Bones (2)

BONE
www.indiandentalacademy.com

Bones are the units of the
skeletal system.

Classification of bone tissues
1. Shape of bones
• Long,short,flat,irregular,pneumatic,
sesamoid,supernumerary
2. Regions of long bone
• Epiphysis
• Diaphysis
• Metaphysis
3. Macroscopic appearance
• Compact bone
• Trabecular/cancellous/spongy bone
4. Developmental origin
• Intramembranous/dermal bone
• Intracartilaginous/endochondral bone

Morphology of bones

Histology of bone
• Periosteum
White fibrous layer
Elastic osteogenic layer

Histology of bone
• Haversian system
Haversian canals
Volkmann’s canals
Lamellae
Lacunae
Canaliculli

Histology of bone
• Types of lamellae:
Osteonic
Interstitial
Circumferential

High power view of part of an osteon in transverse section seen with transmitted
light.

Single osteon viewed with polarization optics to illustrate lamellar structurewww.indiandentalacademy.com

Histological sections of bone illustrating the various kinds of lamellaewww.indiandentalacademy.com

Osteocyte in lacuna.Arrow shows canalliculi.www.indiandentalacademy.com

Histogenesis of bone
• Intramembranous & Endochondral ossification.
• Histologically both bones are identical.
• Both are formed from mesenchymal tissue.

Intramembranous bone formation
A. Condensation of
mesenchyme around
capillary network at
specific points-Centres of
ossification
B. Cells converted into
osteoblasts
• Open faced
• nucleus,prominent
nucleolus
• RER & Golgi bodies
• Lysosomes containing
alk.phos.
C. Matrix(osteoid)
production:collagen,proteo
glycans etc.
Osteoblasts,blood vessels line the
growing bone spicule which is full
of osteocytes.
matrix

D. Calcification & woven
bone formation

Bone deposition
Osteoblast
Osteoid
Mineralized bone

Endochondral bone formation
A. Mesenchymal condensation
B. Cartilaginous model formed in
hyaline cartilage.

• Cartilage cells
enlarge(beginning from
ossification centre)
• Surrounding cartilage matrix
calcifies
• Cartilage cells die
• Calcified matrix left
behind(primary areolae)
• Perichondrium forms.

• Blood vessels invade from
perichondrium
• Perivascular cells
(OSTEOBLAST) and
OSTEOCLAST come along
with blood vessels.
• Osteoclast erode the primary
alveolae (secondary alveolae)
• Osteoblast form new bone
over secondary alveolae
• Woven bone formed.

Endochondral bone formation.
OB=osteoblasts
BM=bone
matrix
CM=cartilage
matrix
CE=capillary
epithelium

Development of cranium

An alizarin stained & cleared
fetus of about 14 weeks in
utero.Note the degree of
progression of ossification
from primary centres.Sternum,
carpals, tarsals & secondary
ossification centres are yet to
ossify.

Further development, growth & remodelling
All bone initially
formed is woven
bone(seen in infants,
alveolar bone in
which orthodontic
tooth movement has
recently occurred &
fracture repair sites)

Conversion of woven bone to mature bone

Bone remodelling = resorption + deposition
Old bone is being removed in segment A by osteoclasts,forming the cutting cone.In
segment B, osteoblasts begin to synthesize the osteoid(filling cone), the osteoid
mineralizes, becoming new bone.www.indiandentalacademy.com

Origin of the cells of the bone
•Osteoblasts are derived from
paravascular connective
tissue as an independent
process.
•Circulating osteoclast
precursor cells derived from
marrow,are the origin of the
osteoclasts.

Bone resorption
Classical features of a osteoclast:multinucleation, numerous
mitochondria(M), ruffled border(RF), golgi saccules(G)

Re(modelling).
A schematic cross section
of cortical bone shows
surface modelling (M),
which is the process of
uncoupled resorption and
formation.
Remodelling(R) is the turn
over of existing bone.

Re(modelling).
Surface modelling is noted
the PDL and the periosteal
surfaces. Bone
remodelling assists with
cortical bone resorption on
the right and replaces
immature bone on the left
side the alveolar process

Bone growth & modelling

Secondary ossification centres

Secondary ossification centres appear
at a later stage of growth.

Bone growth-the epiphysial growth plate
Hyaline cartilage
Zone of cell
multiplication
Zone of cell
hypertrophy
Matrix
calcification
Chondrolysis &
ossification

Bone growth & modelling
Scheme of the patterns of remodelling
occuring in the growth of a long bone
Periosteal resorption
Endosteal resorption
Endochondral bone formation
Periosteal deposition
Endosteal deposition

Bones & their response to applied stresses
• 1867 Meyer(anatomist) &
Culman(mathematician): propounded the
Trajectorial theory of bone formation.Trabeculae
develop along lines of stresses calculated
mathematically that enable it to best resist stresses
to which it is subjected during function.
• 1870’s Julius Wollf: trabecular arrangement can
change with a change in intensity & direction of
forces.

