Introduction
Landmarks in periodontal classification
Need for classification
Classification 1989 – with limitation
Classification 1993 – with limitation
Classification 1999 – changes made from 1989 classification and its limitation
Consensus report 2017classification
Classification 2017
Key features in 2017 classification
Gingival and periodontal health – induced and reduced periodontium
Gingivitis – biofilm induced
Gingivitis – non biofilm induced
Conclusion
References
This document provides an overview of diabetes mellitus and its relationship to periodontal disease. It begins with definitions of diabetes and classifications of the different types. It then discusses the history, epidemiology, diagnosis, complications, and relationship between diabetes and periodontal disease. Specifically, it notes that diabetes is a risk factor for more severe periodontal disease and periodontal disease can worsen glycemic control in diabetes patients. The two-way relationship between periodontal infections and diabetes is explored.
This document discusses periodontal regeneration and repair. It defines regeneration as the replacement of damaged tissues with new tissues that restore the original structure and function, while repair involves the reattachment of existing fibers and is inferior. True regeneration requires the formation of a new epithelial seal, connective tissue fibers inserted into the root, and new cementum and alveolar bone. However, complete regeneration may be difficult to achieve due to the complexity of biological factors involved. New approaches utilize scaffolds, growth factors, stem cells, and tissue engineering to help guide and stimulate regeneration. The future of regeneration may rely on combining technologies and biological concepts to attract cells needed for full regeneration.
This document provides an overview of cementum, the mineralized tissue that covers tooth roots. It defines cementum and discusses its development, physical and chemical characteristics, classification, cells, functions, and involvement in periodontal disease. Cementum is composed of collagen fibers embedded in mineralized matrix. It provides attachment for periodontal ligament fibers and aids in tooth function and repair. The document also examines cementum at the microscopic level and various proteins and cells involved in its formation and remodeling.
Porphyromonas gingivalis is a gram-negative, anaerobic bacterium implicated as a primary pathogen in periodontal disease. It produces several virulence factors that allow it to invade tissues, evade the host immune system, and cause damage. These include proteolytic enzymes, lipopolysaccharide, capsular polysaccharides, fimbriae, and outer membrane proteins. Fimbriae aid in adhesion to host cells, while enzymes degrade host proteins and tissues. Capsular polysaccharides and outer membrane structures help resist phagocytosis. P. gingivalis is strongly associated with periodontitis and its virulence factors contribute directly to tissue destruction and immune evasion during infection.
This document provides classifications for various conditions affecting the periodontium, including:
- Gingival diseases such as dental plaque-induced and non-plaque induced gingivitis.
- Periodontitis, which is further classified into necrotizing periodontitis, periodontitis as a manifestation of systemic diseases, and other forms.
- Other conditions like periodontal abscesses, endo-peridontal lesions, mucogingival deformities, traumatic occlusal forces, and teeth/prosthesis factors.
It also defines terms like peri-implant mucositis and peri-implantitis, and discusses factors associated with soft and hard tissue deficiencies around dental
THIS PRESENTATION INCLUDES:
INTRODUCTION
MAIN BLOOD SUPPLY BRANCHES TO PERIODONTIUM
BLOOD SUPPLY TO MAXILLARY TEETH AND PERIODONTIUM
BLOOD SUPPLY TO MANDIBULAR TEETH AND PERIODONTIUM
VENOUS DRAINAGE OF MAXILLARY AND MANDIBULAR TEETH AND PERIODONTIUM
BLOOD SUPPLY TO EACH COMPONENT OF PERIODONTIUM
CLINICAL SIGNIFICANCE OF BLOOD SUPPLYING THE PERIODONTIUM
CLINICAL CORELATIONS WITH GINGIVITIS AND PERIODONTITIS
CONCLUSION
REFERENCES
This document provides an overview of resective osseous surgery techniques. It discusses the anatomical forms of bone, osteoplasty and ostectomy procedures, surgical approaches, and techniques. Osteoplasty involves reshaping bone without removing tooth-supporting bone through techniques like grooving and blending. Ostectomy involves removing tooth-supporting bone to eliminate osseous deformities. Specific techniques like horizontal grooving, scribing, and hand instrumentation are described. Post-operative maintenance and expected osseous changes are also summarized.
