Suture Materials and Suturing Techniques - Presented by Dr. Prasanjit Das and group as a part of Dhaka Dental College, OMS Department weekly presentation program.
Suture Materials and Suturing Techniques - Presented by Dr. Prasanjit Das and group as a part of Dhaka Dental College, OMS Department weekly presentation program.
Wound healing refers to a living organism's replacement of destroyed or damaged tissue by newly produced tissue. In undamaged skin, the epidermis and dermis form a protective barrier against the external environment
WOUND HEALING. wound healing in general, wound healing in dentistry.YasminShaik16
Wound Healing:
Wound healing is a complex and dynamic process that restores the integrity of the skin and underlying tissues after injury. This essential biological function involves a well-orchestrated interplay of cellular and molecular mechanisms. Understanding wound healing is crucial for healthcare professionals, researchers, and anyone interested in medical science. This comprehensive overview will cover the phases of wound healing, factors affecting the process, advanced wound care techniques, and current research trends. This presentation delves into the four distinct phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. Each phase plays a crucial role in repairing damaged tissue and involves complex interactions between cells, growth factors, and the extracellular matrix.
Key topics include:
Hemostasis: The immediate response to injury, where blood clotting mechanisms are activated to prevent excessive bleeding.
Inflammation: The body's defense mechanism against infection, involving white blood cells, cytokines, and other inflammatory mediators.
Proliferation: The phase where new tissue forms, characterized by the proliferation of fibroblasts, collagen deposition, and angiogenesis.
Remodeling: The final phase where the newly formed tissue matures and strengthens over time, ensuring functional and aesthetic restoration.
This presentation also covers factors that influence wound healing, such as age, nutrition, underlying health conditions, and external factors like infection and mechanical stress. Additionally, it highlights advanced wound care techniques and the latest research in enhancing the healing process through innovative therapies and technologies.
Ideal for healthcare professionals, students, and anyone interested in understanding the science behind wound healing, this presentation provides valuable insights into how our bodies repair themselves and the advancements in medical science that support this vital process.
Factors Affecting Wound Healing
Wound healing can be influenced by various intrinsic and extrinsic factors. Understanding these factors is crucial for optimizing healing outcomes.
Intrinsic Factors
Age: Healing capacity declines with age due to reduced cellular proliferation, slower immune response, and decreased collagen synthesis.
Genetics: Genetic predispositions can affect the efficiency of the healing process and the likelihood of developing chronic wounds or hypertrophic scars.
Nutrition: Adequate nutrition is essential for wound healing. Proteins, vitamins (especially vitamins A and C), and minerals (like zinc) play vital roles in cell proliferation, collagen synthesis, and immune function.
Health Conditions: Chronic conditions such as diabetes, obesity, and cardiovascular diseases can impair wound healing. Diabetes, for example, can lead to poor blood circulation and reduced immune response, increasing the risk of infection and delayed healing.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Wound healing
1. WOUND HEALING
Resource Faculties:
Prof. Dr.TR Manandhar
Dr. Navin Agrawal
Dr. Mannu Vikram
Dr. Vimmi Singh
Dr. Ashok Ayer
Presenter:
Dr.Ravi Acharya
JR-2014
Dept.of Conservative
Dentistry and Endodontics
2. Contents:
• Wound definition
• Classification of wounds
• Healing
• Types of wound healing
• Stages of wound healing
• Phases of wound healing
• Hard tissue healing
• Factors affecting wound healing
• Complication
3. • Systemic medication affecting wound healing
• Healing of sinus tract
• Wound healing after pulpectomy
• Wound healing of Apical Periodontitis
• Healing of root fracture
• Healing in patients on chemotherapy/radiotherapy
• Perforation and prognosis of healing
• Conclusion
• References
4. WOUND
• It is a circumscribed injury which is caused by
external force and it can involve any tissue and
organ.
5. • A wound is a break in the integrity of the skin or
tissues often which may be associated with
disruption of the structure and function.
(SRB 4th edition)
• A cut or break in the continuity of any tissue, caused
by injury or operation.
