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
Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations”
Bowen , 1976
Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003
INTRODUCTION
DEFINITION
TYPES OF TRAUMA FROM OCCLUSION
GLICKMAN CONCEPT
WAERHAUG CONCEPT
STAGES OF TISSUE RESPONSE TO INJURY
CLINICAL AND RADIOGRAPHIC FEATURES OF TFO
CLINICAL DIAGNOSIS OF TFO
TFO AND IMPLANTS
TREATMENT OF TFO
CONCLUSION
REFRENCES
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
Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations”
Bowen , 1976
Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003
INTRODUCTION
DEFINITION
TYPES OF TRAUMA FROM OCCLUSION
GLICKMAN CONCEPT
WAERHAUG CONCEPT
STAGES OF TISSUE RESPONSE TO INJURY
CLINICAL AND RADIOGRAPHIC FEATURES OF TFO
CLINICAL DIAGNOSIS OF TFO
TFO AND IMPLANTS
TREATMENT OF TFO
CONCLUSION
REFRENCES
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
mucogingival surgery or plastic surgery of muco-gingival tissue is a surgical procedure targeted to correct and eliminate anatomic, developmental and traumatic alterations of gingiva.
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
Certains medications have been associated with gingival enlargement.
the seminar gives a complete analysis of etilogy and pathogenesis involved in digo as well as sequlae of it
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
The etiology of a disease refers to the causative trigger(s), whereas pathogenesis refers to the mechanism(s) by which the disease progresses.
In other words, while the microbial biofilm developing on the tooth surface constitutes a necessary etiological factor, its mere presence is insufficient for the initiation of the disease.
Further risk factors, such as host genetics, lifestyle, stress, and systemic conditions, that dictate the immunopathogenesis are crucial for the transition from a healthy to a diseased state.
mucogingival surgery or plastic surgery of muco-gingival tissue is a surgical procedure targeted to correct and eliminate anatomic, developmental and traumatic alterations of gingiva.
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
Certains medications have been associated with gingival enlargement.
the seminar gives a complete analysis of etilogy and pathogenesis involved in digo as well as sequlae of it
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
The etiology of a disease refers to the causative trigger(s), whereas pathogenesis refers to the mechanism(s) by which the disease progresses.
In other words, while the microbial biofilm developing on the tooth surface constitutes a necessary etiological factor, its mere presence is insufficient for the initiation of the disease.
Further risk factors, such as host genetics, lifestyle, stress, and systemic conditions, that dictate the immunopathogenesis are crucial for the transition from a healthy to a diseased state.
The etiology of a disease refers to the causative trigger(s), whereas pathogenesis refers to the mechanism(s) by which the disease progresses.
In other words, while the microbial biofilm developing on the tooth surface constitutes a necessary etiological factor, its mere presence is insufficient for the initiation of the disease.
Further risk factors, such as host genetics, lifestyle, stress, and systemic conditions, that dictate the immunopathogenesis are crucial for the transition from a healthy to a diseased state.
Microbiology of Periodontal diseases with its introduction history, plaque hypothesis, Microbial complexes, Individual pathogens, Advances in microbiological diagnosis,
Control of bacterial biofilms.
ORAL MICROBIOME.pptx by UMNA FATIMA- BIOMEDumnajmi123
This PowerPoint presentation provides a thorough exploration of the oral microbiome and its significance in both maintaining health and contributing to disease. Beginning with an introduction to the oral microbiome, the presentation outlines its diverse composition and its crucial role in oral health. It further examines the concept of dysbiosis within the oral microbiome, highlighting the factors contributing to imbalance and its implications for oral and systemic health. The presentation also delves into emerging research linking oral microbiome dysbiosis to systemic diseases, shedding light on potential mechanisms and clinical implications. Methods for studying the oral microbiome are discussed, along with recent advancements in research methodologies and therapeutic strategies targeting microbial dysbiosis. Additionally, the presentation explores the evolving field of precision dentistry and its integration with oral microbiome analysis for personalized treatment approaches. Through case studies and examples, the audience gains insight into the practical applications of oral microbiome research. The presentation concludes with a summary of key points and an invitation for questions and discussion, emphasizing the importance of ongoing research in understanding and harnessing the potential of the oral microbiome for improving health outcomes.
Pathogenesis is derived from the Greek work ‘pathos’ meaning suffering and ‘ genesis’ meaning generation or creation. Plaque is considered as the main etiologic factor in the pathogenesis of periodontal disease.
