The document discusses wound healing and its various aspects in 3 parts. It begins by defining a wound and the process of healing. It describes the 4 main phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. It then discusses different types of wounds, tissues involved in healing, and factors that affect the process. The document concludes by noting the complexity of wound healing and importance of addressing underlying issues to ensure proper repair.

1. Presented by:
Dr U Bharath kumar
1st year PG trainee
Moderator :
Dr Abhivyakti Tewari
Assistant professor 1

2.  Introduction
 Types of wounds
 Types of wound healing
 Mechanism of wound healing
 Wound healing in specialized tissues
 Factors affecting wound healing
 Complications
 Advancements
 conclusion 2

3.  A wound is a disruption in the normal
anatomic structure and function of
tissue and is accompanied by cellular
damage
 Healing is a tightly choreographed array
of cellular, physiologic, biochemical,
processes directed toward restoring the
integrity and functional capacity of the
damaged tissue (peterson’s principles of surgery)
3

4.  Physical
• Incision
• Crushing
• Over heating
• Over cooling
• Desiccation
• Irradiation
• blood flow↓
 Chemical
• agents with unphysiologic
pH
• agents with unphysiologic
tonicity
• vasoconstrictors
• proteases
• thrombogenic agents
4Ref: contemporary peterson

5. Injury to
normal cell
Reversible injury
Regeneration
Repair
Adaptations
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Irreversible
injury
Cell death
5Ref : Robin’s basic pathology

6.  When restitution occurs by means of tissue that is
structurally and functionally indistinguishable from
native tissue, it is regeneration
 If tissue integrity is reestablished primarily through
the formation of fibrotic scar tissue , it is known as
repair
 Repair is the body’s version of a spot weld
 With the exception of bone and liver, tissue
disruption invariably results in repair rather than
regeneration.
6Ref: Peterson’s principles

7.  Initial Haemostasis
 Inflammation
 Proliferation
 Remodelling
8Ref: Peterson’s principles

8.  Usually lasts for seconds to minutes
 Tissue trauma and local bleeding
activate factor XII (Hageman factor)
 complement, plasminogen, kinin,
and clotting systems are induced
 primary platelet plug organized
within a fibrin matrix
9Ref: laskin, contemporary peterson

9. 10Ref: Peterson’s principles

10.  Under the influence of histamines,kinins and prostaglandins, vasodilation
occurs followed by diapedisis of neutrophils
 The cytokines released by perishing neutrophils, like TNF-α and
interleukins serves as chemotactic agents for lymphocytes and monocytes.
 Macrophages break down injured tissue and phagocytose bacteria and cell
debris
 Macrophages taper off by the 5th post injury day
 Lag phase- wound strength
11Ref: Peterson’s principles

11. 12Ref: Peterson’s principles

12.  The remodeling/maturation phase can
last for several years
 On and off sequence of matrix
degradation and formation.
 Type III collagen is replaced by
stronger type I collagen
 Tensile strength gradually increases to
form 80% of original tissue strength
13Ref: peterson’s principles., contemporary omfs

13. Type of collagen Commonly seen in
Type 1 Bone
Type 2 Cartilage
Type 3 Skin, lung, liver, intestine
Type 4 Basement membrane
14

14. 15

15.  Healing by primary intention
 Healing by secondary intention
 Healing by tertiary intention
16

16.  Healing by first intention occurs when a clean laceration or surgical
incision is closed primarily with sutures or other means
 Healing proceeds rapidly with no dehiscence and minimal scar
formation.
 Strictly speaking, healing by primary intention is only theoretically
ideal, impossible to attain clinically
17Ref: Peterson’s principles

17. 18Ref: Robin’s

18.  If conditions are less favorable, wound healing is more
complicated and occurs through a protracted filling of the
tissue defect with more granulation and connective
tissue.
 It is commonly associated with avulsive injury, local
infection,or inadequate closure of the wound
19Ref: Peterson’s principles

