The document discusses wound healing and periodontal wound healing in particular. It describes the processes of regeneration and repair. Regeneration involves renewal of tissues through growth of same tissue type, while repair involves replacement of tissues through scar formation. The molecular biology of wound healing is explained, including roles of fibrin clot, growth factors, matrix degradation and connective tissue formation. Healing by primary and secondary intention is also defined. Healing processes following various periodontal procedures like scaling, root planing, flap surgery and implant placement are outlined. Factors influencing wound healing and potential complications are briefly mentioned.
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
The future of dentistry and periodontics lies in regeneration. The goals of periodontal therapy lies in not only the arrest of periodontal disease progression but also regeneration of the lost periodontal structures. This presentation provides a review of the current understanding of the regeneration of the periodontium and the procedures involved to restore the periodontal tissues around the teeth.
Pericoronitis is defined as inflammation of the oral soft tissues surrounding the crown of a partially erupted tooth. its treatment- operculectomy i.e. removal of the inflammed operculum
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
Jbhzj gccycgccychcvycyxfthvyc4dygih8h me feel so special daughter is in the given questions and answers in love you so much to do but I have to be with me and my friends and my friends are not at
Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
The future of dentistry and periodontics lies in regeneration. The goals of periodontal therapy lies in not only the arrest of periodontal disease progression but also regeneration of the lost periodontal structures. This presentation provides a review of the current understanding of the regeneration of the periodontium and the procedures involved to restore the periodontal tissues around the teeth.
Pericoronitis is defined as inflammation of the oral soft tissues surrounding the crown of a partially erupted tooth. its treatment- operculectomy i.e. removal of the inflammed operculum
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
Jbhzj gccycgccychcvycyxfthvyc4dygih8h me feel so special daughter is in the given questions and answers in love you so much to do but I have to be with me and my friends and my friends are not at
Dentist in pune.(BDS. MDS) - Dr. Amit T. Suryawanshi. Wound healing in Dentis...All Good Things
entist in pune. (BDS. MDS) - Dr. Amit T. Suryawanshi. Seminar- Wound healing in dentistry.
Email ID- amitsuryawanshi999@gmail.com
Contact -Ph no.-9405622455
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
2. Contents
1. Introduction
2. Regeneration & repair
3. Healing by primary and secondary intension
4. Molecular biology of wound healing
5. Factors influencing/ complications of wound healing
6. Healing of oral wounds
7. Role of saliva and GCF in wound healing
8. Wound healing following various periodontal therapies
9. Use of lasers in wound healing
10. conclusion
3. Introduction
A wound/Injury is
a disruption of
the anatomic
structure and
function in any
body part.
Wound
healing
Healing on the other
hand is a cell response
to injury in an attempt
to restore the normal
structure and function.
4. Periodontal wound healing
A more complex situation presents itself when a
mucoperiosteal flap is apposed to an instrumented root surface
deprived of its periodontal attachment.
In this case, the wound margins are not two opposing vascular
gingival margins but comprise the rigid nonvascular
mineralized tooth surface, on the one hand, and the connective
tissue and epithelium of the gingival flap, on the other hand.
5. Process of healing
It involves 2 distinct processes :
At times, both the processes take place
simultaneously
Regeneration Repair
6. Regeneration
Natural renewal of a structure, produced by growth &
differentiation of new cells and intercellular substances to
form new tissues or parts which function the same as
original tissues.
Growth from the same type of tissue that has been destroyed
or from its precursors.
Periodontal tissues are limited in their regenerative
capacity.
9. Regeneration related to periodontal tissues
Manifested by:
Mitotic activity in the epithelium of the gingiva and connective tissue
of PDL
Bone remodelling
Continuous deposition of cementum
Most gingival and periodontal diseases are chronic inflammatory
process and, as such are, healing lesions.
10. Repair- “healing by scar”
Replacement of one tissue with another tissue,
such as fibrous connective tissue, which may not function the
same as the tissue replaced.
Two processes are involved in the repair:
1. Granulation tissue formation
2. Contraction of wounds
11. Granulation tissue formation
Each granule histologically corresponds to proliferation of new
small blood vessels which are slightly lifted on the surface by a
thin covering of fibroblasts and young collagen
Granulation tissue
formation
Phase of
inflammation
Phase of clearance
Phase of ingrowth
of granulation
tissue
Angiogenesis
(neovascularization)
Formation of
fibrous tissue
(fibrogenesis)
12. Angiogenesis
necessary to sustain newly formed granulation tissue
proliferation of endothelial cells from the margins of the severed
vessels
13. fibrogenesis
Emigration and proliferation of the fibroblasts at the site of injury
Deposition of these cells which in turn increases collagen synthesis
As the maturation proceeds: there is an increase in the collagen, and a
decrease in the fibroblasts and blood vessels .