Classification of chemical antiplaque agents
1. FIRST GENERATION AGENTS
Poor substantivity and thus used 4-6 times daily.
Reduces plaque score by 20-50%
Examples:
Antibiotics like Penicillin, Erythromycin, Metronidazole
2. SECOND GENERATION AGENTS
Reduce plaque score by 70-90%
Used twice daily
Example: Bisbiguanides, Chlorhexidine, Alexidine
3. THIRD GENERATION AGENTS
Effective against specific periodontal pathogens
Example: Delmopinol
II. Vehicles for delivery of chemical agents
a. Toothpastes
b. Sprays
c. Irrigators
d. Chewing gums
e. Mouthwashes (Listerine, Chlorhexidine, Triclosan, Fluorides, Hydrogen peroxides, Povidone iodine)
Analgesic is a drug that relieves pain by acting on the CNS or on the peripheral pain mechanism without altering consciousness
Opioid analgesics
Non Opioid analgesics (NSAIDs)
NSAIDs are non-steroidal anti-inflammatory drugs. These are not only pain killers but also are anti-inflammatory drugs that are widely used in dentistry. These are weaker analgesics, also called nonnarcotic or aspirin-like or antipyretic analgesics. They do not depress CNS, do not produce physical dependence, and have no abuse liability. They act primarily on peripheral pain mechanisms.
It is a naturally occurring, semi-synthetic, or synthetic type of anti-infective agent that destroys or inhibits the growth of selective microorganisms, generally at low concentrations.
These drugs are used extensively in dentistry for two main reasons: to prevent an infection (chemoprophylaxis) and in the treatment of an infection. Their use in the management of periodontal diseases is often as an adjunct to conventional treatment.
INDICATIONS IN PERIODONTAL DISEASES
1. Patients who do not respond to conventional mechanical periodontal therapy
2. Patients with Aggressive periodontitis and other types of early-onset periodontitis
3. Patients with acute or recurrent periodontal infection
(Periodontal abscess, NUG / NUP, Peri-implantitis, Pericoronitis) associated with/without systemic manifestation)
4. Prophylaxis for medically compromised patients, endocarditis
Soft deposit that form the biofilm on teeth. Plaque is defined as structured, resilient, yellow grayish colored substance that adheres tenaciously to intra oral hard surfaces including restorations. The term plaque is derived from French word, meaning ‘to form a coverage’.Marginal plaque – cause gingivitis.
Supragingival plaque and tooth-associated subgingival plaque – cause calculus formation and root caries. Tissue-associated subgingival plaque- cause tissue destruction in periodontitis.
Cementum is the mineralized dental tissue covering the anatomical root of teeth. It begins at the cervical portion of the tooth at the cementoenamel junction till the apex. It is one of the four tissues that support the tooth in the jaw (the periodontium).
The primary function- Provides attachment to collagen fibres of the periodontal ligament. It therefore is a highly responsive tissue maintaining the integrity of the root, helping to maintain the tooth in its functional position in the mouth, and being involved in tooth repair and regeneration.
Recent advances in periodontal diagnosisPerio Files
First generation:- Conventional probes.
Second generation:- Pressure controlled visual measurement recording probes
Third generation:-Pressure controlled electronic probes with direct computer data capture.
Fourth generation : Aim at recording sequential probing positions along the gingival sulcus.
Fifth generation : Ultrasonic device attached to the 4th generation probe.
Hormonal changes in female patients and periodontal diseasesPerio Files
Hormonal fluctuations and gingival changes in female patient occurs during Puberty, Menstruation, Pregnancy, Menopause,
Oral Contraceptives, Osteoporosis.
NEED FOR ASSESSMENT: To identify high-risk stages of female patients in prior so that preventive and treatment procedures can be tailored
During pregnancy, women undergo certain hormonal and physiological changes that can affect their mouths.
EFFECT OF PREGNANCY ON PERIODONTAL TISSUES
PREGNANCY GINGIVITIS
EFFECT OF PERIODONTITIS ON PREGNANCY
PRETERM LOW BIRTH WEIGHT (PLBW) INFANTS
PREECLAMPSIA
Oral-systemic link has been termed Periodontal Medicine. Significance: Periodontal disease is preventable and readily treatable, thus providing many new opportunities for preventing and improving several systemic diseases.
FOCAL INFECTION: Localized or Generalized infection caused by dissemination of microorganisms or toxic products from focus of infection.