19. Angiogenesis
Cellular infiltrate
scar
20

20.  For more complex wounds, healing is acheived
through a staged procedure that combines
secondary healing with delayed primary closure.
 wound is debrided and allowed to granulate and
heal by second intention for 5 to 7 days
 Once adequate granulation tissue has formed,
wound is sutured close to heal by first intention.
 Using of grafts also considered as tertiary intention
21Ref:Peterson’s principles

21. FEATURES PRIMARY SECONDARY
CLEANLINESS CLEAN UNCLEAN
INFECTION UNINFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES PLACED NOT PLACED
HEALING MINIMAL GRANULATION TISSUE LARGE GRANULATION
OUTCOME LINEAR SCAR IRREGULAR
COMPLICATIONS NOT FREQUENT FREQUENT
22

22.  LOCAL FACTORS:
 Foreign bodies
 Venous insufficiency
 Pressure, trauma
 Ischaemia, hypoxia
 Radiation
 Salivary contamination
 Electrocautery
 SYSTEMIC FACTORS
 Aging
 Smoking
 Diabetes
 Corticosteroids
 Immunocompramised state
 Malnutrition
 Cytotoxic chemotherapy
 Chronic illness
 Peripheral artery disease
23Ref: contemporary omfs

23.  There are notable intrinsic and extrinsic factors that differ between dermal
and oral mucosal tissue repair which result in scar less healing.
 Saliva supports wound repair by assisting oral fibroblasts in wound
closure, increasing cell turnover and stimulating the release of growth
factors in order to achieve rapid oral wound healing.
 Saliva contains EGF, histatins, peptides with antimicrobial properties that
promote fibroblast and keratinocyte migration, further enhancing the
minimally scarring wound healing response in the oral cavity.
24Ref: shafers oral pathology

24.  Bone
 Nerve
 Muscle
25

25.  Trauma
 Post – extraction
 Implant
Image depecting rigid fixation – contact vs gap healing
Cartilage
Rigid
fixation
collagen
Haversian system
Vascular bundles
26Ref: Peterson’s principles

26.  Immediate reaction to trauma
 Chondrogenesis
 Endochondral ossification
 Bone formation
 Bone remodeling.
27

27. Fracture hematoma Callus formation
Cartilage formation mineralization remodelling 28

28.  Haversian remodelling
 Little to no callus
 Good bone opposition and no motion at fractured or osteotomy site
Contact healing
 Direct contact between cortical bone ends laid down by lamellar bone
at fractured site parallel, by direct union of osteons
Gap healing
 Osteoblast differentiate and deposit osteoids on exposed fractured
fragments that convert into lamellar bone later.
29

29. Schenk R, Willenegger, H. 30

30.  Anchoring
 Bridging
 Sealing
 Uniting
31

31. Fracture healing
Direct healing
Contact healing
gap healing
Indirect healing
Hematoma phase Repairative phase
Soft callus Hard callus
Remodelling phase
32

32.  Sockets heal by secondary intention
 Occurs in 5 stages
 Complications –
 Drysocket
 septic periostitis
 Complete healing is achieved by roughly
4-6 weeks
33Ref: Laskin vol 1, contemporary omfs

33. The discovery of osseointegration forced us to rethink
basics of wound healing
Wound healing in implants involves
Healing of bone to the implant
Healing of alveolar soft tissue to the implant
Healing should occur on implant interface first
Minimal implant force loading during healing time
Bone implant interface should be contaminant free
Implant –bone
interface
Epithelium
neovascularisation
Medullary
bone
34Ref: contemporary omfs, misch

34.  Neurapraxia
 Axonotmesis
 Neurotmesis
35Ref: contemporary omfs

35.  Degenerative changes at distal stump.
 Nerve separated from its nutritive center.
 break in myelin-atrophy of axon.
 retrograde degeneration upto few blocks.
Neuroma formation
36Ref: contemporary omfs

