deformity which refers to coxa varus angulation
of proximal femur.
⢠Cause of transformation is not completely known,
however levels of transcription factor C-fos are raised
which leads to gene over expression & tumor formation.
18. Types
⢠Monostotic: Involvement of a single bone.
⢠Polyostotic: Many bones are involved.
Most severe form is McCune Albright
Syndrome
19. Clinical Features
⢠Four disease patterns are recognised:
i. Monostotic
ii. Polyostotic
iii. Craniofacial form
iv. Cherubism
Age : 3-15 years
2/3 of patients with polyostotic disease are asymptomatic before
they are aged 10 years.
Monostotic patients as old as 20-30 years are asymptomatic.
Males and females are equally affected.
Clinical findings of increasing pain & an enlarging soft tissue
mass suggest malignant change.
20. Monostotic Fibrous Dysplasia
70-80% of the lesions.
Most frequently occurs in the ribs(28%),
femur(23%) and humerous in decreasing order of
frequency.
The clinical term âLeontiasis Osseaâ has often been
applied to cases of fibrous dysplasia which affect the
maxilla or facial bones & give the patient a leonine
appearance.
21. Clinical Features
⢠Age: children & young adults.
⢠Sex: equally affects males &
females
⢠Painless swelling or bulging of
jaws.
(usually involves labial/buccal
plate; when it involves
mandible, sometimes it causes a
protruberant excrescence of
inferior border)
⢠Malalignment, tipping of teeth
due to progressive expansile
nature of lesion & tenderness
may develop.
⢠Malocclusion
⢠Mucosa over the lesion is
invariably intact.
(Fibrous Dysplasia of maxilla is
a serious form of disease since it
has marked predilection for
occurrence in children & is
impossible to eradicate without
radical, mutilating surgery).
⢠lesions extend locally to involve
maxillary sinus, zygomatic
process & floor of orbit & base of
skull.
⢠Bulging of canine fossa
⢠Extreme prominence of
zygomatic process
⢠Marked facial deformity
22. Radiographic Features
⢠Has 3 basic patterns:
i. Small, unilocular/large, multilocular with well
circumscribed border containing a network of fine
bony trabeculae.
ii. Increased trabeculations render the lesion more
opaque-Mottled Appearance
iii. Many delicate trabeculations-Ground Glass or peau
dâ orange appearance; it is not well circumscribed
and blends into adjacent normal bone.
⢠In all types, cortical plate is thinned because of
expansile nature of growth.
24. Histopatholgy
⢠Lesion is fibrous composed of proliferating
fibroblasts in compact stroma of interlacing
collagen fibres.
⢠Irregular bony trabeculae are scattered
throughout the lesion without any definite
pattern- âChinese Characterâ shaped.
⢠Trabeculae are of coarse, woven bone.
25.
26. Treatment
⢠Surgical removal of lesion.
⢠Lesions with type III radiographic findings
should be block resected.
⢠Malignant transformation into osteosarcoma.
27. Mc Cune Albright Syndrome
or
Polyostotic Fibrous Dysplasia
Defined as association of polyostotic
fibrous dysplasia, precocious puberty,
cafĂŠ-au-lait spots & other
endocrinopathies due to hyperactivity
various endocrine glands.
28. Etiology
⢠Post zygotic activation mutation of GS alpha
gene in affected tissues.
⢠GS alpha subunit is a component of G-protein
complex, which couples hormone receptors to
Adenylyl Cyclase (intracellular second
messenger) in a submembrane site.
29. Clinical Features
⢠Precocious puberty associated with the condition is gonadotrophin-
independent.
⢠Acromegaly
⢠Gonadotrophin-McCune Albright Syndrome
⢠Hyperprolactinemia
⢠Some severely affected patients may present with associated
hepatic, cardiac and GI dysfunction.
⢠Cutaneous pigmentation is the most common extraskeletal
manifestation & is ipsilateral to side of bony lesions.
⢠CafÊ-au-lait spots are related to amount of melanin in basal cells
of epidermis.
⢠Pigmentation may occur at birth & may precede the development of
skeletal & endocrine abnormalities.
