Periodontal abcess in dentistry concise view.pptxHazimrizk1
Periodontal abscess concise view discussing its Definition, Etiology and risk factors,
Pathogenesis,signs and symptomes,Clinical features
Diagnosisand diffrential diagnosis
Management
Everything a dentist needs to know about a periodontal abscess is here.
Along with all the relevant facts, references, definitions, classifications, and each and every statement is given with proper detail
Periodontal abcess in dentistry concise view.pptxHazimrizk1
Periodontal abscess concise view discussing its Definition, Etiology and risk factors,
Pathogenesis,signs and symptomes,Clinical features
Diagnosisand diffrential diagnosis
Management
Everything a dentist needs to know about a periodontal abscess is here.
Along with all the relevant facts, references, definitions, classifications, and each and every statement is given with proper detail
about pathophysiology behind endo perio lesion and various methods for it. it also explains various complications related to it, dental anomalies associated.
Non Surgical Periodontal Therapy by Dr Santosh Martandesantoshmds
Review and Essay Material on Non Surgical Periodontal Therapy. Illustrative Contents for proper presentation on all aspects of NSPT. The Presentation helps in drafting A to Z of NSPT. Readers are encouraged to add newer studies and ideas under each aspect of NSPT.
Introduction
Definition
Pathway of odontogenic infection
Classification
Maxillary space infection
Mandibular space infection
Ludwigs angina
Cavernous sinus thrombophlebitis
Occurrence of infectious disease is determined by interaction of host , the microorganism and the environment
In healthy state there is balance among these factors and when the balance is lost disease occurs
Most odontogenic infections arise as a sequel of pulp necrosis caused by caries, trauma, periodontitis
Definition : the fascial spaces are the potential spaces between the various layers of fascia normally filled with loose connective tissue and bounded by anatomical barriers , usually of bone , muscle or fascial layers.
(Moore – 1975)
Invasion of dental pulp by bacteria after decay of a tooth
inflammation edema and lack of blood supply
Venous congestion ,pulpal tissue death
Reservoir for bacterial growth
Periodic egress of bacteria into surrounding alveolar Acute stage
in acute stage ,infection spreading in the soft tissues can take the following forms of in the clinical situation
Abscess
Cellulitis
Fulminating infections
CONSCIOUS SEDATION USE ON ANXIETY REDUCTION, AND PATIENT AND SURGEON SATISF...Dr. B.V.Parvathy
EFFECT OF CONSCIOUS
SEDATION USE ON ANXIETY REDUCTION, AND PATIENT
AND SURGEON
SATISFACTION IN DENTAL
IMPLANT SURGERIES: A
SYSTEMATIC REVIEW AND META-ANALYSIS
Orthodontics-Periodontics Relationship
ntroduction
Biological basis for orthodontic therapy
Periodontal tissue response to orthodontic force
Effects of orthodontic tooth movement on the periodontium
Orthodontic tooth movement in adults with periodontal tissue breakdown
Specific factors associated with orthodontic tooth movement
Implants and orthodontic therapy
Systematics of combined ortho – perio treatment
Periodontally Accelerated Osteogenic Orthodontics (PAOO)
Minor periodontal surgery and orthodontic treatment
Review of literature
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about pathophysiology behind endo perio lesion and various methods for it. it also explains various complications related to it, dental anomalies associated.
Non Surgical Periodontal Therapy by Dr Santosh Martandesantoshmds
Review and Essay Material on Non Surgical Periodontal Therapy. Illustrative Contents for proper presentation on all aspects of NSPT. The Presentation helps in drafting A to Z of NSPT. Readers are encouraged to add newer studies and ideas under each aspect of NSPT.
Introduction
Definition
Pathway of odontogenic infection
Classification
Maxillary space infection
Mandibular space infection
Ludwigs angina
Cavernous sinus thrombophlebitis
Occurrence of infectious disease is determined by interaction of host , the microorganism and the environment
In healthy state there is balance among these factors and when the balance is lost disease occurs
Most odontogenic infections arise as a sequel of pulp necrosis caused by caries, trauma, periodontitis
Definition : the fascial spaces are the potential spaces between the various layers of fascia normally filled with loose connective tissue and bounded by anatomical barriers , usually of bone , muscle or fascial layers.