(Baillière’s 23rd Ed)
7. Classification based on type of wound
i. Clean incised wound
ii. Lacerated wound
iii. Bruising and contusion
iv. Haematoma
v. Puncture wound
vi. Abrasion
vii. Crush injury
viii. Injuries to bone and joint (maybe open or closed)
ix. Injuries to nerve (either clean cut or crush)
x. Injuries to arteries and veins
xi. Penetrating wounds
8. Classification based on thickness of wound
a) Superficial wound
b) Partial thickness
c) Full thickness
d) Deep wounds
e) Complicated wounds
f) Penetrating wound
Superficial
Partial thickness
Full thickness
Deep wound
9. Classification of surgical wounds
a) Clean wound
b) Clean contaminated wound
c) Contaminated wound
d) Dirty infected wound
10. HEALING
• Healing is the body’s response to injury in
an attempt to restore normal structure and
function.
11. The process of healing involves 2 distinct
processes:
A. REGENERATION
B. REPAIR
12. • Regeneration: Is when healing takes place by
proliferation of parenchymal cells and usually
results in complete restoration of the original
tissues.
• The goal of all surgical procedures should be
regeneration which returns the tissues to their
normal microstructure and function.
13.
14. • Repair: It is a healing outcome in which tissues
do not return to their normal architecture and
function.
• Repair typically results in the formation of scar
tissue.
15. TYPES OF WOUND HEALING
• Healing by first intention (wounds with opposed
edges)
• Healing by secondary intention (wounds with
separated edges)
16. Healing by first intention (wounds
with opposed edges)
Healing of wound with following characteristics:
Clean and uninfected
Surgically incised
Without much loss of cells and tissue
Edges of wound are approximated by surgical sutures.
Wounds with opposed edges
Primary union
17. • The incision causes
death of a limited number of epithelial cells
and connective tissue cells
disruption of epithelial basal membrane
continuity
• The narrow incisional space immediately fills
with clotted blood containing fibrin and blood
cells; dehydration of the surface clot forms the
well known scab that covers the wound.
18. Within 24 hours
• Neutrophils appear at margins
of incision, moving toward fibrin
clot
• Epidermis at its cut edges
thickens as a result of mitotic
activity of basal cells
• Within 24 to 48 hours, spurs
of epithelial cells from the both
edges migrate and grow along
the cut margins of the dermis,
depositing BM components as
they move. They fuse in the
midline beneath the surface
scab, thus producing a
continuous but thin epithelial
layer.
19. By day 3,
• Neutrophils replaced by macrophages
• Granulation tissue progressively invades incision space
• Collagen fibers are now
present in the margins of the
incision, but at first these are
vertically oriented.
• Epithelial cell proliferation
continues, thickening epidermal
covering layer
20. By day 5,
• Incisional space is filled with granulation tissue
• Neovascularisation is maximal
• Collagen fibrils become more abundant and begin to bridge
incision
• The epidermis recovers its normal thickness, and differentiation
of surface cells yields a mature epidermal architecture with
surface keratinization
21. During the second week
• Continued accumulation of collagen and
proliferation of fibroblasts
• Leukocytic infiltrate, edema, and increased
vascularity have largely disappeared.
22. By the end of the first month,
• Scar comprises a cellular connective tissue devoid of
inflammatory infiltrate, covered now by intact epidermis.
• Dermal appendages that have been destroyed in the line
of the incision are permanently lost.
• Tensile strength of the wound increases thereafter, but it
may take months for the wounded area to obtain its
maximal strength.
23. Healing by second intention
• Wounds with separated edges
• Secondary union
• When there is more extensive loss of
cells and tissue
• Regeneration of parenchymal cells
cannot completely reconstitute the
original architecture.
• Abundant granulation tissue grows in
from the margin to complete the repair.