FOCUS OF INFECTION Confined area that
(1) contains pathogenic microorganisms
(2) can occur anywhere in body
Diseases/Conditions affected by periodontitis
A PREGNANCY, PREECLAMPSIA
B ISCHEMIC HEART DISEASES, STROKE
C DIABETES MELLITUS
D PNEUMONIA, COPD
E OSTEOPOROSIS
F CANCER
G ALZHEIMER’S DISEASE
H. RHEUMATOID ARTHRITIS
*Increase in size of gingiva. Lead to false pockets.
*Difficulties associated with it are:
Difficulty in plaque control; Aesthetic concerns; Affect mastication
Interfere with speech
*TREATMENT:
Gingivectomy is the treatment of choice to remove false pockets.
In case of true pockets (osseous defects), gingivectomy with Flap surgery is done. First Gingivectomy is done. After that flap is raised and osseous surgery is performed (either osteotomy or regenerative depending upon the type of defect). Gingivectomy is done by scalpel or electro cautery/lasers (to minimize bleeding). Gingivectomy can be done only where at least 3mm of keratinized gingiva remains after completion of surgery. So it is contraindicated in patients with lack of sufficient keratinized gingiva
*REASONS OF RECURRENCE:
Responsible factors: Residual local irritation; and systemic or hereditary conditions causing noninflammatory gingival hyperplasia.
Recurrence of chronic inflammatory enlargements immediately after treatment indicates that all irritants have not been removed. Contributory local conditions like food impaction and overhanging margins of restorations are commonly overlooked.
If the enlargement recurs after healing is complete and normal contour is attained, inadequate plaque control by the patient is the most common cause.
All about gingivitis
*definition
*classification
*Signs and Symptoms: Increased GCF, Gingival Bleeding, Color change, Consistency, Surface texture (STIPPLING), Position of Gingiva, Gingival Contour, Size.
Treatment consisits of scaling and root planing. The more inflamed a gingival unit appears clinically, the better the chances of therapeutic measures resulting in a return to normal gingival health
2017 classification of periodontal and periimpalnt diseasesPerio Files
In World Workshop 2017, American Academy of Periodontology (AAP) and European Federation of Periodontology (EFP) with expert participants updated the 1999 classification of Periodontal Diseases.
Since 1999, new evidences have emerged regarding environmental and systemic risk factors, prompting the experts to develop new classification.
All furcation defects need to be classified and their possible prognosis should be defined. The treatment of the furcation defects should be carried out accordingly. Treatment include
Osteoplasty, Odontoplasty, Tunnel preparation, Root resection, Hemisection
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
It restore alveolar bone to the level existing at the time of surgery or slightly more apical to this level. Aim is to achieve positive bony architecture.
STEPS INCLUDE:
1.VERTICAL GROOVING
2. RADICULAR BLENDING
3. FLATTENING INTERPROXIMAL BONE
4. GRADUALIZING MARGINAL BONE
PREFERRED TREATMENT FOR ONE WALLED PERIODONTAL BONE DEFECTS (HEMISEPTUM)
Evidence based practice is Integration of best research evidence with clinical expertise and patient values.
Advantages: QUALITY OF CLINICAL PRACTICE IMPROVES BY INCORPORATING LATEST EFFECTIVE CLINICAL TECHNIQUES INTO PATIENT CARE.
Dental practitioner should try to adopt quality evidences in dental practice, accept evidence based new practices and letting go existing theories.
Evidence collected should be combined with clinical experience and patient preferences. Positive environment with advancement in science can help facilitate evidence based change in future.
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.
This topic include all the drugs that are locally applied in periodontal pocket so that their levels in GCF should be more than blood.
Advantages:
Can attain higher concentrations at base of pocket
Can use drugs that are not suitable for systemic administration
Patient compliance is not required
Alternative for patients predisposed to adverse drug reactions from systemic administration.
Reduced risk for drug resistant microbe development
Lower total drug dose
INDICATIONS:
As an adjunct to mechanical therapy in pockets of 5 mm or greater depth
In patients who are systemically compromised & cannot undergo periodontal flap surgery
Localized recurrent pockets with supportive periodontal therapy
In refractory periodontitis (that is resistant to treatment)
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3. CONTENTS
• Introduction
• Definitions
• Non specific plaque hypothesis
• Specific plaque hypothesis
• Updated plaque hypothesis
• Ecological plaque hypothesis
• Keystone pathogen plaque hypothesis
• Conclusion
4. INTRODUCTION
• Plaque is the primary etiological factor of
periodontal diseases
• Also evidences support that periodontal disease
acts as contributor factor for various systemic
diseases (Diabetes, Heart Diseases, Lung
Diseases, Preterm low birth weight infants….....)