Porphyromonas gingivalis is a gram-negative, anaerobic bacteria implicated in periodontitis. It is a late colonizer that survives and proliferates in the subgingival biofilm through invasion of host cells and evasion of the immune system. P. gingivalis functions as a keystone pathogen in the polymicrobial synergy and dysbiosis model of periodontal disease, where it can elevate the virulence of the entire microbial community and impair host immune responses, leading to tissue destruction. Targeting the pathogenic microbial community as a whole, rather than P. gingivalis alone, may be a more effective therapeutic strategy for treating periodontitis.
This document provides an overview of diabetes mellitus and its relationship to periodontal disease. It begins with definitions of diabetes and classifications of the different types. It then discusses the history, epidemiology, diagnosis, complications, and relationship between diabetes and periodontal disease. Specifically, it notes that diabetes is a risk factor for more severe periodontal disease and periodontal disease can worsen glycemic control in diabetes patients. The two-way relationship between periodontal infections and diabetes is explored.
This document discusses periodontal regeneration and repair. It defines regeneration as the replacement of damaged tissues with new tissues that restore the original structure and function, while repair involves the reattachment of existing fibers and is inferior. True regeneration requires the formation of a new epithelial seal, connective tissue fibers inserted into the root, and new cementum and alveolar bone. However, complete regeneration may be difficult to achieve due to the complexity of biological factors involved. New approaches utilize scaffolds, growth factors, stem cells, and tissue engineering to help guide and stimulate regeneration. The future of regeneration may rely on combining technologies and biological concepts to attract cells needed for full regeneration.
This document provides an overview of cementum, the mineralized tissue that covers tooth roots. It defines cementum and discusses its development, physical and chemical characteristics, classification, cells, functions, and involvement in periodontal disease. Cementum is composed of collagen fibers embedded in mineralized matrix. It provides attachment for periodontal ligament fibers and aids in tooth function and repair. The document also examines cementum at the microscopic level and various proteins and cells involved in its formation and remodeling.
Porphyromonas gingivalis is a gram-negative, anaerobic bacterium implicated as a primary pathogen in periodontal disease. It produces several virulence factors that allow it to invade tissues, evade the host immune system, and cause damage. These include proteolytic enzymes, lipopolysaccharide, capsular polysaccharides, fimbriae, and outer membrane proteins. Fimbriae aid in adhesion to host cells, while enzymes degrade host proteins and tissues. Capsular polysaccharides and outer membrane structures help resist phagocytosis. P. gingivalis is strongly associated with periodontitis and its virulence factors contribute directly to tissue destruction and immune evasion during infection.
This document provides classifications for various conditions affecting the periodontium, including:
- Gingival diseases such as dental plaque-induced and non-plaque induced gingivitis.
- Periodontitis, which is further classified into necrotizing periodontitis, periodontitis as a manifestation of systemic diseases, and other forms.
- Other conditions like periodontal abscesses, endo-peridontal lesions, mucogingival deformities, traumatic occlusal forces, and teeth/prosthesis factors.
It also defines terms like peri-implant mucositis and peri-implantitis, and discusses factors associated with soft and hard tissue deficiencies around dental
THIS PRESENTATION INCLUDES:
INTRODUCTION
MAIN BLOOD SUPPLY BRANCHES TO PERIODONTIUM
BLOOD SUPPLY TO MAXILLARY TEETH AND PERIODONTIUM
BLOOD SUPPLY TO MANDIBULAR TEETH AND PERIODONTIUM
VENOUS DRAINAGE OF MAXILLARY AND MANDIBULAR TEETH AND PERIODONTIUM
BLOOD SUPPLY TO EACH COMPONENT OF PERIODONTIUM
CLINICAL SIGNIFICANCE OF BLOOD SUPPLYING THE PERIODONTIUM
CLINICAL CORELATIONS WITH GINGIVITIS AND PERIODONTITIS
CONCLUSION
REFERENCES
This document provides an overview of resective osseous surgery techniques. It discusses the anatomical forms of bone, osteoplasty and ostectomy procedures, surgical approaches, and techniques. Osteoplasty involves reshaping bone without removing tooth-supporting bone through techniques like grooving and blending. Ostectomy involves removing tooth-supporting bone to eliminate osseous deformities. Specific techniques like horizontal grooving, scribing, and hand instrumentation are described. Post-operative maintenance and expected osseous changes are also summarized.