24. Secondary healing differs from primary healing in several
respects:
Inflammatory reaction is more intense
Much larger amounts of granulation tissue are formed
Wound contraction occurs in large surface wounds
Substantial scar formation and thinning of the
epidermis occurs
25. Difference between 1˚ & 2˚ union
of wound
FEATURES PRIMARY SECONDARY
CLEANLINESS CLEAN NOT CLEAN
INFECTION NOT INFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES USED NOT USED
HEALING SMALL GRANULATION
TISSUE
LARGE GRANULATION
TISSUE
OUT COME LINEAR SCAR IRREGULAR WOUND
COMPLICATION NOT FREQUENT FREQUENT
26. STAGES OF WOUND HEALING
1. Stage of inflammation.
2. Stage of granulation tissue formation and organisation.
3. Stage of epithelialisation.
4. Stage of scar formation and resorption.
5. Stage of maturation.
27. PHASES OF WOUND HEALING
For soft tissue wound healing:
1. Inflammatory phase: It can be broken down into further
a) Clot formation
b) Early inflammation
c) Late inflammation
2.Proliferative phase
3.Maturation phase
28. Inflammatory phase
a) Clot formation:
- Begins with three events:
i. Blood vessel contraction initiated by platelet
degranulation of serotonin, which acts on endothelial
cell and increases the permeability of the vessel,
allowing a protein rich exudate to enter the wound
site
ii. A platelet plug formation
iii. Activation of extrinsic and intrinsic clotting
mechanism
30. • These events stabilize hemostasis, begins production of
chemoattractants and initiate the process of wound
decontamination.
• This result in formation of a coagulum.
31. • Compression of surgical flap with sterile iced
gauze immediately after surgery is designed to
minimize the thickness of fibrin clot and thereby
accelerate optimal wound healing.
32. b) Early inflammation:
• Characterized by production of polymorphonuclear
neutrophils (PMNs)
• Begin to enter the wound site within 6 hours of clot
stabilization.
• The number of PMNs increases steadily, peaking at
about 24 to 48 hours after the injury.
33. • Three key steps mark PMN migration into the wound
site: a) Pavementing
b) Emigration
c) Migration
• Main role of PMNs is wound decontamination by
phagocytosis of bacteria.
• The number of PMNs drop rapidly after the third day.
34. c) Late inflammation:
• Presence of macrophages.
• Reaches peak concentration by approximately
third or fourth day.
• They have longer life than PMNs and remain in
wound till healing is completed.
35. • Are more bioactive then PMNs – secrete a vast array of
cytokines – leads to initiation of proliferative phase of
wound healing.
• Major functions of macrophages:
wound decontamination through phagocytosis and
digestion of microorganisms and tissue debris.
ingestion and processing of antigens for
presentation to T lymphocytes
regulation of wound healing
36. Proliferative Phase
• Characterized by formation of granulation tissue
in the wound.
• 2 key cell types are present in this phase:
a) fibroblasts
b) endothelial cells
37. • Granulation tissue:
It is a fragile structure composed of an extracellular
matrix of fibrin, fibronectin, glycosaminoglycans,
proliferating endothelial cells, new capillaries, and
fibroblasts mixed with inflammatory macrophages and
lymphocytes.
38. • Epithelial cells are active during this phage and
are responsible for initial wound closure.
• GTR procedures are based on control of the
epithelial cell growth rate during this phase.
39. a) Fibroblasts: Fibroplasia
– They migrate into the wound site on the 3rd day after
injury and achieve their peak numbers by
approximately 7th day.
– This action is stimulated by combination of cytokines
produced initially by platelets and subsequently by
macrophages and lymphocytes.
40. – As the number of macrophages declines and
fibroblasts population increases the wound transforms
from granulomatous tissue to granulation tissue.
– Fibroblasts produces collagen (first detected in the
wound about the third day of injury) .
– Fibroblasts produce type III collagen initially and as
the wound matures type I collagen is formed.
41. – As wound healing progresses, the collagen fibers become
organized by cross-linking.
– A focused type of fibroblast known as a myofibroblast plays a
significant role in wound contraction, particularly in incisional-
type wounds.