36. 37

37.  It is a well known fact that healing is impaired in diabetes
mellitus.
 higher incidence of wound infection associated with
diabetes has less to do with the patient having diabetes and
more to do with hyperglycemia
 It is attributed to the fact uncontrolled blood glucose
hinders red blood cell permeability and impairs blood flow
through the critical small vessels at the wound surface
 In diabetes the terminal collagen formation is also impaired
so wound proliferation occurs but wound maturation is
impaired.
38

38.  Following grafting, nutritional support for a free skin graft is initially
provided by plasma that exudes from the dilated capillaries of the host bed.
 A fibrin clot forms at the graft-host interface, fixing the graft to the host
bed
 Host leukocytes infiltrate into the graft through the lower layers of the
graft.
 Graft survival depends on the ingrowth of blood vessels from the host into
the graft (neovascularization) and direct anastomoses between the graft
and the host vasculature (inosculation)
 Reinnervation of the skin graft occurs by nerve fibers entering the graft
through its base and sides.
39

39.  Infection
 Dehisence of wound
 Implantation (Epidermal) Cyst Formation
 Pigmentation
 Deficient Scar Formation
 Hypertrophic Scars and Keloid Formation
 Excessive Contraction
 Neoplasia
40Ref : Collective information

40. KELOID
 Proud flesh
 Extends the boundary of wound
 Occur on the sternal, shoulders
upper arms, earlobes, and cheeks
 Appear at three months or later
HYPERTROPHIC SCAR
 With in the wound margin
 Regress with time
 commonly occur on extensor
surfaces of joints
 Appear within one month
41Jackson IT, Bhageshpur R, DiNick V, Khan A, Bhaloo S. Investigation of recurrence rates among earlobe keloids utilizing various postoperative therapeutic modalities. Eur J
Plast Surg. 2001;24(2):88,

41.  Growth factors
 Gene theraphy
 Dermal mucosal substitutes
42Ref: Wound Healing and Perioperative Care Vivek Shetty, DDS, DrMedDenta,T, Harry C. Schwartz, DMD, MD, FACS

42.  Through their central ability to orchestrate the various cellular activities
that underscore inflammation and healing, cytokines have profound effects
on cell proliferation, migration, and extracellular matrix synthesis.
 Exogenous growth factors, such as PGDF, angiogenesis factor, epidermal
growth factor (EGF), TGF, bFGF, and IL-1, applied directly to the wound.
 To date only a single growth factor, recombinant human platelet-derived
growth factor-BB (PDGF-BB), has been approved by the United States
Food and Drug Administration
 Experimental studies suggest potential for the use of growth factors in
facilitating peripheral nerve healing.
 The bone morphogenetic proteins (BMPs) belonging to the TGF-β
superfamily have osteoinductive capacities
43

43.  It should be clearly understood that the healing of wound is not an
isolated, solitary phenomenon but actually a very complex series of
biologic events.
 Wound healing in the maxillofacial region occurs in the presence of
many challenges, usually proceeds undisturbed and with preserved
oral function.
 When a facial or intra-oral wound presents a disturbed healing
process, it is recommended to conduct a thorough and judicious
examination to eliminate or correct underlying local or general
factors.
44

44.  Robbins basic pathology
 Peterson’s principles of oral and maxillofacial surgery
 Laskin volume 1
 Shafer’s oral pathology
 Contemporary omfs
 Misch : Implantology
 Wound Healing and Perioperative Care Vivek Shetty, DDS, DrMedDenta,T, Harry C.
Schwartz, DMD, MD, FACS
 Investigation of recurrence rates among earlobe keloids utilizing various
postoperative therapeutic modalities. Eur J Plast Surg. 2001;24(2):88
Jackson IT, Bhageshpur R, DiNick V, Khan A, Bhaloo S.
45

45. Thank you
46

46. 47

47.  Types of callus
 Delayed union vs mal unioun
 Contact and gap healing distance
 Local and systemic factors
 3 types of nerve degeneration
 Osteoconduction vs osteo
induction
 How keloid forms
 Healing in diabetic patients
 Factors promoting wound
healing(growth factors etc)
 Flaps on wounds
 Types of collagen
48