Porphyromonas gingivalis is a gram-negative, anaerobic bacteria implicated in periodontitis. It is a late colonizer that survives and proliferates in the subgingival biofilm through invasion of host cells and evasion of the immune system. P. gingivalis functions as a keystone pathogen in the polymicrobial synergy and dysbiosis model of periodontal disease, where it can elevate the virulence of the entire microbial community and impair host immune responses, leading to tissue destruction. Targeting the pathogenic microbial community as a whole, rather than P. gingivalis alone, may be a more effective therapeutic strategy for treating periodontitis.
This document discusses genetics in relation to periodontitis. It provides background on genetic study designs like segregation analysis, twin studies, and linkage/association studies that are used to identify genes associated with periodontal diseases. Specific genes linked to aggressive periodontitis are mentioned, including mutations in the alkaline phosphatase, cathepsin C, and CD18/CD11 genes. Studies finding autosomal dominant and recessive inheritance of aggressive periodontitis in different populations are summarized. The role of HLA antigens and IL-1 gene polymorphisms in periodontitis susceptibility is also briefly covered.
Periodontal medicine is the study of the relationship between periodontal health and systemic health. Periodontal disease can influence systemic health through direct effects of bacteria or indirect host-mediated inflammatory responses. Periodontitis has been linked to increased risk of cardiovascular disease, diabetes, and preterm low birth weight. Treatment of periodontal infection may help improve glycemic control in diabetic patients and reduce systemic inflammation.
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Periodontal disease results from a complex interplay between subgingival biofilm and the host immune-inflammatory response. While several bacteria are found in periodontal pockets, no single organism causes the disease. The pathogenesis involves the host response to the bacterial challenge, which can remain at a low, asymptomatic level or progress to tissue destruction if left unchecked. Understanding these disease processes is important for developing improved treatment strategies.
3.b)diabetes mellitus and periodontal disease iipunitnaidu07
This document provides an overview of diabetes and its relationship to periodontal disease. It begins by outlining various classifications and clinical presentations of diabetes, as well as its complications. It then discusses the oral manifestations that can be seen in diabetics, including infections, burning mouth, and increased dental caries. The document explains that diabetes is a risk factor for periodontal disease, increasing its severity and incidence. It explores various mechanisms by which diabetes may influence periodontitis, such as changes to subgingival flora and microvasculature, as well as defects in host immune response. The relationship between diabetes and periodontal disease is proposed to be bidirectional, with each condition exacerbating the other through chronic inflammation. Prevention, medical management
Emdogain is a gel containing enamel matrix proteins that has been shown to regenerate hard and soft tissues lost to periodontal disease. It works by attracting mesenchymal cells to the root surface, promoting attachment, proliferation, and differentiation which results in new cementum, bone, and periodontal ligament formation. Over 20 years of clinical studies involving over 2 million patients have demonstrated its effectiveness and safety in treating intra-bony and gingival recession defects.
Periodontitis is a chronic infectious inflammatory disease caused by microbes; however the presence of microbes is not enough for the cause of its complex nature of disease. Inflammation is the prime cause of periodontal disease. It commences with the aggregation of pathogenic microbes that induce the host to stimulate a cascade of inflammatory response reactions which in-turn leads to the destruction of the host tissues itself. There is a complex interplay of innate and adaptive immune responses which fights against the pathogens by direct interaction or by release of certain molecules including cytokines.
Cytokines are cell signalling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma. Cytokine biology reveals that there are some subsets of cytokines which are pro-inflammatory cytokines which stimulate the inflammatory responses and cause tissue destruction.
A periodontist is expected to have a sound basis of the cytokine profile to understand the pathogenesis of periodontitis and also to discover the new treatment modality of anti-cytokine therapy.
Classification Systems of Periodontal Diseases Manu Bhaskaran
This document discusses the history and development of classification systems for periodontal diseases. It begins with early classification attempts in the late 19th century based primarily on clinical features. In the 1920-1970 period, classifications were dominated by the "classical pathology" paradigm focusing on non-inflammatory degenerative forms of periodontitis. Starting in the 1970s, the "infection/host response" paradigm emerged as the dominant view, recognizing periodontitis as inflammatory diseases caused by bacterial infection. The document reviews several influential classification systems developed under this new paradigm from the 1970s to present day.