– Myofibroblasts align themselves parallel with the wound
surface and then contract, drawing the wound edges
together.
– These cells are eliminated by apoptosis after wound closure.
42. b)Endothelial cells: Angiogenesis
–Formation of new blood vessels at the site of injury
takes place by proliferation of endothelial cells from the
margins of severed blood vessels.
–The newly formed blood vessels are more leaky
accounting for the more edematous appearance of new
granulation tissue.
43. Epithelium:
• The first step is formation of an epithelial seal on the surface
of the fibrin clot. It begins at the edge of the wound, where the
basal and suprabasal prickle cells rapidly undergo mitosis.
• Migration stops as a result of contact inhibition of the
epithelial cells from the opposing wound edge.
• In wounds healing by primary intention, formation of an
epithelial seal typically takes 21 to 28 hours after
reapproximation of the wound margins.
44. Maturation Phase
• Begins 5 to 7 days after injury.
• There is conversion of granulation tissue to fibrous
connective tissue and decrease parallelism of collagen
to the plane of the wound.
• Maturation of the epithelial layer quickly follows
formation of the epithelial seal.
45. • Scar strength is:
– 3% in 1 week
– 20% in 3 weeks
– 80% in 12 weeks
47. HARD TISSUE HEALING
• The inflammatory and proliferative phases are
similar to those for soft tissue.
• The maturation phase differs markedly from that
for soft tissues because of the tissue involved.
48. Osteoblasts: Osteogenesis
• A major difference lies in the role of the osteoclast.
• Osteoclasts acts as an organizational unit to debride
necrotic bone from the wound margin similarly as
macrophages remove tissue debris from the clot.
• New bone formation is apparent about 6 days after
surgery.
49. • Bone formation is categorized into two types:
a) Matrix vesicle – based process
b) Osteoid secretion
50. a) Matrix vesicle – based process
• Woven bone formation occurs by this process.
• In this process osteoblasts produce matrix vesicles through
exocytosis of their plasma membrane.
• It begins with the deposition and growth of hydroxyapatite
crystals in the pore regions.
• The crystals amalgamate to form spherulites whose union
results in mineralization.
51. b)Osteoid secretion
• Lamellar bone formation occurs by this process.
• Osteoblasts secrete an organic matrix composed of
longitudinally arranged collagen matrix fibrils.
• Mineralization occurs by mineral deposition directly
along the collagen fibrils.
52. • In this stage alkaline phosphatase plays an important
role in mineralization.
• Several growth factors identified as a key components in
the production of osseous tissue are:
a. TGF- ß
b. BMP
c. PDGF
d. FGF
e. IGF
53. • The osseous defect is filled with bone tissue by
16 weeks after surgery.
54. Cementoblasts: Cementogenesis:
• Begins 10 to 12 days after root end resection.
• The exact sequence leading to the formation of new
cementum remain unidentified.
• Cementum covers the resected root end in
approximately 28 days.
55. FACTORS AFFECTING WOUND
HEALING:
1) Local factors:
i. Infection
ii. Presence of necrotic tissue and foreign body
iii. Poor blood supply
iv. Venous or lymph stasis
v. Tissue tension
vi. Hematoma
vii. Large defect or poor apposition
56. viii. Recurrent trauma
ix. X-ray irradiated area
x. Site of wound, eg.wound over the joints and back has
poor healing
xi. Underlying diseases like osteomyelitis and malignancy
57. 2) General factors:
i. Age, obesity,smoking
ii. Malnutrition, zinc, copper
iii. Vitamin deficiency (vit C, vit A)
iv. Anemia
v. Malignancy
vi. Jaundice
vii. Diabetes
viii. HIV and immunosupressive diseases
ix. Steroids and cytotoxic drugs
58. COMPLICATION:
1. Deficient scar formation:
a) Wound dehiscence
b) Ulceration
2. Excessive formation of the repair components:
a) Aberrations of growth: -hypertrophic scar
-keloid
b) Excessive amount of granulation tissue
formation
59. c) Exuberant proliferation of fibroblasts and other
connective tissue elements: Desmoids or Aggressive
fibromatoses
3. Formation of contractures
62. HEALING OF SINUS TRACT:
• Sinus is a tract leading from an enclosed area of
inflammation to an epithelial surface, and is one of the
sequelae of inflammatory disease.