(Moore – 1975)
Invasion of dental pulp by bacteria after decay of a tooth
inflammation edema and lack of blood supply
Venous congestion ,pulpal tissue death
Reservoir for bacterial growth
Periodic egress of bacteria into surrounding alveolar Acute stage
in acute stage ,infection spreading in the soft tissues can take the following forms of in the clinical situation
Abscess
Cellulitis
Fulminating infections
CONSCIOUS SEDATION USE ON ANXIETY REDUCTION, AND PATIENT AND SURGEON SATISF...Dr. B.V.Parvathy
EFFECT OF CONSCIOUS
SEDATION USE ON ANXIETY REDUCTION, AND PATIENT
AND SURGEON
SATISFACTION IN DENTAL
IMPLANT SURGERIES: A
SYSTEMATIC REVIEW AND META-ANALYSIS
Orthodontics-Periodontics Relationship
ntroduction
Biological basis for orthodontic therapy
Periodontal tissue response to orthodontic force
Effects of orthodontic tooth movement on the periodontium
Orthodontic tooth movement in adults with periodontal tissue breakdown
Specific factors associated with orthodontic tooth movement
Implants and orthodontic therapy
Systematics of combined ortho – perio treatment
Periodontally Accelerated Osteogenic Orthodontics (PAOO)
Minor periodontal surgery and orthodontic treatment
Review of literature
To evaluate the effects of B. lactis HN019 on clinical periodontal parameters (plaque accumulation and gingival bleeding), on the immunocompetence of gingival tissues [expression of BD-3, Toll-like receptor 4 (TLR4), cluster of differentiation (CD)-57 and CD-4], and on immunological properties of saliva (IgA levels) and adhesion to buccal epithelial cells and antimicrobial properties in non-surgical periodontal therapy in GCP patients.
INTRODUCTION
KEY ELEMENTS IN TISSUE ENGINEERING
- Progenitor cells
- Scaffold
- Signalling molecules
DESIRED PROPERTIES AND WAYS TO ENHANCE THE REGENERATIVE CAPACITY OF SCAFFOLDS
4. GENE THERAPY IN PERIODONTAL TISSUE ENGINEERING
5. RECENT DEVELOPMENTS
6. CRITICAL ANALYSIS OF PRESENT STATUS OF TISSUE ENGINEERING FOR PERIODONTICS.
4. CONCLUSION
5. REFERENCES
To evaluate the efficacy of the GPCS for palatal hemostasis during and after the FGG harvesting procedure.
A secondary objective was to evaluate if the placement of the suture improved the operator
visibility thereby reducing the surgical time.
Comparative study of DFDBA and FDBA block grafts.pptxDr. B.V.Parvathy
To evaluate and compare the effectiveness of demineralized freeze dried block graft and freeze dried block graft with chorion membrane as barrier membrane clinically and radiographically for the treatment of residual deep intra bony defects.
Abstract
Focused Clinical Question: Debates and questions related to the newly developed two-vector system
for classification of periodontal diseases have emerged as to how to accurately assign stage and grade
to the periodontitis cases. The aim of the present manuscript is to demonstrate the essential thought
processes that are needed in utilizing the new periodontitis classification system to diagnose two gray
zone cases.
Summary: Clinical case 1 includes an 83-year old patient diagnosed with periodontitis and classified as
Generalized Stage III Grade B periodontitis, while clinical case 2 , a 73-year old male was classified as
presenting Generalized Stage IV Grade B periodontitis. Although clinical and radiographic evaluations
revealed similarities between the cases, the thought process that includes clinical judgement is
described to guide a more accurate diagnosis following the guidelines of the new classification
system.
Conclusion: The two cases demonstrated here offer an opportunity for clinicians to recognize the
essential role of sound clinical judgment in certain cases when applying the new periodontal disease
classification system and also to clarify questions emerging from implementing this classification
system.
Key words: Staging and grading of periodontal diagnosis, Periodontal Diseases, Periodontal Diagnosis,
Abstract
Aim: The aim of this study was to determine whether the combined connective tissue
graft (CTG) with injectable platelet‐rich fibrin (i‐PRF) with coronally advanced flap
(CAF) improved root coverage of deep Miller Class I or II gingival recessions com‐
pared with CTG alone with CAF.
Material and Methods: Seventy‐two patients with Miller class I and II gingival reces‐
sions were enrolled. Thirty‐six patients were randomly assigned to the test group
(CAF+CTG+i‐PRF [700 rpm for 3 min]) or control group (CAF+CTG). Clinical evalua‐
tions were made at 6 months.
Results:At 6months, complete root coveragewas obtained at 88% of the sites treated
with CAF+CTG+i‐PRF and 80% of the sites treated with CAF+CTG. Difference be‐
tween the two groups was not statistically significant. At 6 months, the recession
depth (RD) reduction and increase in keratinized tissue height (KTH) of the test sites
were significantly better compared with the control sites.
Conclusions: According to the results, the addition of i‐PRF to the CAF+CTG treat‐
ment showed further development in terms of increasing the KTH and decreasing
RD. However, this single trial is not sufficient to advocate the true clinical effect of
i‐PRF on recession treatment with CAF+CTG and additional trials are needed.
KEYWORDS
connective tissue graft, injectable platelet‐rich fibrin, root coverage
DEFINITION
ETIOLOGY
HISTORICAL PRESPECTIVE
TERMINOLOGIES WHICH HAVE BEEN USED TO DESCRIBE OCCLSAL TRAUMA
REVIEW OF LITERATURE
OCCLUSAL FORCES DURING JAW MOVEMENTS
CLASSIFICATION
STAGES OF TISSUE RESPONSE TO EXCESSIVE OCCLUSAL FORCES
EXAMINATION AND DIAGNOSIS
DEFINITION
INDICATION AND OBJECTIVES
PROCEDURES FOR INCREASING WIDTH OF ATTACHED GINGIVA
PROCEDURES FOR ROOT COVERAGE
TECHNIQUES FOR CORRECTION OF ABERRANT FRENUM
PAPILLA RECONSTRUCTION
RIDGE AUGMENTATION
PROCEDURES FOR INCREASING VESTIBULAR DEPTH
CROWN LENGTHENING PROCEDURES
The Efficacy of Pocket Elimination/Reduction Compared to Access Flap Surgery: A SystematicReview and Meta-analysis
To assess the efficacy and adverse effects of resective
surgery compared to access flap in patients with
periodontitis.