This document discusses the influence of systemic conditions on the periodontium. It begins by introducing periodontitis as a chronic bacterial infection and how host responses can vary between individuals. Systemic disorders can impair the host's immune defenses, creating opportunities for more severe periodontal disease. Several specific systemic factors are then examined in more detail, including hormonal changes, diabetes mellitus, and female sex hormones. The effects of these conditions on the periodontium are explored through their impact on factors like subgingival microbiota, polymorphonuclear leukocyte function, collagen metabolism, and wound healing. Treatment considerations for periodontal disease in systemic disease patients are also briefly addressed.
This document discusses the historical background and various methods of root biomodification, which involves chemically or mechanically modifying the root surface to promote periodontal regeneration. It describes how citric acid, tetracycline, fibronectin, and EDTA work to demineralize and detoxify the root surface in order to remove the smear layer and expose collagen fibers, making the surface more biocompatible and conducive to new attachment of periodontal tissues. Register and Burdick's 1975 technique using citric acid application for 2-3 minutes is outlined, along with modifications by Miller. The mechanisms and benefits of different agents are explained.
"INFLUENCE OF SYSTEMIC DISEASES (CONDITIONS) ON PERIODONTIUM" -PART-2Perio Files
This document discusses various systemic conditions and disorders that can influence periodontal disease, including:
1. Hematologic disorders like red blood cell disorders (such as sickle cell anemia), platelet disorders, and white blood cell disorders (such as leukemia) which can cause bleeding, infection, and gingival enlargement.
2. Systemic drug therapy that can cause gingival enlargement as a side effect, such as from anticonvulsants, immunosuppressants, and calcium channel blockers.
3. Psychosomatic disorders like stress, which may exacerbate periodontal disease through its effects on the immune system and increased production of pro-inflammatory mediators.
This document outlines a proposed new classification scheme for periodontal and peri-implant diseases and conditions. It discusses the need to update the 1999 classification scheme and develop a similar scheme for peri-implant diseases to align with current understanding. Key areas covered include definitions of periodontal health, gingivitis, and periodontitis at both the patient and site levels. Factors that determine the development and severity of gingivitis are summarized. Diagnostic criteria for gingivitis and approaches to classifying mild, moderate, and severe cases are discussed. The document also addresses non-dental plaque induced gingival conditions and future research needs.
This document discusses periodontal regeneration and the various factors involved. It begins by defining key terminology related to grafting and regeneration. It then discusses the biology and objectives of periodontal regeneration, including the ideal outcome of new attachment formation and factors that can influence outcomes. The document outlines various techniques for periodontal regeneration including non-graft associated approaches involving removal of epithelium and surgical techniques, as well as graft-associated approaches using various graft materials. Requirements for predictable regeneration and assessment methods are also summarized.
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.
Localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP) are rare, severe forms of periodontitis that primarily affect younger individuals. LAP is characterized by localized periodontal destruction limited to first molars and incisors, while GAP affects at least three permanent teeth. Both forms have a familial pattern and rapid progression of attachment and bone loss. The main pathogens associated with LAP and GAP are Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, respectively. Patients generally present with deep pockets and bone loss disproportionate to plaque levels.
This document discusses potential biomarkers for periodontal disease. It begins by defining biomarkers and explaining their advantages over traditional diagnostic methods. It then explores various categories of biomarkers, including microbiological markers like bacterial species and their products, as well as immune and inflammatory markers like cytokines. Specific biomarkers that have shown promise are discussed, such as GCF levels of PGE2, AST, and IgG subclasses. The document also notes challenges with biomarkers, like the polymicrobial nature of periodontal disease making it difficult to choose single bacterial species markers. Overall, the document provides a comprehensive overview of the types of biomarkers studied for periodontal disease and their potential for diagnosis and monitoring disease activity.