• A sinus tract is a drainage duct for the suppuration
produced by abscesses.
63. • Suppuration from the periapical inflammatory process
may be resorbed by the host organism, otherwise it will
flow through the less resistant tissue area.
• It drains onto the epithelial tissue through either a
mucosal, or occasionally, a cutaneous sinus tract.
64. • Sinus tract adjacent to teeth or near the apex of the tooth
is usually considered to be of endodontic origin and root
canal therapy is the primary treatment to achieve its
healing.
• The presence of a sinus tract in the oral cavity is usually
considered of pulpal origin, but it can also be caused by
periodontal disease.
65. Draining sinus Healed sinus
Sinus is active with pus drainage Sinus has healed with pus discharge
absent
Surrounding mucosa reddish pink in
color
Surrounding mucosa presents normal
tissue coloration
Gutta- percha point can be inserted Gutta- percha cannot be inserted
66. Treatment:
• Treatment is directed towards elimination of the source
of infection.
• The offending tooth is removed if it is too badly decayed,
or if there is extensive loss of the surrounding alveolar
bone.
• In most cases, the sinus tract heals spontaneously if the
infected pulp is removed, and the root canal debrided
and filled.
67. • Some chronic sinus tracts heal leaving behind a
small residual scar, excision may not be
required unless its appearance is of concern to
the patient.
• If there is fibrosis of the sinus tract trajectory
then surgical removal is necessary.
68. WOUND HEALING AFTER
PULPECTOMY
• The healing pattern following pulpectomy is
characterized by an initial inflammatory reaction in
the apical tissue due to the trauma induced by the
cutting procedure.
• In the absence of wound infection, reorganization
soon occurs. This involves replacement of the
injured tissue by connective tissue derived from the
periapical region.
69. • Materials used to fill root canals may compromise the
normal healing pattern, owing to their irritating capacity,
and result in a longstanding inflammatory lesion.
• Inflammatory cells accumulate close to the root filling
material and remain for as long as toxic components are
released. Eventually the material will be lined off by
fibrous connective tissue.
• When overfilling occurs, the process of phagocytosis
may eliminate the excess root filling material and
occasionally also material inside the canal.
70. WOUND HEALING OF APICAL
PERIODONTITIS
• Follows the general principle of wound healing of
connective tissues elsewhere in the body, with the
formation of fibrovascular granulation tissue, removal of
necrotic tissue and dead bacteria by activated
macrophages, and finally repair and/or regeneration of
the wounded tissue.
• Healing is largely accomplished by regeneration and to
some degree by fibrosis.
71. • Local tissue resident cells involved in periapical wound
healing are osteoblasts and bone marrow stromal cells in
alveolar bone and multipotent stem cells in periodontal
ligament.
• The extracellular matrix and growth factors of cementum
(i.e., IGF-1, FGFs, EGF, BMP, TGF-β, PDGF) are
capable of inducing proliferation, migration, attachment,
and differentiation of multipotent stem cells in the
periodontal ligament into cementoblast-like cells and
produce cementoid tissue on the root surface denuded
of periodontal ligament.
72. During periapical wound healing, the osteoblasts or
mesenchymal cells lining the surfaces of endosteum
Stimulated by TGF-β, BMPs, IGFs, PDGF, VEGF, and
cytokines released by stromal cells, osteoblasts,
platelets, and bone matrix after bone resorption
Undergo proliferation and differentiation into
osteoblasts
Produce bone matrix
73. • When one of the cortical bone plates (buccal or
lingual/palatal) is destroyed
• Mesenchymal cells in the inner layer of
periosteum beneath the oral mucosa –
stimulated by TGF-β, BMPs,IGFs, PDGF, and
VEGF
• Undergoes proliferation and differentiation into
osteoblasts and produces bone matrix
74. • If both cortical bone plates are destroyed by large apical
periodontitis lesions, it is possible that the lesion may be
repaired with fibrous scar tissue because of extensive
destruction of the periosteum beneath the oral mucosa.