Impact of Different Surgical Protocols on Dimensional Changes of Free Soft Ti...Dr. B.V.Parvathy
To determine if there is a difference in the amount of shrinkage during
healing of free soft tissue autografts (FSTA) using different surgical
techniques—suturing the vestibular flap margin apically to the base of
the recipient bed versus leaving the flap margin free and unsutured.
Regenerative Surgical Treatment of Furcation Journal PresentationDr. B.V.Parvathy
AIM
To evaluate the performance and the added values of surgical regenerative techniques in terms of tooth loss, furcation closure/conversion, horizontal bone level gain and other periodontal parameters of teeth affected by periodontitis-related furcation defects, at least 12 months after surgery.
i-prf &MN in gingival augmentation in thin phenotypeDr. B.V.Parvathy
To evaluate the effect of gingival thickness (GT) and keratinized tissue width (KTW) using injectable platelet rich fibrin (i-PRF) alone and with microneedling (MN) in individuals with thin periodontal phenotypes.
Local Treatment in Periodontal pocket Journal PresentationDr. B.V.Parvathy
It was a systematic review and network meta-analysis aimed to evaluate the efficacy of adjunctive locally delivered antimicrobials, compared to sub gingival instrumentation alone or plus a placebo, on changes in probing pocket depth (PPD) and clinical attachment level (CAL), in patients with residual pockets during supportive periodontal care.
2 Stage Crown Lengthening VS 1 Stage Journal PresentationDr. B.V.Parvathy
This randomized controlled trial aimed to assess the efficacy of a two-
stage crown lengthening intervention (SCL) in the aesthetic zone
compared with a one-stage crown lengthening procedure (CCL).
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
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.
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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.
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
3. ABSCESS IN PERIODONTIUM
Definition
1) A localized purulent infection in the periodontal tissues.
Meng H X et al; 1999
2) A lesion with an expressed periodontal breakdown occurring during a limited
period of time, and with easily detectable clinical symptoms, including a
localised accumulation of pus located within the gingival wall of the periodontal
pocket.
Herrera et al; 2000
4.
5. Classification
By the Location of the Abscess Gillets et al; 1980
Gingival Abscess Periodontal Abscess
Localised painful swelling,
affecting only the marginal
and interdental
gingiva. [Due to impacted
foreign objects]
Localised painful swelling,
affecting deeper periodontal
structures, including deep
pockets, furcations and
vertical osseous defects.
Affects only marginal soft
tissues.
Located beyond mucogingival
line.
Histologically, both lesions are identical.
6. Course of Lesion: Pini Prato et al; 1988
Acute Periodontal
Abscess
Chronic Periodontal
Abscess
Symptoms; pain, tenderness,
sensitivity to
palpation, and suppuration
upon gentle pressure.
Associated with a sinus tract,
and it is usually
asymptomatic, although the
patient can
refer mild symptoms. May
have an acute exacerbation.
A localised acute abscess may become a chronic abscess
when drainage is established through a sinus or through the
sulcus.
7. Number of Abscess: Topoll H H et al; 1990
Single Periodontal
Abscess
Multiple Periodontal
Abscess
Associated with local factors,
which contribute to the
closure of the drainage of a
periodontal pocket.
Reported in uncontrolled
diabetes mellitus, medically
compromised patients, and
in patients with untreated
periodontitis after systemic
antibiotic therapy for non‐oral
reasons.
Seen in a patient with
multiple external root
resorptions
8. According to the International Workshop for a Classification of Periodontal
Diseases and Conditions, 1999:
Gingival Abscess
A localized, painful, rapidly expanding lesion involving the marginal gingiva or interdental
papilla sometimes in a previously disease-free area.
Periodontal Abscess (Acute or Chronic)
A localized accumulation of pus within the gingival wall of a periodontal pocket resulting in
the destruction of the collagen fibre attachment and the loss of nearby alveolar bone.
Pericoronal Abscess
A localized accumulation of pus within the overlying gingival flap surrounding the crown of
an incompletely erupted tooth.
Periapical Abscess
9. Periodontal Abscess
In periodontitis patients, there are different subgroups:
• Acute exacerbation of an untreated periodontitis.
Dello Rurso N M et al, 1985
Periodontitis-affected sites (with a pre-existing
periodontal pocket)
Healthy sites (without a pre-existing pocket)
10. • After non-surgical periodontal therapy: after scaling or professional prophylaxis,
dislodged calculus fragments can be pushed into the tissues or inadequate scaling may
allow calculus to remain in deep pocket areas, while the coronal part will occlude the
normal drainage.
