Repair and Regeneration of Oral Tissues Ten Cate Chapter

15
1. Difference between regeneration and repair
a. Regeneration the complete restoration of tissue
architecture and function
b. Repair restoration of function and of tissue continuity
BUT with distortion of the normal architecture
Wound healing in Oral Mucosa
- Skin and oral mucosa have the primary function of protecting
the underlying tissues from MOs and toxins
- The oral mucosa can be damaged by: direct physical insult,
radiation, chemical irritation, colonisation by microorganisms.
Initial response to wound healing
- HAEMOSTASIS
- When the mucosal surface is damaged there is vascular
damage and haemorrhaging into the tissue defect
o FIBRIN deposited, PLATELET aggregation, CLOT
formation
o Time frame: MINUTES
- FUNCTION of CLOT
o to unite the wound margins and protect from exposed
tissues
o provisional scaffold for subsequent migration of
REPARATIVE CELLS
- Moist environment means clot is not hard and dry like that in
skin, rather it is a SOFT COAGULAM that is easily lost.
o The integrity of the clot as a protective barrier is
compromised after several minutes
o This is due to
VASODILATION and INCREASED VASCULAR
PERMEABILITY allow PLASMA PROTEINS to enter
the wound site and this stimulates LEUKOCYTE
MIGRATION
- MOs, toxins, and antigens are also likely to have entered into
the mucosal tissues leading to an INFLAMMATORY RESPONSE
Inflammatory cell activation, migration, and function
- Immediate acute inflammatory reaction
- Inflammatory cells come from
o Cells normally present in tissues
o Cells extravsated when BVs are damaged
o Cells carried in intact BVs adjacent to a wound that exit
by a process called diapedesis.

Chemotaxis is the process by which platelet

derived cytokines recruit leukocytes to the site of
tissue damage
Major cells involved in inflammation and wound healing
o PMNs
Mainly NEUTROPHILS the FIRST to invade the
wound
Time frame: a FEW HOURS
Activation: phagocytic stimuli OR binding of
chemotactic mediators, antigen-antibody
complexes to specific receptors on the cell
membrane, and components of the complement
system.
Max concentration 24 hours, short life span at
the wound site before they die.
How do neutrophils work?
Various enzymes and reactive oxygen
metabolites (O2 derived free radicals) that
kill engulfed bacteria and can also destroy
damaged and normal tissue when the cells
die
PRIMARY FUNCTION: manage bacterial
invasion and hence infection
o Mononucelar leukocytes
Phagocytic cell macrophages
Time frame: 24 hours
Predominant cell at 5 days
Mediated by:
o Platelet factors in the fibrin clot
o Keratinocytes at the wound margins
o Fibroblasts
o Leukocytes
Result of macrophage presence
o Cellular and humoral responses
o Phagocytosis of damaged tissue
components and foreign material
In the absence of macrophages, fewer
fibroblasts are stimulated during healing
o This means that healing is slower
o TGF-beta in particular simulates
fibroblasts to proliferate and
synthesise extracellular matrix
proteins
Other growth factors released
include PDGF and IL1
Lymphocytes

Lymphocyte chemotaxis is macrophage

related

o Mast cells
Important source of PROINFLAMMATORY mediators
and CYTOKINES
Promotes inflammation and vascular changes
Reparative phase
- The acute inflammatory phase needs to subside to ensure
successful repair of the injured tissues.
- Regeneration of the tissues begins first in epithelium and then
in the connective tissue
- Mobilisation and migration of epithelial cells at the wound
margin
o Cells lose their close attachment to each other and to
the underlying CT within 24 hours of wounding
HISTOLOGICALLY you see a widening of the
intercellular spaces
o 24-48 hours later
Cell division in the basal epithelium increases a
short distance behind the wound margin
Cells immediately adjacent to the margin begin to
migrate laterally beneath the clot or coagulum
Epithelial cells continue to migrate until they
reach the cells from the opposing wound margin,
when contact inhibition restricts further
movement