• Guided tissue regeneration procedure and bone grafts is
recommended to prevent ingrowth of fibroblasts from
periosteum or submucosa into the bony defect and to
enhance periapical wound healing if periapical surgery is
necessary.
75. ENDODONTIC IMPLICATIONS (PATHOGENESIS
OF APICAL PERIODONTITIS AS EXPLAINED BY
FISH)
• Described the reaction of the periradicular tissues to
bacterial products, noxious products of tissue necrosis,
and antigenic agents from the root canal
• FISH in 1939 theorized that the zones of infection are
not an infection by themselves but the reaction of the
body to infection. Thus he concluded that the removal of
this nidus of infection will result in resolution of infection.
76. • Four well defined zones of reaction were found during
the experiment:
a. Zone of infection or necrosis (PMNLs)
b. Zone of contamination (Round cell infiltrate –
lymphocytes)
c. Zone of irritation (Histiocytes and osteoclasts)
d. Zone of stimulation (Fibroblasts, capillary buds and
Osteoblasts)
80. PERIAPICAL WOUND HEALING AFTER
SURGICAL ENDODONTIC THERAPY
• Faster than nonsurgical endodontic therapy.
• Surgical debridement is done.
• Goal of surgical endodontic therapy is to seal microbial
etiology within the root canal system by root- end filling
in most cases.
82. HEALING OF ROOT FRACTURE
• Healing of root fracture depends upon:
a) Site of the fracture
b) Status of the pulp
• Two directions of wound healing response are expected:
a) At the pulpal side
b) At periodontal ligament side
83. • If pulp is intact at the fracture site, the odontoblastic
progenitor cells will create a hard tissue bridge uniting
the fractures fragments.
• During initial stage of wound healing, traumatized tissue
stimulate an inflammatory response and trigger the
release of a series of osteoclastic activity ,subsequently
obliterating the fracture site.
84. Any of the following types of resorption may occur:
i. External surface resorption surrounding the proximal
fracture edges at the periodontal side of fracture.
ii. Internal surface resorption surrounding the fracture
edges centrally at the pulpal side of the fracture.
iii. Internal tunneling resorption burrows behind the pre-
dentin layer and along the root canal walls of the
coronal fragment.
85. The pattern of healing of root fracture are:
a) Healing with calcified tissue
b) Healing with interproximal calcified tissue
c) Healing with interposition of bone and
connective tissue
d) Interposition of granulation tissue
86. Healing With Calcified Tissue
• The calcified tissue is formed at the fracture site.
• The innermost layer of repair maybe of dentin
while the more peripheral portion of the fracture
is incompletely repaired with cementum.
87. • Clinically the teeth appears normal.
• Radiographically, the fracture line is discernible,
but the fragments are in close contact.
88. Healing With Interproximal Calcified
Tissue
• Characterized by presence of connective tissue between
the fragments.
• The fracture surfaces are covered by cementum along
with connective tissue fibres running parallel to the
fracture surface or from one fragment to the another.
89. • Clinically the teeth are firm or may be slightly
mobile.
• Radiographically, the fragments appear
separated by a narrow radiolucent line, and the
fractured edges appear rounded.
90. Interposition Of Granulation Tissue
• The fracture site is obliterated with granulation
tissue.
• The coronal portion is necrotic while the apical
portion is vital.
91. • Radiographically, widening of the fracture line
and/or a developing radiolucency corresponding
to the fracture line becomes apparent.
92. Healing with interposition of bone and
connective tissue
• This mode of healing is a sequelae of trauma prior to
completed growth of the alveolar process
• Thus, the coronal fragment continues to erupt while the
apical fragment remains stationary.
• Interposition of bone and connective tissues is seen
along the fracture site.