• After surgical periodontal therapy: associated with the presence of foreign bodies such
as membranes for regeneration or sutures.
• Acute exacerbation in refractory periodontitis Fine D H et al, 1994
• Acute exacerbation in supportive periodontal therapy.
• Systemic antimicrobial intake without subgingival debridement, in patients with
advanced periodontitis may also cause abscess formation, probably related to an
overgrowth of opportunistic bacteria.
11. In Non-Periodontitis patients:
• Different foreign bodies have been described to be associated with the development of a
periodontal abscess, an orthodontic elastic, a piece of dental floss, a dislodged cemental
tear, a piece of a toothpick or pieces of nails in subjects with nail-biting habits. Also
termed ‘oral hygiene abscesses’.
• The root surface may be altered by different factors: perforation by an endodontic
instrument, cervical cemental tears, external root resorption, an invaginated tooth or a
cracked tooth.
12. Pathogenesis
The invasion of bacteria into the soft tissues surrounding the periodontal pocket
Inflammatory process through the chemotactic factors released by bacteria that attract
inflammatory cells
The destruction of the
connective tissues, the encapsulation of the bacterial
infection and the production of pus
DeWitt G V et al, 1985
Once the abscess is formed, the rate of destruction within the abscess will depend on the
growth of bacteria inside the focus, their virulence and the local pH.
13. Histopathology
• A normal oral epithelium and lamina propria.
• An acute inflammatory infiltrate.
• An intense focus of inflammation, with presence of neutrophils and lymphocytes in an area
of destroyed and necrotic connective tissue.
• A destroyed and ulcerated pocket epithelium.
• Gram-negative bacteria.
DeWitt G V et al, 1985
14. Microbiology
The most prevalent bacterial species identified in periodontal abscesses, using culture-based
or molecular-based diagnostic techniques, is:
o Porphyromonas gingivalis
o Prevotella intermedia
o Prevotella melaninogenica
o Fusobacterium nucleatum
o Tannerella forsythia
o Treponema spp.
o Parvimonas micra
o Actinomyces spp.
o Bifidobacterium spp
o Campylobacter spp.
o Capnocytophaga spp.
o Aggregatibacter actinomycetemcomitans
15. Based on Symptoms:
• Severe pain
• Tenderness of gingiva
• Swelling
• Tooth mobility
• Tooth elevation
• Sensitivity of the tooth to palapation
Based on Oral examination,
Clinically:
• Presence of an ovoid elevation in the gingiva along the lateral part of the root.
• Found as a diffuse swelling or simply as a red area.
16. • Suppuration either through a fistula or, most commonly, through the pocket opening,
spontaneous, or occur after applying pressure on the lesion.
• Bleeding on probing.
• Increased tooth mobility.
Radiographically:
• Normal appearance
• Some degree of bone loss [In previous pockets]
General Examination:
• Body temperature
• Malaise
• Regional lymphadenopathy
• Increased blood leukocytes
17. Differential diagnosis
Other abscesses in the mouth: periapical or dento-alveolar or endodontic abscesses, lateral
periapical cyst, vertical root fractures, endo-periodontal abscess, postoperative infection.
Tumor lesions, including metastatic tumoral lesions, odontogenic myxoma, non-Hodgkin´s
lymphoma, squamous cell carcinoma, metastatic carcinoma.
Other oral lesions: pyogenic granuloma, osteomyelitis, odontogenic keratocyst, eosinophilic
granuloma.
Self-inflicted gingival injuries.
Sickle cell anemia.
Abscesses after surgical procedures.
18. Problems in 1999 Classification
(1) The differentiation between gingival and PA, which could be confusing, because
this differentiation was simultaneously based on location and etiology.
(2) Considering a PA as chronic or acute may not be adequate, because an abscess, by
definition, is an acute lesion.
(3) The inclusion of pericoronitis and periapical abscesses in the classification together
with PA might not be appropriate.
20. Treatment
Two distinct phases:
1. Control of the acute condition
2. Management of a pre‐existing and/or residual lesion
Control of the acute condition:
Four therapeutic alternatives;
1. Tooth extraction
2. Drainage and debridement
3. Systemic or local antimicrobials
4. Surgery
21. • Tooth extraction: If severely damaged, and prognosis is hopeless after the destruction
caused by the abscess.
• Drainage and debridement: Through the pocket or through an external incision, compression
and debridement of the soft tissue wall, and the application of topical antiseptics after the
drainage. If associated with a foreign body impaction, the object has to be eliminated
through careful debridement.
• Systemic or local antimicrobials:
Smith & Davies 1986 -evaluated the incision and drainage of the abscess, together with
adjunctive systemic metronidazole (200 mg, tid, 5 days), followed by a delayed periodontal
therapy
Hafström et al, 1994 -drainage through the periodontal pocket, irrigation with sterile saline,
supragingival scaling and tetracycline for 2 weeks (1 g/day).
Herrera et al, 2000 -compared azithromycin (500 mg, once per day, 3 days) versus
amoxicillin plus clavulanate (500+125 mg, tid, 8 days), with delayed scaling (after 12 days).