This document discusses aggressive periodontitis, including its definition, classification, clinical characteristics, diagnostic criteria, and treatment modalities. Aggressive periodontitis is defined as a rare, severe form of periodontitis characterized by early onset and familial aggregation. It can be localized or generalized. Treatment involves nonsurgical and surgical therapies like scaling and root planing as well as adjunctive systemic or local antibiotics. Maintaining frequent periodontal maintenance visits is important for long-term disease control.
AAP 2017 CLASSIFICATION OF PERIODONTAL DISEASE PART 1Babu Mitzvah
This document outlines the proceedings of a world workshop on classifying periodontal and peri-implant diseases and conditions. It discusses the need to update the 1999 classification system to current understanding. The outline covers periodontal health, gingival diseases, periodontitis, peri-implant diseases and key changes. Specifically, it defines periodontal health as having less than 10% bleeding sites and no probing depths over 3mm. It also discusses categories for periodontal health with an intact versus reduced periodontium, such as for successfully treated periodontitis patients.
Classification of Diseases & Conditions Affecting the Periodontium.pdfssuseraf61fb
This document discusses the classification of periodontal diseases and conditions over time. It describes four major attempts at classification between 1989-2017 based on criteria like etiology, histopathology, and genetics. The 1989 classification categorized periodontitis into prepubertal, juvenile, and adult types. The 1993 classification grouped periodontitis into adult and early onset types. The 1999 classification revised categories to include chronic, aggressive, and necrotizing periodontitis as well as periodontitis associated with systemic diseases. The 2017 classification framework characterized periodontitis based on multidimensional staging and grading that can be adapted over time with new evidence.
This document discusses genetics in relation to periodontitis. It provides background on genetic study designs like segregation analysis, twin studies, and linkage/association studies that are used to identify genes associated with periodontal diseases. Specific genes linked to aggressive periodontitis are mentioned, including mutations in the alkaline phosphatase, cathepsin C, and CD18/CD11 genes. Studies finding autosomal dominant and recessive inheritance of aggressive periodontitis in different populations are summarized. The role of HLA antigens and IL-1 gene polymorphisms in periodontitis susceptibility is also briefly covered.
Periodontal medicine is the study of the relationship between periodontal health and systemic health. Periodontal disease can influence systemic health through direct effects of bacteria or indirect host-mediated inflammatory responses. Periodontitis has been linked to increased risk of cardiovascular disease, diabetes, and preterm low birth weight. Treatment of periodontal infection may help improve glycemic control in diabetic patients and reduce systemic inflammation.
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Periodontal disease results from a complex interplay between subgingival biofilm and the host immune-inflammatory response. While several bacteria are found in periodontal pockets, no single organism causes the disease. The pathogenesis involves the host response to the bacterial challenge, which can remain at a low, asymptomatic level or progress to tissue destruction if left unchecked. Understanding these disease processes is important for developing improved treatment strategies.
3.b)diabetes mellitus and periodontal disease iipunitnaidu07
This document provides an overview of diabetes and its relationship to periodontal disease. It begins by outlining various classifications and clinical presentations of diabetes, as well as its complications. It then discusses the oral manifestations that can be seen in diabetics, including infections, burning mouth, and increased dental caries. The document explains that diabetes is a risk factor for periodontal disease, increasing its severity and incidence. It explores various mechanisms by which diabetes may influence periodontitis, such as changes to subgingival flora and microvasculature, as well as defects in host immune response. The relationship between diabetes and periodontal disease is proposed to be bidirectional, with each condition exacerbating the other through chronic inflammation. Prevention, medical management
Emdogain is a gel containing enamel matrix proteins that has been shown to regenerate hard and soft tissues lost to periodontal disease. It works by attracting mesenchymal cells to the root surface, promoting attachment, proliferation, and differentiation which results in new cementum, bone, and periodontal ligament formation. Over 20 years of clinical studies involving over 2 million patients have demonstrated its effectiveness and safety in treating intra-bony and gingival recession defects.
Periodontitis is a chronic infectious inflammatory disease caused by microbes; however the presence of microbes is not enough for the cause of its complex nature of disease. Inflammation is the prime cause of periodontal disease. It commences with the aggregation of pathogenic microbes that induce the host to stimulate a cascade of inflammatory response reactions which in-turn leads to the destruction of the host tissues itself. There is a complex interplay of innate and adaptive immune responses which fights against the pathogens by direct interaction or by release of certain molecules including cytokines.