Trajectorial theory

• 1925 Beninghoff:Studied architecture of cranial &
facial skeleton & so called stress trajectories. The
trajectories obeyed no bone limits but rather the
demands of the functional forces.
• 1955 Sicher: Pillars of trajectories.

Pillars of trajectories

Frontal section of the maxilla and the
mandible in the plane of the first
molars.Because it transmits masticatory
load to the entire cranium the maxilla has
thin cortices connected by fine
trabeculae.the mandible is however loaded
in bending and torsion;it therefore is
composed of thick cortical bone connected
by coarse oriented trabeculae.

2D vectorial analysis of stress in the frontal section of the human
skull.relative to a bilateral bitting force 100 arbitary units , the load
is distributed to the vertical components of the mid face as
compressive stress(-ve).the horizontal structures are loaded in
tension (+ve)

• 1990 Frost : Mechanostat theory-Mechanical
loading is essential to skeletal health.Control of
most bone modelling & some remodelling process
is related to strain history.
The mechanostat provides a useful reference for
the hierarchy of biomechanical responses to
applied loads.

Mechanostat theory
Schematic drawing of the
Mechanostat concept of
Frost. Bone formation(F)
& resorption(R) are the
remodelling phenomena
that change the shape or
form (or both) of a
bone.The peak strain
history determines
whether atrophy,
maintenance, hypertrophy
or fatigue failure occurs.
uE= microstrain=
percent of deformation x
1/10000

Joints of the cranium
• Temporomandibular joints
• Sutures
• Synchondroses
• Gomphoses
• Symphysis ?

Sutures: Limited to the skull.
Bones are separated by
sutural ligament.growth
occurs by apposition by
cambial layer.
Finally obliterated 20’s

Types of sutures:
• Plane
• Serrate
• Denticulate
• Squamous
Joints of the
cranium

Synchondrosis: temporary cartilaginous junctions between
the skull components developing in chondrocranium.
These are :
Spheno occipital: 13-15 years.
Spheno ethmoidal: 6 years
.
Intrasphenoidal & intraerthmoidal:
at birth.
Histologically:a two sided epiphysis.

Synchondroses
bone bone
Hyaline
cartilagewww.indiandentalacademy.com

Symphysis
bone bone
hyaline
cartilage
hyaline
cartilage
fibrous cartilagewww.indiandentalacademy.com

Is ‘symphysis menti’ a symphysis really?
The articulation between the two halves of the mandible is
usually described as a symphysis & the symphysis menti
does bear some resemblance histologically.It is rapidly
abolished during the 1st postnatal year 7 since it is
improbable that it is the site of any functionally significant
movement while present,it is of doubtful propriety to
assign it to this group of joints.

Chemical composition of bone

Calcium metabolism
ICF
11000 mg
ECF
900 mg
Glomerular
Filtrate
10,000 mg
Excretion
in urine
100 mg
Bone
exchangeable
400 mg
Stable
1000 mg
Diet
1000 mg
GIT
1000 mg
Excretion
in faeces
900 mg
Absorption
600mg
Rapid exchange
Resorption
300mg
Deposition
300mg

Decreased blood Ca level
parathyroid kidney
parathormone Vitamin D
Bone
Increase in
resorption &
release of Ca
Intestine
Increase in
absorption of
Ca
Increased blood Ca level
thyroid
calcitonin
Bone
Inhibition of bone
resorption and
deposition of Ca
Normal calcium levelwww.indiandentalacademy.com

Factors affecting bone metabolism
Stimulation Inhibition
Bone formation GH
Calcitonin
Insulin
Testosterone
Estrogen
Cortisol
Mineralization Calcitonin
Insulin
Vit D
Cortisol
Bone resorption Parathormone
Thyroxine
Cortisol
Testosterone

Cholecalciferol
LIVER (inactive form of Vit D3)
25 Hydroxycholecalciferol
KIDNEY 1,25 Dihydroxycholecalciferol
(active form Vit D)
INTESTINE Absorption of CALCIUM
Vitamin D metabolism

Orthodontics is a bone manipulative therapy & favourable
calcium metabolism is an important consideration.
Because of the interaction of structure & metabolism,a
through understanding of the osseous structure & function
is fundamental to patient selection,risk
assessment,treatment planning & retention of desired
denofacial relationsips.
Orthodontics:current principles & technique
T.M. Graber & R.L.Vanarsdall

However if the metabolic problems (particularly –ve calcium balance) are
resolved with medical treatment, these patients can be treated orthodontically
assuming sufficient skeletal structure remains.
No age limit is specified for orthodontic treatment; however the clinician must
carefully assess the probability of metabolic bone disease.In addition to
osteoporosis orthodontist must be particularly vigilant for osteomalacia and
renal osteodystrophy.
Orthodontics:Current principles & techniques
T.M. Graber & R.L. Vanarsdall;225,3rdEd
Orthodontics is contraindicated in patients with active metabolic bone
disease because of excessive resorption and poor bone formation.