22. Eguchi et al, 2008 -compared irrigation with sterile physiological saline and 2% minocycline
hydrochloride ointment, versus irrigation with sterile physiological saline without the local
antibiotic.
• Surgery: Abscesses associated with deep vertical defects, or in cases occurring after
periodontal debridement in which calculus is left subgingivally after the treatment.
The drug with the most adequate profile is metronidazole (normally prescribed, for acute
conditions, at 250 mg, tid). Azithromycin (500 mg, once per day) and amoxicillin plus
clavulanate (500+125 mg, tid) have also shown good clinical results. The duration of the
therapy should be restricted to the duration of the acute lesion, which is normally 2‐3 days.
23.
24. Management of a pre‐existing and/or residual lesion:
Since most periodontal abscesses occur in a previously existing periodontal pocket,
periodontal therapy should be evaluated.
• If not been treated previously→ appropriate periodontal treatment should be provided.
• If within the active phase of therapy → once the acute lesion is treated the periodontal
therapy should be completed.
• If patients during SPT → a careful evaluation of the recurrence of the abscesses should
be made as well as an adequate evaluation of the tissue damage and how this affects
tooth prognosis.
25. CONTENTS - PART 2
Necrotizing Periodontal Diseases
• Definition
• Classification
• Etiology – Host Immune Response
• Microbiology
• Pathophysiology & Histological features
• Diagnosis
• Problems in 1999 Classification
• 2017 Classification
• Differential diagnosis / Other Acute Conditions in Periodontium
• Treatment
26. NECROTIZING PERIODONTAL
DISEASES
NPD is a group of infectious diseases that includes:
• Necrotizing ulcerative gingivitis (NUG)
• Necrotizing ulcerative periodontitis (NUP)
• Necrotizing stomatitis (NS)
27. Older names of NUG:
• Vincent’s disease
• Trench‐mouth disease
• Necrotizing gingivo‐estomatitis
• Fusospirochaetal stomatitis
• Ulcerative membranous gingivitis
• Acute ulcerative gingivitis
• Necrotizing ulcerative gingivitis or Acute necrotizing ulcerative gingivitis
NUP was defined by:
- 1989 World Workshop
- 1993 European Workshop
- International Workshop for a Classification of Periodontal Diseases and Conditions in 1999
28. Classification
According to the location of the tissue affected by the acute disease process, NPD can
be classified as:
• Necrotizing gingivitis: when only the gingival tissues are affected.
• Necrotizing periodontitis: when the necrosis progresses into the periodontal
ligament and the alveolar bone, leading to attachment loss.
• Necrotizing stomatitis: the necrosis progresses to deeper tissues beyond the
mucogingival line, including the lip or cheek mucosa, the tongue, etc.
Horning G M et al, 1995
29. Etiology
Host Immune Response
Non HIV patients;
• Previous history of NPD
• Poor oral hygiene
• Inadequate sleep
• Unusual psychological stress
• Poor diet
• Recent systemic diseases
• Alcohol abuse
• Tobacco smoking
• Caucasian ethnicity
• Age below 21
30. HIV Patients; Winkler et al,1988
• NPD are more frequent and show a faster progression.
• The reduction in the counts of peripheral CD4 lymphocytes.
Malnutrition;
• “Protein‐energy malnutrition”, a marked reduction in key antioxidant nutrients and an
altered acute phase response against infection.
• An inversed proportion in the ratio of helper/suppressor T‐lymphocytes, histaminemia,
increased free cortisol in blood and saliva.
• Defects in mucosal integrity.
Psychological stress and insufficient sleep;
• Associated with NG.
• Military personnel in wartime.
• New recruits for military services.
• Drug‐abusers during abstinence syndrome.
• Students during exam periods
• Patients with depression or other psychological conditions
31. • During these stress periods, not only the immune response is altered, but also the
subject’s behavior, leading to inadequate oral hygiene, poor diet or increased tobacco
consumption.
• Mechanism; a reduction in the gingival microcirculation and salivary flow and an
increase in serum and urine levels of 17‐hydroxycorticosteroid (17‐OHCS), which are
associated with an alteration in the function of polymorphonuclear leukocytes (PMN)
and lymphocytes, or even an increase in the levels of periodontal pathogens, such as P.
intermedia.
• In patients with NG, higher urine levels of 17‐OHCS have been reported, when
compared with healthy or treated patients.
• Patients with NG also contained PMNs with altered functions, since their bactericidal,
phagocytic and chemotactic capacities were depressed.
32. Inadequate oral hygiene, pre‐existing gingivitis and previous history of NPD;
• Plaque accumulation due to ulcer and crater lesions that may limit tooth brushing due to
pain.
• Usually occurs over a previously existing periodontal disease, usually chronic gingivitis.
Alcohol and tobacco consumption;
• Smoking is a risk factor.
• Mechanisms; effect of smoking on inflammation and tissue response, since smoking
interferes with both PMN and lymphocyte function and nicotine induces
vasoconstriction in gingival blood vessels.
