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
Dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.
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
Dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.
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
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
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
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
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
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
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
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
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Abscess of periodontium is a topic which is must to be read by a dentist or dental surgeon. Also the slide is made from carranza's periodontology, which can help the readers to grasp the concepts in few minutes. thank you.
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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).
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2. 2
TABLE OF CONTENTS
o INTRODUCTION
o DEFINITION
o NORMAL ANATOMY OF THE PERIODONTIUM
o CLASSIFICATION OF POCKETS
o DIFFERENCES BETWEEN SUPRABONY AND INFRABONY POCKETS
o PATHOGENESIS OF PERIODONTAL POCKETS
o POCKET CONTENTS
o CLINICAL SIGNS AND SYMPTOMS
o CLINICAL AND HISTOPATHOLOGIC CORRELATIONS
o ASSESSMENT AND DIAGNOSIS
o TREATMENT MODALITIES
o CONCLUSION
o REFERENCES
3. 3
INTRODUCTION
o The word ‘pocket’ originated from the French word ‘pochette’ which
means a cul-de-sac or a pouch-like cavity.
o A sulcus depth up to 3mm is usually considered to be normal (provided
the patient can maintain oral hygiene). Beyond 3mm, it is considered to
be a pocket.
o The cause of this is mainly the extension of inflammation leading to a
pathologic deepening of gingival sulcus and the eventual destruction of
supporting periodontal tissues (if left untreated).
o A periodontal pocket is one of the most important clinical features of
periodontal diseases.
4. 4
DEFINITION
o Periodontal pockets are simply defined as a “deepening of the gingival
sulcus.”
o If this happens due to the coronal migration of the marginal gingiva it is
referred to as “gingival or pseudo-pocket”.
o Deepening due to apical migration of the junctional epithelium is
referred to as “true pocket.”
5. 5
NORMAL ANATOMY OF THE PERIODONTIUM
o The periodontium is a complex structure composed of-
• Gingiva
• Periodontal ligaments (PDL)
• Cementum
• Alveolar bone
o The primary functions of the periodontium is to allow the tooth to be
attached to the bone and to provide a barrier for the underlying
structures from the oral microflora.
9. 9
CLASSIFICATION OF POCKETS
1. Depending upon its morphology
a. Gingival/false/relative pocket.
b. Periodontal/absolute/true pocket.
c. Combined pocket.
2. Depending upon its relationship to crestal bone
a. Suprabony/supracrestal/supra-alveolar pocket.
b. Infrabony/intrabony/subcrestal/intra-alveolar pocket.
3. Depending upon the number of surfaces involved
10. 10
CLASSIFICATION OF POCKETS
a. Simple pocket—involving one tooth surface.
b. Compound pocket—involving two or more tooth surfaces.
c. Complex pocket—where the base of the pocket is not in direct
communication with the gingival margin. It is also known as spiral
pocket.
4. Depending upon the nature of the soft tissue wall of the pocket
a. Edematous pocket.
b. Fibrotic pocket.
5. Depending upon the disease activity
a. Active pocket.
b. Inactive pocket.
12. Suprabony pockets
A) The base of the pocket is coronal to
the crest of the alveolar bone.
B) The pattern of bone destruction is
horizontal.
C) Interproximally, the transseptal fibres
are arranged horizontally.
D) On the facial and lingual surfaces,
the periodontal ligament fibres follow
normal horizontal-oblique course
between the tooth and the bone.
Infrabony pockets
A) The base of the pocket is apical to
the crest of the alveolar bone.
B) The pattern of bone destruction is
vertical/angular
C) Interproximally, the transseptal fibres
are arranged in an oblique pattern.
D) On the facial and lingual surfaces,
the periodontal ligament fibres follow
the angular pattern of the adjacent
bone.
12
DIFFERENCES BETWEEN SUPRABONY AND INFRABONY POCKETS
14. 14
PATHOGENESIS OF PERIODONTAL POCKETS
FIRST EVENT
o Colonization of Gram-positive bacteria supragingivally and its
extension into the gingival sulcus and conversion of Gram-positive
aerobes to Gram-negative anaerobes
16. 16
POCKET CONTENTS
It consists of debris principally containing micro-organisms and their products-
o Enzymes
o Endotoxins and other metabolic products
o Dental plaque
o Gingival fluid
o Food remnants
o Salivary mucin
o Desquamated epithelial cells and leukocytes.
If purulent exudate is present, it consists of-
o Living, degenerated and necrotic leukocytes (PMNLs)
o Living and dead bacteria (Treponema denticola, Porphyromonas gingivalis)
o Serum
o A scanty amount of fibrin.