This leads to the formation of scar know as CICATRISATION.
14. Wound contraction
It starts after 2-3 days and the process is completed by the 14th day.
Wound is reduced by 80% of its original size which helps in rapid
healing since lesser surface area of the injured tissue has to be
replaced.
Mechanisms
of wound
contraction
dehydration
myofibroblasts
Contraction of
collagen
15. Repair related to periodontal tissues
Simply restores the continuity of the diseased marginal
gingiva and re-establishes a normal gingival sulcus at the
same level on the roots as the base of the pre-existing
periodontal pocket.
Arrests bone destruction but does not result in gain of
gingival attachment or bone height.
16. wound strength- extracellular matrix
The wound is strengthened by proliferation of fibroblast and myofibroblast
which get structural support from the extracellular matrix
ECM has five main components:
1. collagen
2. adhesive glycoprotein
fibronectin - plasma/ tissue type
tenascin or cytotactin
thrombospondin
3. basement membrane
4. elastic fibres
5. proteoglycans
17. Healing by first intention
(Primary union)
This is defined as healing of a wound which has the following
characteristics:
Clean and uninfected
Surgically incised
Without much loss of cells and tissue
Edges of wound are approximated by surgical suture
18. Primary union involves the following sequence of events:
Initial hemorrhage
Acute inflammatory response- within 24 hours
Epithelial changes- completes by 48 hours
Organization of fibroblasts- starts around 3rd day
Wound maturation- starts after 1 week and completes
around 4 weeks
19. The incised wound as well as suture
track on either side are filled with
blood clot and there is inflammatory
response from the margins
spurs of epidermal cells migrate along the
incised margin on either side as well as round the
suture track, formation of granulation tissue also
begins from below.
removal of sutures at around 7th day
result in scar tissue at the sites of
incision and suture track
20.
21. Healing by secondary intention
(secondary union)
This is defined as-
Open wound with a large tissue defect, at times infected
Extensive loss of cells and tissues
Not approximated by sutures, but is left open
22. Secondary union consists of the following events :
Initial hemorrhage
Inflammatory process
Epithelial changes
Granulation tissue formation
Wound contraction
23. A. The open wound is filled with blood clot and there is inflammatory response at
the junction of viable tissue
B. Epithelial spurs from the margins of wound meet in the middle to cover the gap
and separate the underlying viable tissue from necrotic tissue at the surface forming
scab
C. After contraction of the wound ,a scar smaller than the original wound is left
A B C
24. Molecular biology of wound healing
1. The fibrin clot and inflammatory cells
The important functions of the clot are:
plugs the cut blood vessels and also serves to protect the
denuded tissues temporarily.
reservoir of growth factors and cytokines that are released by the
degranulation of activated platelets and serving as a provisional
matrix for cell migration and might be providing the start signals
for wound repair.
25. 2. Re-epithelialization of wounds
keratinocytes start moving into the defect about 24 hours after the
injury
The keratinocytes use receptors on their surface, known as integrins
to bind to laminin in the basal lamina.
Integrins are a family of cell adhesion receptors that mediate cell
surface interactions with extracellular matrix and in some cases
with other cells
26. At this edge, the cells will have to dissolve the hemidesmosome
attachment, downregulate the expression of α6β4, and upregulate
integrin receptors α5β1, αVβ6 and αVβ5 that are suitable for adhesion
to provisional matrix components.
epidermal growth factor
transforming growth factor-α
heparin-binding epidermal growth factor and
keratinocyte growth factor are involved in stimulating the
proliferation of the epithelial cells here.
27. 3. Matrix degradation and the wound-cleaning
process
creation of a migrating path for keratinocytes is achieved by
the dissolution of the fibrin barrier by the enzyme plasmin
that is derived from the activation of plasminogen in the clot.
The two activators, tissue-type plasminogen activator and
urokinase-type plasminogen activator along with its receptor,
are upregulated in the migrating keratinocytes
28. MMP-1 degrades native collagens and aids cell migration by
destroying collagens I and III.