• Alcohol consumption has also been associated with the physiological and psychological
factors favoring NPD.
Young age and ethnicity;
• In developed countries, young people are more prone to suffer NPD, mostly between 21-
24 years, usually combined with other predisposing factors, such as smoking and stress.
• NPD affects even younger people, being malnutrition and occurrence of infections.
33. Microbiology
• Spirochetes and fusiform bacteria Plaut et al, 1894 and Vincent et al, 1896 – Vincent’s
Infection
• Culture studies:- P. intermedia, and Treponema, Selenomonas and Fusobacterium species,
“constant flora”.
• In HIV patients:- along with other species, invasion of Candida albicans, herpes viruses or
superinfecting bacterial species.
34. Pathophysiology & Histological features
In NG lesions observed through light microscopy have shown a distinct pathology, with
presence of an ulcer within the stratified squamous epithelium and the superficial layer of the
gingival connective tissue surrounded with a non‐specific acute inflammatory reaction.
Four regions are:-
(1) Superficial bacterial area: [Fibrous mesh]
composed of degenerated epithelial cells, leukocytes, cellular rests, and a wide variety of
bacterial cells, including rods, fusiforms and spirochetes.
35. (2) Neutrophil-rich zone:
composed of a great number of leukocytes, especially neutrophils, and numerous
spirochetes of different sizes and other bacterial morphotypes located between the host
cells.
(3) Necrotic zone:
presence of disintegrated cells, together with medium and large size spirochetes and
fusiform bacteria.
(4) Spirochetal infiltration zone:
tissue components are adequately preserved, but infiltrated by large and medium size
spirochetes.
36.
37. Diagnosis
Based on the clinical findings:
Necrotizing gingivitis:
• Based on the presence of necrosis and ulcers in the free gingiva.
• Start at the interdental papilla with the typical “punched‐out” appearance.
• A marginal erythema, named “lineal erythema”, may be present, separating the healthy
and the diseased gingiva.
• Necrotic lesions can progress to the marginal gingiva.
• Most typical location is the anterior teeth, especially in the mandible.
• Gingival bleeding is a frequent finding, usually spontaneous or after minimal contact.
• Painful with severity.
38. Other less common findings are:
• Pseudo‐membranous formation over the necrotic area. It consists on a meshwork of whitish-
yellow color, composed of necrotic tissue, fibrin, erythrocytes, leukocytes and bacterial
cells. When this “membrane” is removed, the underlying connective tissue becomes
exposed and bleeds.
• Halitosis.
• Adenopathies, if present, submandibular lymph nodes.
• Fever and a general feeling of discomfort.
39.
40. Necrotizing periodontitis:
• Along with clinical features of NG; affects the periodontal ligament and alveolar bone,
leading to loss of attachment.
• On progression, the interdental papilla is divided in a buccal and a lingual/palatal part,
with a necrotic area in the middle, known as interproximal crater. If the craters are deep,
the interdental crestal bone becomes exposed and denudated. In addition, crater
formation favors disease progression by allowing the accumulation of more bacteria.
Interproximal necrotic areas spread laterally and merge with the neighboring areas,
creating an extensive zone of destruction.
• Immune‐compromised patients, bone sequestrum (necrotic bone fragments within the
tissues but separated from the healthy bone) may occur, mainly interdentally, but also in
buccal or lingual/palatal alveolar bone.
41. Necrotizing stomatitis:
• When bone denudation extends through the alveolar mucosa, larger bone sequestra may
occur, with large areas of osteitis and oral‐antral fistulae.
• Severity of these lesions is associated with severely compromised systemic patients,
including AIDS patients and severe malnutrition.
Problems in 1999 Classification
1. Did not consider the huge differences in prevalence, risk of progression, and extent and
severity of NPD among patients with different predisposing conditions.
43. Differential diagnosis / Other Acute Conditions in Periodontium
Gingival lesions of specific bacterial origin
• Group B streptococci → Gingival lesion- Streptococcal gingivostomatitis
Treated with re-hydration, resting, systemic antimicrobials
• Staphylococci aureus → with vesicles & desquamation, affecting lips, oral mucosae.
Appearance similar to multiform erythema or impetigo.
Treated with, systemic antimicrobials.
• Neisseria gonorrhoeae → white‐yellowish plaques or pseudo‐membranes when
removed → bleeding ulcer
Salivary flow ↓ → denser saliva
Treated with, systemic antimicrobials
Erythematous Erosive
44. • Treponema pallidum → Primary syphilis → chancre on the lips, tongue or tonsils.
Secondary syphilis → gingiva later with presence of plaque
(elevated papillae with central erosion)
Tertiary syphilis → affect palate and tongue
Treated with, specific systemic antimicrobials.
Virus infections
• Varicela → Herpusvirus varicella (HSV-3) → Vesicles in oral cavity, including
gingiva
Treated with, antiviral agents & adequate nutritional support.
• Recurrent herpetic infection → Herpessimplex virus type 1(HSV-1) → Primary
Herpetic Gingivostomatitis
Intraoral or labial, itching & stinging feelings.