Osteoporosis: Generic term for low bone mass.
Risk factors:
• Age (after 3rd decade).
• Long term glucocorticoid therapy.
• Slight stature.
• Menopause.
• Excessive smoking,alcohol.
• Low physical activity.
• Low calcium,vit. D diet.
• Kidney failure,liver disease.
Features:
Low bone mass,low radiographic density of jaws, thin cortices, excessive
bone resorption

Vitamin D deficient rickets
Any disorder in the vit.D-Calcium
phosphorus axis which results
in hypomineralized bone
matrix.
Cessation of calcification of
epiphysial growth plate
cartilage.However the cartilage
continues to grow.Since
unmineralized bone canot bear
weight they bow.

Adult rickets
Seen in postmenopausal women with low calcium intake and little
exposure to UV light.
Features:softening,distortion,increased tendency towards fracture.
Stress bearing bones have asymmetric deformities & long bones
have hairline fracture.

Vitamin D resistant rickets
(familial hypophosphatemia,refractory rickets,phosphate diabetes)
• Hypophosphatemia & hyperphosphaturia associated with decreased
renal tubular reabsorption of inorganic phosphates.
• Familial occurrence,X-linked dominant trait.
• Do not respond to the usual doses of vit. D.
• Normocalcaemia with high normal PTH levels.
• Diminished intestinal calcium & phosphate absorption.
• Decreased growth & short stature.
• Normal vit. D metabolism.

Renal rickets(renal osteodystropy)
Common finding in patients with chronic renal disease.Results from the
inability of diseased kidneys to convert 25-hydroxy cholecalciferol to
the active form of vit.D.
Hypophosphatasia
Low alkaline phosphatase levels.Results in rachitic deformity.

Vitamin C
It has a role in the hydroxylation of proline in collagen synthesis.
Vit C furthers the normal development of intercellular ground substance
in bone,dentin & connective tissue.
Effects on bone:
Osteoblasts fail to form osteoid.Calcified cartilage (scorbutic lattice) is
formed but no bone develops.The calcified cartilage is liable to
fracture (trummerfeld zone or zone of complete destruction).

Hyperparathyroidism
Bone pain,pathologic fractures,gerneralized osteoporosis,giant cell
tumours of the jaw.
Histologically: The most characteristic change in bone is osteoclastic
resorption of the trabeculae of the spongiosa & along the blood vessels
in the haversian system of the cortex. Fibroblasts are found as a mass
in some areas.

Clinical considerations
Is it easier to move teeth in younger patients?
The alveolar bone in young persons who comprise the majority of our
patients is not very dense. It contains large marrow spaces. Since tooth
movement is facilitated by the formation of resorptive cells,whose
number again increases according to the number of marrow spaces, the
anatomic condition can hardly be more favourable than in the
supporting structures of majority of the young orthodontic patients.

Clinical Considerations
Is it easier to move teeth in younger patients?

Why does cortical bone offer good anchorage?
The marrow space contains a large surface area for cellular activity which is
indispensable for tooth movement.On the other hand if bone involved in tooth
movement is of a compact character the surface area where the cellular reaction
can take place is greatly reduced.
When one is planning orthodontic treatment ,the tooth should remain in spongy
bone during movement.On the other hand when teeth are pitted against cortical
bone they can be used to our advantage to provide more anchorage.

How soon after extraction can we start treatment ?
Extraction spaces contain tissue undergoing reconstruction which is rich in
cells & vascular supply.Such an area is ideally suitable for tooth
movement & due advantage should be taken of this by commencing
treatment as soon as possible following extraction. Thereby one avoids
atrophy & narrowing of the alveolar process,resulting in bone loss &
cortical bone formation at the extraction site.

Why do teeth move faster in the upper arch?
A common example is space closure in a Class I four premolar extraction
case.It is often necessary to use headgear on the maxillary 1st molars
to maintain the Class I relationship.The relative resistance of the
mandibular molars to mesial movements is well known.

Why do teeth move faster in the upper arch?
Why are mandibular molars more difficult to move mesially than
maxillary molars ?
2 physiologic factors hold the answer:
• Thin cortices & trabecular bone of the maxilla offer less resistance to
resorption than thick cortices & more coarse trabeculae of the
mandible.
• The leading root of mandibular molars being translated mesially
forms bone that is far more dense than the bone formed by translating
maxillary molars mesially.Why this occurs is not known.

Why teeth move faster in the upper arch …

Why do I have to be careful with cases suffering from
periodontitis?
Moving teeth when progressive periodontal disease is present
invites disaster.
Osteoclasts thrive in the diseased tissue environment.
On the other hand osteoblast histogenesis is suppressed
by inflammatory disease.
When teeth are moved in the presence of active periodontal disease resorption is
normal or even enhanced & bone formation inhibited.this may exacerbate the
disease process,resulting in a rapid loss of supporting bone.

We need healthy bone for adequate retention..
Teeth that have been moved recently are surrounded by lightly calcified
woven bone.Thus the teeth are not adequately stabilized & have a
tendency to move to their original position.During retention phase the
bone matures.

Thank you

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