93. • Clinically the teeth are firm and react normal to
pulp tests.
• Radiographically, the fragments are seperated
by a distinct bony ridge.
94. HEALING IN PATIENTS ON
CHEMOTHERAPY/ RADIATION
THERAPY
• These patients have impaired healing responses.
• Pulp may become necrotic during radiation therapy.
• Symptomatic nonvital teeth should be endodontically
treated 1 week before initiating radiation or
chemotherapy whereas asymptomatic nonvital teeth may
be delayed.
95. PERFORATION AND PROGNOSIS
FOR HEALING
• An endodontic perforation is an artificial opening in the
tooth or its root, created by the clinician during entry to
the canal system or by a biologic event such as
pathologic resorption or caries that results in a
communication between the root canal and the
periodontal tissues.
• A furcation perforation refers to a mid-curvature opening
into the periodontal ligament space and is a worst
possible outcome in root canal treatment.
96. • A post space perforation is defined as a
communication between the lateral root surface
and the surrounding periodontal structures due
to misdirection or an excessively large post
enlargement.
97. Timing Of Perforation Repair
• The main complication arising from perforation is the
potential for secondary inflammation of the periodontal
attachment with eventual infection and ultimately tooth
loss if untreatable.
• The timing of repair categorized into immediate or
delayed.
• Immediately closing the communication between the
periodontal tissues and the root canal system promotes
a superior healing potential.
98. Location Of Perforation
• Perforations can be categorized by location:
a) Subgingival
b) Midroot
c) Apical
• Once perforations exhibit the formation of
osseous defects, the prognosis is compromised
significantly.
99. • Any perforation located near the gingival sulcus
promoted inflammation and loss of epithelial
attachment, resulting in periodontal pocket
formation.
• Apical and midroot perforations without
communication to the oral cavity has a good
prognosis provided an immediate seal was
obtained .
100. Size Of Perforation
• Small perforations of the canal space promote a
direct and immediate restoration of the defect.
• It offers fewer chances for periodontal
breakdown and epithelial proliferation within the
perforation site.
101. Conclusion:
• Understanding of wound healing is as important as
knowing the pathogenesis of disease, because
satisfactory wound healing is the ultimate goal of
treatment.
• If we are able to understand the mechanism of periapical
wound healing, we can design treatment approaches
that maximize favorable conditions for wound healing to
occur.
102. References:
• Robbins and Cotran, Pathologic Basis Of Disease, 7th
edition
• SRB’S Manual Of Surgery, Sri Ram Bhatt, 4th Edition
• Cohen’s Pathways Of the Pulp,9th edition
• Ingle’s Endodontics,6th edition
• Textbook of Endodontology, Gunnar Bergenholtz,
Preben Horsted- Bindslev, Claes Rait, 2nd Edition
• Essentials of Endodontics, Vimal K Sikri
• Textbook of Endodontics, Nisha Garg, 2nd Edition
At this time, the long process of blanching begins, accomplished by the increased accumulation of collagen within the incisional scar, accompanied by regression of vascular channels.
When there is more extensive loss of cells and tissue, as occurs in infarction, inflammatory ulceration, abscess formation, and surface wounds that create large defects, the reparative process is more complicated.
The common denominator in all these situations is a large tissue defect that must be filled.
trabeculae
Healing walton torabinejad principle and practice of endodontics 3rd edition
There is a popular concept that healing in older
individuals is impaired, compromised, or delayed
compared with that in younger patients. This is
not necessarily true. Studies in animals have
shown remarkably similar patterns of repair of
oral tissues in young versus old, but with a slight
delay in healing response.'' Radiographic evidence
of healing of younger versus older patients
after root canal treatment demonstrated no apparent
difference in success and failure.1 9 There is
no evidence that vascular or connective tissue
changes in older individuals result in significantly
slower or in impaired healing. Overall, there is little
difference in the speed or nature of healing between
the different age groups; this includes both
bone and soft tissue. Critical to healing is vascularity.
In healthy individuals, blood flow is not impaired
with age .z°