MMP-9 (also known as gelatinase B) can cleave the collagen in basal
lamina (type IV) and the collagen that forms the anchoring fibrils
(type VII)
MMP10 (also known as stromelysin-2) is also expressed in wounds
and is thought to have a wide spectrum of substrate specificity for
collagen
29. Connective tissue repair by:
Activation of fibroblasts by platele granules
Angiogenesis by VEGF and b-FGF
Formation of Granulation tissue by TGF, PDGF, FGF and EGF
contraction of the wound by myofibroblasts.
30. Wound repair involves phenotypic change of fibroblasts from
quiescent to proliferating cells, and subsequently to migratory, and
then to stationary matrix producing and contractile cells.
In the connective tissue, fibroblasts are surrounded by a matrix
that contains collagen and cellular fibronectin as the major
components. Consequently, quiescent fibroblasts express collagen
receptors α1β1 and α2β1 and the major fibronectin receptor α5β1
integrin which they use for adhesion to the matrix
34. Healing of oral wounds
Oral wounds heals faster and with less scarring
than extra oral wounds
It is mainly due to:
factors in saliva
specific microflora of the oral cavity
resemblance of fetal fibroblast with gingival
fibroblast
35. Role of saliva & GCF in oral wound healing
Physico-chemical factors favoring healing are:
appropriate PH
ionic strength
calcium and magnesium ions
Saliva has an efficient capacity to reduce redox activity
caused by transitional metal ions and inhibit the
production of free radicals that may be beneficial for the
healing process
36. Lubrication of oral mucosa is beneficial for
wound healing
Advantages of moist environment:
Prevention of tissue dehydration and cell death
accelerated angiogenesis
incremental breakdown of fibrin and tissue debris
Presence of growth factor – produced by saliva
37.
38. Healing following scaling & root planing
Numerous polymorphonuclear leucocytes can be seen between
residual epithelial cells & crevicular surface in about 2 hrs
There is dilation of blood vessels, oedema & necrosis in the
lateral wall of the pocket
24 hrs after scaling a widespread infiltration of inflammatory
cells and migration of keratinocytes have been observed, in
all areas of the remaining epithelium& in 2 days the entire
pocket is epithlialized.
39. In 4-5 days a new epithelial attachment may appear at bottom of
sulcus.
Depending on the severity of inflammation & the depth of
the gingival crevice, complete epithelial healing occurs in 1-2
weeks
connective tissue repair by Immature collagen fibers occur within
21days.
healing occurs with the formation of a long thin junctional
epithelium with no connective tissue attachment.
40. Healing following curettage
A blood clot forms between the root surface & the lateral wall
of the pocket, soon after the curettage
Large number of polymorphonuclear leucocytes after the procedure
rapid proliferation of granulation tissue
Epithelisation of the inner surface of the lateral wall is completed
in 2-7 days
The junctional epithelium is also formed in about 5 days
41. Healing after surgical gingivectomy
Initial response- formation of a protective surface clot
Clot is then replaced by granulation tissue
By 24 hours there is an increase in new connective tissue cells,
mainly angioblasts just beneath the surface layer of inflammation and
necrosis
42. By the 3rd day numerous young fibroblasts are located in
the area which start granulation tissue formation.
The highly vascular granulation tissue grows coronally,
creating a new free gingival margin and sulcus
Capillaries derived from the blood vessels of the
periodontal ligament migrate in to the granulation tissue
and within 2 weeks they connect with gingiva vessels
43. After 5-14 days: surface epitheliazation is complete
During first 4 weeks: keratinization is less than it was
before surgery
Complete epithelial repair takes 1 month.
Complete repair of the C.T. takes about 7 weeks
Flow of GCF is initially increased after gingivectomy and
diminishes as healing progresses.
44. Healing following electrosurgical gingivectomy
There appears to be little difference in the results obtained after
shallow gingival resection with electrosurgery and that with
periodontal knives.
when used for deep resection close to bone, electrosurgery can
produce gingival recession, bone necrosis and sequestration, loss of
bone height, furcation exposure, and tooth mobility, which do not
occur with the use of periodontal knives.
45. Healing following depigmentation of gingiva
Healing after surgical depigmentation:
After surgery it was found necessary to cover the exposed lamina propria
with periodontal packs for 7 to 10 days.
After 6 weeks the attached gingiva regenerated by only a delicate scar
present. The newly formed gingiva was clinically non-pigmented.
Healing following cryosurgical depigmentation:
At 2nd to 3rd day: superficial necrosis becomes apparent and a whitish
slough could be separated from the underlying tissue, leaving a clean
pink surface.
