2. Lecture outline
Learning
Outcomes
At the end of the session, the learners should be able to:
1. Describe the normal structure and histology of jaw bone and tooth socket. (C3)
2. Describe the process of healing of fracture and extraction socket. (C3)
3. Discuss the causes and types of complications associated with healing of jaw fracture and tooth
extraction socket. (A2)
Lecture Outline 1. Introduction
1. Structure and histology of jaw bone
2. Structure and histology of tooth socket
2. Pathogenesis of healing
1. Jaw bone fracture
2. Extraction socket
3. Healing process
1. Promoting and inhibiting factors
2. Complications
3. Introduction
• Alveolar bone proper or bundle
bone (histological term)
– Inner portion of socket walls
– Lamellar bone
– Sharpey’s fibers insertion
– Lamina dura (radiographically)
• Alveolar bone
– Remaining hard structure
– Comprise cortical and
cancellous bone
Structure of tooth socket
5. Healing of extraction sockets
Divided into 3 sequential and frequently overlapping phases:
I. Inflammatory
a) Hemostatic response
b) Inflammatory response
II. Proliferative
a) Fibroplasia
b) Woven bone formation
III. Remodeling
7. INFLAMMATORY PHASE
• Hemorrhage post extraction creates blood clot within socket
• Clot plugs severed vessels and stops bleeding
• Inflammatory cells migrate to wound to remove necrotic debris
– Acute inflammation (24hr) – polymorphonuclear leukococytes
– Chronic inflammation (72hr)– macrophages, lymphocytes, plasma cells
• Proliferating endothelial cells and immature fibroblasts forms the
granulation tissue which gradually replaces the blood clot “organization
of the clot” (1 wk)
• As the site becomes sterilized, the granulation tissue is gradually replaced
with a provisional connective tissue matrix rich in collagen fibers and cells
(inflammatory cells ↓, collagen fibers ↑ )
8. PROLIFERATIVE PHASE
• Characterized by intense and rapid tissue formation
• Fibroplasia involves rapid deposition of a provisional matrix
• Matrix then penetrated by vessels and bone forming cells (cells with
osteogenic potential from adjacent bone marrow –osteoprogenitor cells)
• Finger-like projections of woven bone laid down around vessels
• Projections completely surround vessel primary osteon
• Woven bone formation starts at the base and periphery of socket –
gradually fill up the socket by replacing granulation tissue
• Woven bone can be identified in socket as early as 2 weeks post extraction
and remains in the wounds for several weeks
10. REMODELING PHASE
• Bone remodeling involves replacement of woven bone with
lamellar bone
• After approximately 6 wk, the socket is filled with woven bone but
outline of socket is still discernable histologically and
radiographically
• Subsequently woven bone is remodeled with cortical and
cancellous bone and lamina dura disappears
• Remodeling also includes reduction in alveolar bone height
• Radiographically, socket is generally obliterated 20 to 30 weeks
after extraction
11. Buccal-lingual section of socket wall
a few months after extraction
The intense remodeling process is characterized
by the presence of bone multicellular units and
reversal lines
12. HEALING OF
MUCOSAL SOFT
TISSUE
• Epithelial cells
bordering the
socket rim migrate
between the blood
clot and the
proliferating
granulation tissue
• Epithelial
14. STIMULATING factors
• Initial healing responses are regulated by signaling
molecules (i.e. growth factors and cytokines) such as:
– platelet-derived growth factors
– insulin-like growth factors
– transforming growth factor- beta
– fibroblastic growth factors
• Initiate cell migration, differentiation and proliferation
• Act as mitogenic and angiogenic signals at the early stage
of bone healing
15. COMPLICATIONS
Causes of delayed healing of extraction socket
1. INFECTIONS
2. TRAUMATIC EXTRACTION
3. DRY SOCKET
4. DISEASED BONE
16. References
• Antonio nanci (2008). Ten cate’s oral histology. Elsevier, india
• J.v Soames, j.c.southam (2005). Oral pathology. Oxford university press, new york
• M.G.Araujo, c.o. silva, m.misawa, f.sukekava (2015) Alveolar socket healing: what can we learn? Periodontology
2000, 68:122-134
• Sanjay saraf (2008) Textbook of oral pathology. Jaypee Brothers Publishers, india
• Kumar Purkait (2011) Essential of oral pathology. JP Medical Ltd, india
19. Lecture outline
Learning
Outcomes
At the end of the session, the learners should be able to:
1. Describe the normal structure and histology of jaw bone and tooth socket. (C3)
2. Describe the process of healing of fracture and extraction socket. (C3)
3. Discuss the causes and types of complications associated with healing of jaw fracture and tooth
extraction socket. (A2)
Lecture Outline 1. Introduction
1. Structure and histology of jaw bone
2. Structure and histology of tooth socket
2. Pathogenesis of healing
1. Jaw bone fracture
2. Extraction socket
3. Healing process
1. Promoting and inhibiting factors
2. Complications
20. What are the normal
components of bone
structurally?