Erythema, grouped lesions break forming an erosion in oral mucosae gingiva or lip.
DD to recurrent aphthous stomatitis. Treated with, antiviral agents.
45. • Epstein Barr Virus (EBV) → Herpessimplex virus type 4 (HSV-4), Cytomegalovirus
or Herpes Simplex Virus Type-5 (CMV or HSV-5) or Coxsackie virus → specific
oral manifestations: infectious mononucleosis (HSV-4) or hand, foot & mouth
disease (Coxsackie).
Fungal infections
• Candidiasis → in immunocompromised patients.
Treated with, antifungal agents →Nystatin, Amphotercin B or Miconazole in solution
or gels.
Gingival manifestations of systemic conditions
• Mucocutaneous disorders →Chronic autoimmune disease →Vesicle-bullous lesions
with liquid content.
Present in gingiva as desquamative gingivitis, erythematous, vesicle-bullous or erosive
lesions. Reddness in attached and free gingiva.
Treated with, application of topical or systemic corticoids.
46. • Lichen planus → Reticular oral lesions on buccal and cheek mucosa. Erosive forms
in tougue and gingiva cause pain and tenderness, as well as bleeding.
Seen as desquamative gingivitis on attached gingiva.
• Pemphigus →Vulgaris →Desquamative gingivitis.
• Pemphigoid →Benign mucous membrane pemphigoid or Cicatrical phemphigoid
→Desquamative gingivitis including periods of exacerbation & remission.
Allergic reactions
• Exudative erythema multiforme →Desquamative gingivitis.
• Contact allergy →Erythematous & edematous gingival tissues
Treated by, removal of the allergen.
47. Traumatic lesions
• Physical (mechanical & thermal) injury →Erosions or ulcer, associated with gingival
recessions. Hyper-quertosis, vesicles or bullae.
• Ionizing radiations →Mucositis, with erythema followed by epithelial necrosis with
whitish plaques, leaves bleeding surface after dislodging.
• Chemical & pharmacological injury →Macular, vescicles, erosions or ulcers.
48. Treatment
The treatment should be organized in successive stages, including the treatment of the
acute phase and a subsequent treatment phase that should include the treatment of
the pre‐existing condition, the corrective treatment of the disease sequelae, and the
supportive or maintenance phase.
Treatment of the Acute Phase:
Two main objectives- 1) To arrest the disease process and tissue destruction.
2) To control the patient´s general feeling of discomfort and pain, which is interfering
with nutrition and oral hygiene practices.
49. Superficial debridement: Westergaard J et al, 1994
• To remove the soft and mineralized deposits.
• Power‐driven debridement devices (e.g. ultrasonics) are usually recommended exerting
minimum pressure over the ulcerated soft tissues.
• The debridement should be performed daily, getting deeper as the tolerance of the
patient improves, and lasting for as long as the acute phase lasts (normally, 2‐4 days).
• Mechanical oral hygiene measures should be limited, in order to avoid pain, since
brushing directly in the wounds may impair healing.
• During this period the patient is advised to use chlorhexidine‐based mouth rinses (at
0.12‐0.2%, twice daily), 3% hydrogen peroxide diluted 1:1 in warm water, and other
oxygen‐releasing agents.
If unsatisfactory response to debridement or systemic effects (fever,malaise)
50. Systemic antimicrobials:
• Metronidazole, at 250mg, every 8 hours, may represent the first alternative, due to its
action over strict anaerobes.
• Other systemic drugs have also been proposed, with acceptable results, including
penicillin, tetracyclines, clindamycin, amoxicillin or amoxicillin plus clavulanate.
• Conversely, locally delivered antimicrobials are not recommended, due to the large
amount of bacteria present within the tissues, where the local drug will not be able to
achieve adequate concentrations.
• These patients have to be followed‐up very closely, daily if possible, and as the
symptoms and signs improve, strict mechanical hygiene measures should be enforced, as
well as complete debridement of the lesions can be scheduled.
51. Treatment of the pre‐existing condition: Cohen ME et al, 1995
• Once the acute phase has been controlled, the treatment of the pre‐existing chronic
condition should be implemented, including professional prophylaxis and/or scaling and
root planing.
• Oral hygiene instructions and motivation should be enforced.
• Existing predisposing local factors, such as overhanging restorations, interdental open
spaces and tooth malposition should be carefully evaluated and treated.
• At this stage, and also during the acute phase, attention should be paid to the control of
the systemic predisposing factors, including smoking, adequate sleep, reduction of stress
or treatment of the systemic conditions
52. Corrective treatment of disease sequelae: Westergaard J et al, 1994
• The correction of the altered gingival topography caused by the disease should be
considered, since gingival craters may favor plaque accumulation and disease recurrence.
• Gingivectomy and/or gingivoplasty procedures may be helpful to treat superficial
craters; for deep craters, periodontal flap surgery, or even regenerative surgery represent
more suitable options.
53. Supportive or maintenance phase:
• During this phase, the main goal becomes the compliance with the oral hygiene
practices and the control of the predisposing factors.