In 1-2 weeks: normal gingiva
In 3-4 weeks: keratinization completed.
No postoperative pain, hemorrhage, infection or scarring seen in patients.
46. Healing following depigmentation by laser:
During lasing gingiva gets covered with a yellowish layer, that could
be easily removed by a wet gauze.
After 1-2 weeks: completion of re-epithelization.
At 4th week: gingiva is similar to normal untreated gingiva i.e.,
lacking melanin pigmentation completely
47. Healing following flap surgery
Immediately response- clot formation
At edge of flap numerous capillaries are seen
1-3days after surgery space between flap & tooth surface & bone
appears reduced & the epithelial cells along border of the flap start
migrating
By 1 week after surgery
epithelial cells have migrated & established an attachment to root
surface by means of hemidesmosomes.
48. The blood clot is replaced by granulation tissue proliferating from
the gingival connective tissue, alveolar bone and periodontal ligament
By 2nd week collagen fibers begins to appear. Collagen fibers gets
arranged parallel to root surface rather than at right angles. The
attachment between soft tissue & tooth surface is weak
By end of one month following surgery the epithelial attachment is
well formed & the gingival crevice is also well epithealised
There is beginning functional arrangement of supracrestal fibres.
49. In cases where Mucoperiosteal flap…
superficial bone necrosis have been observed during first 3 days
Osteoclastic Resorption occurs in that area which reaches its peak at
4-6 days
Osteoblastic Remodelling occurs subsequently
Loss of alveolar bone height by about 1 mm may be expected after
healing.
50. Healing following osseous resection
Elevation of Mucoperiosteal Flap results in
temporary loss of nutrient supply to the bone
In addition, surgical resection of bone also
contributes to necrosis of the alveolar crest & osteoclastic resorption
of the bone takes place initially
The initial loss in bone height is compensated to some extent by the
osteoblastic repair and remodelling.
Thus final loss in bone height is clinically insignificant
Osteoblastic activity is even seen after 1 yr. post-operatively
51. Healing after implant placement
The interface area consists of bone, marrow tissue, and a hematoma
mixed with bone fragments from the drilling process.
In the early phase of healing, woven bone is formed by osteoblasts at
the surfaces of trabecular and endosteal cortical bone surrounding the
implant.
In the late phases of healing, lamellar bone replaces woven bone in a
process of creeping substitution.
52. Stages of healing of implants
a. Woven Bone Formation: When bone matrix is exposed to extra-cellular
fluid, non-collagenous proteins & growth factors are set free & initiate
repair.
Woven bone formation dominates the first4-6 weeks
b. Lamellar Bone Formation: From 2nd month post-operatively the
microscopic structure of bone changes to lamellar bone
c. Bone Remodelling: It begins around 3rd month post-operatively.
Initially rapid remodeling occurs which slows down & continues
for rest of the life
Thus complete healing probably takes longer than 3 to 6 months.
53. Use of lasers in wound healing
Lasers employing low-level energy have been claimed to produce
a positive effect on the biological and bio-chemical processes of
wound re-constitution.
Dermatologic investigations have demonstrated more rapid
epithelialization, enhanced neovascularization, and increased
production of collagen by fibroblasts in vivo
Ultimately, accelerated wound healing, reduced pain and enhanced
neural regeneration.
54. conclusion
Current scientific evidence points to the presence of:
1. cells originating from the periodontal ligament,
2. wound stability,
3. space provision
4. primary intention healing, as fundamental biologic and clinical
factors that must be met to obtain periodontal regeneration.
55. Wound healing is achieved by a series of coordinated efforts by
inflammatory cells, keratinocytes, fibroblasts and endothelial
cells responding to a complex array of signals.
Future research will have to be directed towards understanding
in more detail the molecular mechanisms of differential gene
expression in healing wounds.
56. References
Harshmohan, Textbook of essential pathology for dental students-3rd ed.
Jan lindhe, Textbook of clinical periodontology & implant dentistry -
F.A. Carranza, Textbook of clinical periodontology- 10th ed.
Lariha¨kkinen,Veli-jukka Uitto & Hannularj Av, cell biology of gingival
wound healing, periodontology 2000, vol. 24, 2000, 127–152.
Guy A. Catone, Edward Halusic. Photobiology of lasers in oral and
maxillofacial surgery. In: Guy A. Catone, Charles C. Alling. Lasers
applications in oral and maxillofacial surgery. USA: W.B. Saunders
company, 1997.