17. 17
CLINICAL SIGNS AND SYMPTOMS
SIGNS
• Enlarged, bluish-red marginal gingiva with a ‘rolled’ edge separated from the tooth
surface.
• A bluish-red vertical zone extending from the gingival margin to the alveolar
mucosa.
• A break in the faciolingual continuity of the interdental gingiva.
• Shiny, discolored and puffy gingiva associated with exposed root surfaces.
• Gingival bleeding, purulent exudate from the gingival margin.
• Mobility, extrusion and migration of teeth.
• The development of diastema where none had existed previously.
18. 18
CLINICAL SIGNS AND SYMPTOMS
SYMPTOMS
• Localized pain or a sensation of pressure in the gingiva after eating, which gradually
diminishes.
• A foul taste in localized areas.
• A tendency to suck material from the interproximal spaces.
• Radiating pain “deep in the bone.”
• A “gnawing’ feeling or feeling of itching in the gums.
• The urge to dig a pointed instrument into the gums and relief is obtained from the
resultant bleeding.
• Patient complains that food “sticks between the teeth” or that the teeth “feel loose”
or a preference to “eat on the other side.”
• Sensitivity to heat and cold; toothache in the absence of caries
19. CLINICAL FEATURES
1) Bluish red discoloration of gingival
pocket wall
2) Flaccidity
3) Smooth and shiny surface
4)Pitting on pressure
5) Bleeding on gentle probing
6) Tender inner pocket wall
7)Pus discharge on application of
digital pressure.
HISTOPATHOLOGIC FEATURES
1) Circulatory stagnation
2) Destruction of gingival fibres and
surrounding tissues
3) Atrophy of the epithelium
4) Edema and degeneration
5) Increased vascularity, thinning of epithelium
and proximity of engorged vessels to inner
surface
6) Ulceration of inner aspect of pocket wall
7) Suppurative inflammation of inner wall.
19
CLINICAL AND HISTOPATHOLOGIC CORRELATIONS
20. 20
ASSESSMENT AND DIAGNOSIS
PERIODONTAL POCKET PROBING
The only reliable method of locating periodontal pockets and determining their
extents is careful probing along each tooth surface. There are two different pocket
depths-
o Biological/histological depth: The distance between the gingival margin and the
base of the pocket.
o Clinical/probing depth: The distance from the gingival margin through which a
probe penetrates into the pocket.
Recommended probing force = 0.75N
23. 23
ASSESSMENT AND DIAGNOSIS
RADIOGRAPHIC ASSESSMENT
With periapical radiographs, we are able to assess-
Amount of bone present
Condition of the alveolar crest
Bone loss in the furcation area
Width of the PDL space
Local factors which can cause or intensify periodontal diseases
25. 25
TREATMENT MODALITIES
o Treatment of periodontal pockets is a great challenge because it occurs due to
bacterial biofilm which is highly resistant to the antimicrobials and host response.
o In the initial stage of the disease, inflammation is limited to the gingiva (gingivitis)
but later extends to the deeper tissues in turn leading to gingival swelling, bleeding
of gums and halitosis.
o In the late phase of disease, the supporting collagen of periodontium begins to
degenerate, resorption of alveolar bone takes place and epithelial tissue of gingiva
migrates which leads to formation of pockets.The choice of the treatment strategy
therefore depends upon the stage of disease.
26. 26
TREATMENT MODALITIES
o Various approaches applied for the treatment of disease include surgical
intervention, mechanical therapy and use of pharmacological agents.
o Medications are specifically used for better management of periodontitis and
include antimicrobials that change microbial flora in periodontal milieu and host
response modulating agents which modify host response like reduction of
excessive enzymes level, cytokines, prostaglandins and osteoclast activity.
30. 30
TREATMENT MODALITIES
New attachment procedures.
o Offers ideal result by reuniting the gingiva to the tooth at a position coronal to the
base of pre-existing pocket. Here all the structures of lost periodontium are
restored.
o Following are the techniques for new attachment-
a. Non-graft associated new attachment procedures
b. Graft associated new attachment procedures
c. Combined techniques
31. 31
CONCLUSION
• Understanding the pathogenesis, histopathology and classification of
periodontal pockets is very essential in order to provide adequate
care to patients with periodontal diseases.
• Thank you for listening.
32. 32
REFERENCES
• Essentials of Clinical Periodontology and Periodontics by Shantipriya
Reddy
• Tariq M, Iqbal Z, Ali J, et al. Treatment modalities and evaluation
models for periodontitis. Int J Pharm Investig. 2012;2(3):106-122.
doi:10.4103/2230-973X.104394
• https://www.slideshare.net/randhawans/periodontal-pocket-
96630611