54. Specific considerations for HIV‐positive patients:
• Occurrence of NPD in systemically healthy individuals is suggestive of HIV infection,
and therefore the affected individuals should be screened for HIV.
• The specific management of NPD in HIV‐positive patients includes debridement of
bacterial deposits combined with the irrigation of the site with iodine povidone, based
on its hypothetic anesthetic and bleeding control effects.
• Careful consideration should be made regarding the use of systemic antimicrobials, due
to the risk of over-infections with Candida spp.
• Metronidazole has been recommended due to its narrow spectrum, with limited effects
on Gram‐positive bacteria, which prevent Candida spp. overgrowth, although HIV-
positive patients may not need antibiotic prophylaxis for the treatment of NPD.
• In non‐responding cases, the use of antifungals may be beneficial, including
clotrimazole lozenges, nystatin vaginal tablets, systemic fluoconazole or itraconazole,
mainly in cases of severe immunesuppression.
56. Clinical Presentation
Involves both the pulp and periodontal tissues and may occur in acute or chronic forms.
Signs and symptoms:
• Deep periodontal pockets reaching or close to the apex and negative or altered response
to pulp vitality tests.
• Bone resorption in the apical or furcation region, spontaneous pain or pain on palpation
and percussion, purulent exudate, tooth mobility, sinus tract, crown and gingival color
alterations.
57. Etiology
Primary etiology:
(1) Endodontic and/or periodontal infections
(2) Trauma and/or iatrogenic factors
(1) Endo-periodontal lesions associated with endodontic and periodontal infections:
Might be triggered;
(i) by a carious lesion that affects the pulp and, secondarily, affects the periodontium;
(ii) by periodontal destruction that secondarily affects the root canal;
(iii)or by both events concomitantly. Less frequently, “true-combined” or “combined”
lesion. Develop in subjects with periodontal health or disease.
58. (2) Endo-periodontal lesions associated with trauma and iatrogenic factors:
Poor prognosis as they affect the tooth structure.
Most common lesions are:
(1) root/pulp chamber/furcation perforation
(2) root fracture or cracking
(3) external root resorption
(4) pulp necrosis draining through the periodontium
Microbiology
Great similarity between the microbiota found in the root canals and periodontal pockets.
Mainly “red” and “orange” complexes, such as P. gingivalis, T. forsythia,or Parvimonas
micra, and species from the genera Fusobacterium, Prevotella and Treponema.
59. Risk factors
• Advanced periodontitis
• Trauma
• Iatrogenic events
• Presence of grooves
• Furcation involvement
• Porcelain-fused-to-metal crowns
• Active carious lesions
In high level of bone destruction around the affected
tooth, and anatomic problems worsen the prognosis
60. Pathophysiology & Histological features
The dental pulp and the periodontium have different communication pathways
• Apical radicular foramina
• Accessory (or lateral) canals, and
• Dentinal tubules
Accessory canals are more prevalent at the apical third of the roots, and furcation regions.
Pathological communication between these structures, includes the migration of
microorganisms and inflammatory mediators between the root canal and the periodontium.
61. Classification
(1) Primary endodontic lesions;
(2) Primary endodontic lesions with secondary periodontal involvement;
(3) Primary periodontal lesions;
(4) Primary periodontal lesions with secondary endodontic involvement; and
(5) “True” combined lesions.
Simon et al, 1972
The three main prognostic groups for a tooth with an EPL are:
(1) hopeless, (2) poor, and (3) favorable.
62. Diagnosis
1. Patient history for occurrence of trauma endodontic instrumentation or post
preparation.
2. Clinical and radiographic examinations presence of perforations, fractures, and
cracking or external root resorption.
If not identified radiographically initially full-mouth periodontal assessment,
including probing depth, attachment level, bleeding on probing, suppuration and mobility, as
well as tooth vitality and percussion tests.
The presence of a periodontal pocket reaching or close to the apex combined with absence of
pulp vitality would indicate the presence of an EPL.
63. Problems in 1999 Classification
(1)Grouping all EPL under a single section entitled “Periodontitis Associated with Endodontic
Lesion” was not ideal, as these lesions may occur in subjects with or without periodontitis.
(2)The single category presented, “Combined Periodontal-Endodontic Lesions”, was too
generic and not sufficiently discriminative to help the clinician to determine the most
effective treatment for a particular lesion.
EPL should be classified according to signs and symptoms feasible to be assessed at the time
that the lesion is detected and that have direct impact on their treatment, such as presence or
absence of fractures and perforations, presence or absence of periodontitis, and the extent of
the periodontal destruction around the affected teeth.
64.
65.
66. REFERENCES
1. David Herrera, Belén Retamal-Valdes, Bettina Alonso, Magda Feres; Acute periodontal
lesions (periodontal abscesses and necrotizing periodontal diseases) and endo-periodontal
lesions; 2017 WORLD WORKSHOP; J Periodontol. 2018;89(Suppl 1):S85–S102.
2. Barry Eley, Mena Soory, J. D. Manson; Periodontics Textbook 6th Edition.
3. Perry R. Klokkevold and Fermin A. Carranza; Acute Gingival Infections.