5. INTRODUCTION
To effectively treat and prevent these diseases, various
hypothesis are proposed to find how healthy plaque
change to pathological plaque
6. PLAQUE HYPOTHESIS-
• Non specific plaque hypothesis
• Specific plaque hypothesis
• Updated plaque hypothesis
• Ecological plaque hypothesis
• Keystone pathogen hypothesis
9. Non-specific plaque hypothesis
Proposed by Miller in 1890;
Name given by Walter Loesche (1976)
States that periodontal disease results from the
noxious products released by entire plaque flora
10. All plaque bacteria
played a role in
periodontal
destruction rather
than any specific
bacteria.
Entire
plaque was
viewed as
bad plaque
11. Plaque induced gingivitis model in support of this theory
• Loe, Theilade, and Jensen in 1965- examined gingival
inflammation in healthy adults who ceased tooth brushing and
any other oral hygiene practices.
• It was observed that as the plaque accumulated, gingivitis
developed
• When plaque was removed by reinstituting adequate oral
hygiene, gingivitis started decreasing
12. Day 0- Mechanical plaque control stopped, plaque
slowly started forming on the teeth.
Day 1-6- Plaque composition changed, with a shift
to more gram-negative species and more rods,
filaments
Day 7- Spirals and spirochetes started appearing
13. • Day 3- First symptoms of gingival
inflammation became visible.
• On re-establishment of proper plaque
control- plaque composition returned
to the initial situation; symptoms of
gingivitis disappeared.
14. Limitations of non- specific plaque
hypothesis
Some individuals with good amount of plaque and
calculus develop gingivitis, but never develop destructive
periodontitis.
Some individuals with periodontitis demonstrate site
specificity in the pattern of disease. Some sites in mouth are
unaffected, whereas deep pockets are found in adjacent sites
17. Specific plaque hypothesis
Given by Walter Loesche
(1976)
Specific bacteria in plaque results in
periodontal disease because that
bacteria produces substances that
mediate the host tissues destruction
18. Specific plaque hypothesis was
accepted
• By the recognition of A. actinomycetemcomitans as a
main causative bacteria in Localized Aggressive
Periodontitis.
• By microbial complexes observed by Socransky et al
21. The primary colonizers (that get attached to
tooth surfaces) are either independent
bacteria (no defined complexes) or member
of yellow, blue or purple complexes.
Secondary colonizers in plaque (that
combine with other bacteria, not on
tooth surfaces) fell into green, orange
or red complexes.
The red complex is particularly associated
with bleeding on probing
22. Socranksy’s complexs
Yellow, blue and
purple associated with
periodontal health
Red, Green and orange
associated with
periodontal disease
23. Limitations
Studies showed that periodontitis occurred even in
absence of pathogens like red/green complex
Sometime these pathogens were found to be present in
absence of disease.
25. UPDATED NON-SPECIFIC PLAOUE
HYPOTHESIS (UNIFIED HYPOTHESIS)
Described by THEILADE IN 1986
Whole plaque contribute to the pathogenic potential to a
greater or lesser extent (Gingivitis), but presence of some
specific virulent bacteria lead to disease progression
(Periodontitis)
26. All bacteria in plaque is virulent by
either involved in invasion, evasion of
the host defenses and/or aggravation
of tissue destruction
But some specific subgingival
bacteria can become virulent than
others (under some favorable
conditions) and cause periodontitis
27. Thus it combines the key concepts of both
the previous hypothesis
28. Theilade’s statement
“any bacterial colonization
(plaque) of sufficient
quantity in the gingival
crevice (sulcus) always
causes at least gingivitis”
Non-pathogenic plaque not
causing gingivitis (in the
absence of oral hygiene)
had never been reported
29. This hypothesis propose
Presence of plaque always lead to gingivitis
Changes occur in plaque leading to growth
of specific virulent bacteria leading to
periodontitis
30. LIMITATION-
CANNOT ANSWER WHY-
In some people, gingivitis
never progress to periodontitis,
whereas some people rapidly
develop periodontitis
32. ECOLOGICAL PLAQUE HYPOTHESIS
Expanded the previous hypothesis by
stating that virulence of specific
micro-organism in plaque occurs by
changes in ecological factors like
change in pH, redox potential,
presence of nutrients etc
33. ECOLOGICAL PLAQUE HYPOTHESIS
Given by Philip D. Marsh in 1994
Periodontitis is caused by overgrowth of
specific micro-organisms of dental plaque
when the local microenvironment changes
(ecological changes), but it is not necessarily
the same bacteria in each case
34. • Changes in microbial composition occurs
due to ecological factors such as change
in pH and redox potential, the presence of
nutrients
35. According to ecological
plaque hypothesis both the
total amount of dental plaque
and the specific microbial
composition of plaque
contribute to transition from
health to disease.