32. Histopathology
⢠Areas of fibrous metaplasia within flat and tubular
bones.
⢠Progressively expanding fibrous lesion of bone
forming mesenchyme.
⢠Concentric expansion in an outward direction within
the medullary bone.
⢠Well-defined, non-encapsulated.
⢠Lesions are rich in spindle shaped fibroblasts with a
swirled appearance within the marrow space.
33. Treatment
⢠Mild cases: surgical radiation
⢠Severe cases: X-ray radiation
⢠Prognosis depends on the degree of skeletal
involvement.
⢠Malignant transformation into osteosarcoma
can also occur.
35. Pathogenesis
⢠Periodontal origin; or
⢠Defect in extraligamentary bone remodelling
that maybe triggered by local factors or possibly
by hormonal imbalance.
36. Types
⢠Based on clinical and radiographic features, it is
divided into three groups:
i. Focal cemento-osseus dysplasia
ii. Periapical cemento-osseus dysplasia
iii. Florid cemento-osseus dysplasia
37. Focal Cemento-Osseus Dysplasia
⢠Exhibits a single site of involvement.
⢠Most commonly in black females with a
predilection for 3-6 decade.
⢠Posterior mandible is the commonest site.
⢠Usually asymptomatic with a positive vitality
test of the affected teeth.
⢠Most of the lesions are smaller than 1.5cm in
diameter.
38. Radiographic Features
⢠Lesions vary from being completely radiolucent to
densely radiopaque with a thin peripheral
radiolucent rim.
⢠Most common is a mixed radiolucent and
radiopaque pattern.
⢠Well defined lesion with a slightly irregular border.
⢠Occurs in both dentulous and edentulous areas.
40. Periapical Cemento-Osseus Lesions
⢠Also called as âCementomaâ,
âFibrocementomaâ, âPeriapical Fibro
Osteomaâ.
⢠Teeth associated with lesion is invariably vital.
⢠Involves periapical region of anterior mandible.
⢠Generally occurs between 30-50 yrs of age.
41. Radiographic Features
⢠Early lesions appear as circumscribed areas of
radiolucency involving periapical areas of tooth.
⢠Mature lesions create a mixed radiolucent and a
radiopaque appearance.
⢠Periodontal ligament is intact.
⢠There is no fusion to the teeth.
43. Florid Cemento-Osseus Lesions
⢠Most clinically extensive form of cemento-osseus dysplasia,
thus the term â âFloridâ.
⢠Common in black females with marked predilection for
middle aged to older adults.
⢠Multifocal involvement, not limited to anterior areas.
⢠May involve all the 4 quadrants.
⢠Asymptomatic.
⢠Dull pain and an alveolar sinus tract maybe present.
⢠Some degree of expansion maybe seen.
⢠Bilateral and symmetric involvement.
44. Radiographic Features
⢠Initially, lesion is predominantly radiolucent,
with time, becomes mixed and then
predominantly radiopaque with a thin
peripheral rim.
⢠Maybe totally radiopaque and blend with
adjacent normal appearing bone.
⢠Both, edentulous and dentulous areas are
affected.
46. Histopathology
⢠All 3 variants present a similar histopathologic picture.
⢠Tissue consist of fragments of cellular mesenchyme
composed of spindle shaped fibroblasts and collagen fibres
with numerous blood vessels.
⢠Free hemorrhage is typically noted interspersed
throughout the lesion.
⢠Within the fibrous connective tissue background is a
mixture of woven bone, lamellar bone & cementum like
particles.
⢠As the lesions mature and become more sclerotic, the ratio
of fibrous connective tissue to mineralised material
decreases.
⢠With maturation, the bony trabeculae become thick,
curvilinear structures that have been said to resemble the
shape of âginger rootsâ.
47.
48. Treatment
⢠For asymptomatic patients: regular recall
examinations with prophylaxis and
reinforcement of good home hygiene care.
⢠For symptomatic patients:
⢠Antibiotics
⢠Sequestration of sclerotic cement like masses
and is followed by healing.
⢠Saucerisation of dead bone.