Cortex
Compact bone
Cortical bone
Medullary cavity
Spongy bone
Cancellous bone
Trabecular bone
Bone marrow
21. Bone tissue types and structure
Based on texture:
● compact bone (dense bone, cortical bone)
● sponge bone (trabecular bone, cancellous bone)
Based on matrix arrangement:
● lamellar bone –
● lamellae of sponge bone are arranged parallel to each other
● lamellae of compact bone are organized concentrically to
around vascular canal (haversian canal)
24. Types of bone
Lamellar bone (mature bone) Woven bone (immature bone)
Woven bone displays a disorganized lamellar appearance due to interlacing appearance of collagen fibers. The cells
(osteoblasts & osteoclasts) are randomly arranged, whereas the cells in mature bone are organized in a circular fashion
that reflects the lamellar structure of the Haversian system.
29. Introduction
• Ossification/osteogenesis - process of laying down new
bone material by osteoblasts. It results in formation of
bone tissue.
• Normal bone ossification is of two tyoes –
1. Endochondral ossification – a cartilage is formed as
precursor on which new bone is laid down
2. Intramembranous ossification - direct laying down of
bone into the primitive connective tissue (mesenchyme).
30. Types of fractures
• Complete / Incomplete
• Closed (simple) – overlying tissue intact
• Compound – fracture site communicates with skin surface
• Comminuted – bone is splintered
• Displaced – ends of bone are not aligned
• Pathologic – diseased bone
• Stress – slow developing fracture that follows a period of
increased physical activity in which the bone is subjected to
31. Healing of fracture
• Bone has remarkable ability to repair and heal without leaving
a scar
• Pattern of bone healing
I. Primary healing
• Under conditions of absolute fracture stability
• By direct osteonal remodeling
• Without callus formation
II. Secondary healing
• Under an environment of relative stability
• With callus formation
32. i. Primary healing
• Attempt to directly reestablish an anatomically
correct and biomechanically competent
lamellar bone structure
• Primary goal of ORIF
• Osteoclasts tunnel across fracture line,
establishing a “cutting cone” between bone
ends
• Osteoblasts follow, laying down bone matrix,
and reestablish continuity between Haversian
systems
• Revascularization occurs, with internal bone
remodeling and bone forms directly with no
callus formation
33. ii. Secondary healing
Three sequential phases:
• Reactive phase (1-7 days post fracture)
– Haematoma and inflammation
– Granulation tissue formation
• Reparative phase (2-12 weeks post fracture)
– Callus formation
– Woven bone
• Remodeling phase (months or years)
– Trabecular bone
34. Reactive phase
• hematoma fills the fracture gap and
surrounds bone injury area
• Clotted blood
– provides a fibrin mesh which helps seal off fracture site
– creates a framework for influx of various migrating cells
(e.g. neutrophils, lymphocytes, monocytes,
macrophages, mast cells, platelets)
35. Reactive phase
• The migrating cells release various cytokines (transforming
growth factor-ᵦ, platelet-derived growth factor, fibroblast
growth factor, interleukins 1 and 6).
• Increased capillary permeability, chemotaxis and small vessel
dilatation
• Ingrowth of fibroblasts and new blood vessels within the
framework form the granulation tissue
• Osteoclasts remove dead bone and phagocytes remove other
necrotic tissue
36. Reparative
phase
• Mesenchymal stem cells are recruited
and differentiate into chondroblasts and
progressively replace the fibrous
granulation tissue with hyaline cartilage
provisional callus/soft callus
undergoes endochondral ossification
hard callus
• Meanwhile, osteoprogenitor cells in the
periosteum and endosteum are activated
and lay down a meshwork of woven
bone within and around the provisional
callus external hard callus
(intramembranous ossification)
37. Remodeling phase
• Occurs once fracture is
satisfactorily bridged by callus
• Excess callus is removed
• Woven bone remodeled into
trabecular lamellar bone
• Medullary canal and bone
shape is restored
38. Factors affecting healing of fracture
• General
– Age, nutrition, drug therapy, bone pathology, type of bone
• Local
– Mobility at fracture site
– Separation of bone ends
– Disturbance of blood supply
– Bone properties (UL> LL, clavicle ++, tibial shaft --)
– Fracture type
– Biomechanical environment (stability and micromotion balance enhance callus formation)
– Irradiation
39. Disorders of bone union
• Delayed union
– Failure of a fracture to consolidate within the expected time
• Non-union
– No signs of healing after >3-6 months
• Malunion
– Bone fragments join in an unsatisfactory position, usually due to
insufficient reduction