39. LIMITATION
Like the other hypotheses, it does not address the
role of host genetic factors that contribute to the
composition of plaque and to susceptibility of
periodontitis; as gingivitis don’t lead to periodontitis
in every case and genetic factors can be
responsible in addition to environmental factors.
41. KEYSTONE PATHOGEN HYPOTHESIS
Certain low-abundant micro-organisms can cause
periodontitis by changing the composition and increasing
the quantity/number of the normal micro-organisms
Given by Hajishengallis et al., 2012
For example Porphyromonas gingivalis ( in small quantities)
has shown to cause periodontitis by manipulating the host
immune system
42. STUDIES
Studies in mouse models showed
Very low amount of P.gingivalis
(<0.01% of total bacteria in plaque)
altered the plaque composition,
causing periodontitis (Hajishengallis et
al.,2011)
43. STUDIES
But in germ-free mice models
P.gingivalis colonized but could
not cause the disease; indicating
the importance of commensal
bacteria in causing the disease
44. P.GINGIVALIS CAUSES three effects
1. “Local chemokine paralysis”
by blocking production of IL-8
produced by gingival epithelial
cells.
Delays the recruitment of
neutrophils, facilitating initial
microbial colonization in
periodontium
Madianos et al.,
1997;
Darveau et al;1998
45. P.GINGIVALIS CAUSES
2. “Manipulate toll like receptor
(TLR) response”
Decrease level of TLR4 activity,
thus facilitate survival and
multiplication of micro-organisms in
periodontium
46. P.GINGIVALIS CAUSES
3. “Inactivate Complement”
Gingipains release by P.Gingivalis
cleave complement factors C3 and
C5 into active C3a and C5a (active
in phagocytosis of microbes). But
these gingipains degraded C3a and
C5a, causing loss of their functions
thus increasing survival of micro-
organisms.
47. P.GINGIVALIS CAUSES
Increasing number of micro-
organisms increase GCF. Increased
GCF is source of more proteins
(utilized as nutrient for other micro-
organisms) and iron (utilized as
source of P.gingivalis)
Thus a vicious cycle is formed in
which P.gingivalis increases
number of other micro-organisms
and its own levels
48. LIMITATION
Like the other hypotheses, it does not address
the role of host genetic factors that contribute to
the composition of plaque and to susceptibility
of periodontitis
Also this hypothesis has yet to be proved in
humans
49. SUMMARY
• Non specific plaque hypothesis: Whole plaque
responsible for disease.
• Specific plaque hypothesis: Specific bacteria in
plaque responsible for disease.
• Updated plaque hypothesis: Whole plaque cause
gingivitis; but progression to periodontitis occurs
by growth of specific bacteria.
50. SUMMARY
• Ecological plaque hypothesis: Whole plaque cause
gingivitis; but progression to periodontitis occurs by
growth of specific bacteria by some ecological
changes in biofilm (like temperature, pH etc.)
• Keystone pathogen hypothesis: Low-abundant micro-
organism like P.gingivalis cause periodontitis by
changing the composition and increasing the quantity
of the normal micro-organisms.
51. Conclusion
It is a proven fact by all hypothesis
that accumulation of plaque always
lead to gingivitis.
52. But progression of disease
from gingivitis to
periodontitis—do not fit to
any hypothesis
‘In some individuals
disease never progress,
whereas in others it rapidly
progress to periodontitis’,
need to be answered
53. Till now, all hypothesis fail to describe actual
relationship between oral microbes and host
response that lead to maintenance of health or its
shift to the disease (periodontitis)
54. A hypothesis is needed, but this is only
possible when complex interaction of
bacteria with the host innate immune
response is fully explored