Cytokines are cell signalling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma. Cytokine biology reveals that there are some subsets of cytokines which are pro-inflammatory cytokines which stimulate the inflammatory responses and cause tissue destruction.
A periodontist is expected to have a sound basis of the cytokine profile to understand the pathogenesis of periodontitis and also to discover the new treatment modality of anti-cytokine therapy.
Classification Systems of Periodontal Diseases Manu Bhaskaran
This document discusses the history and development of classification systems for periodontal diseases. It begins with early classification attempts in the late 19th century based primarily on clinical features. In the 1920-1970 period, classifications were dominated by the "classical pathology" paradigm focusing on non-inflammatory degenerative forms of periodontitis. Starting in the 1970s, the "infection/host response" paradigm emerged as the dominant view, recognizing periodontitis as inflammatory diseases caused by bacterial infection. The document reviews several influential classification systems developed under this new paradigm from the 1970s to present day.
This document discusses the influence of systemic conditions on the periodontium. It begins by introducing periodontitis as a chronic bacterial infection and how host responses can vary between individuals. Systemic disorders can impair the host's immune defenses, creating opportunities for more severe periodontal disease. Several specific systemic factors are then examined in more detail, including hormonal changes, diabetes mellitus, and female sex hormones. The effects of these conditions on the periodontium are explored through their impact on factors like subgingival microbiota, polymorphonuclear leukocyte function, collagen metabolism, and wound healing. Treatment considerations for periodontal disease in systemic disease patients are also briefly addressed.
This document discusses the historical background and various methods of root biomodification, which involves chemically or mechanically modifying the root surface to promote periodontal regeneration. It describes how citric acid, tetracycline, fibronectin, and EDTA work to demineralize and detoxify the root surface in order to remove the smear layer and expose collagen fibers, making the surface more biocompatible and conducive to new attachment of periodontal tissues. Register and Burdick's 1975 technique using citric acid application for 2-3 minutes is outlined, along with modifications by Miller. The mechanisms and benefits of different agents are explained.
"INFLUENCE OF SYSTEMIC DISEASES (CONDITIONS) ON PERIODONTIUM" -PART-2Perio Files
This document discusses various systemic conditions and disorders that can influence periodontal disease, including:
1. Hematologic disorders like red blood cell disorders (such as sickle cell anemia), platelet disorders, and white blood cell disorders (such as leukemia) which can cause bleeding, infection, and gingival enlargement.
2. Systemic drug therapy that can cause gingival enlargement as a side effect, such as from anticonvulsants, immunosuppressants, and calcium channel blockers.
3. Psychosomatic disorders like stress, which may exacerbate periodontal disease through its effects on the immune system and increased production of pro-inflammatory mediators.
This document outlines a proposed new classification scheme for periodontal and peri-implant diseases and conditions. It discusses the need to update the 1999 classification scheme and develop a similar scheme for peri-implant diseases to align with current understanding. Key areas covered include definitions of periodontal health, gingivitis, and periodontitis at both the patient and site levels. Factors that determine the development and severity of gingivitis are summarized. Diagnostic criteria for gingivitis and approaches to classifying mild, moderate, and severe cases are discussed. The document also addresses non-dental plaque induced gingival conditions and future research needs.
This document discusses periodontal regeneration and the various factors involved. It begins by defining key terminology related to grafting and regeneration. It then discusses the biology and objectives of periodontal regeneration, including the ideal outcome of new attachment formation and factors that can influence outcomes. The document outlines various techniques for periodontal regeneration including non-graft associated approaches involving removal of epithelium and surgical techniques, as well as graft-associated approaches using various graft materials. Requirements for predictable regeneration and assessment methods are also summarized.
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.
Localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP) are rare, severe forms of periodontitis that primarily affect younger individuals. LAP is characterized by localized periodontal destruction limited to first molars and incisors, while GAP affects at least three permanent teeth. Both forms have a familial pattern and rapid progression of attachment and bone loss. The main pathogens associated with LAP and GAP are Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, respectively. Patients generally present with deep pockets and bone loss disproportionate to plaque levels.
This document discusses potential biomarkers for periodontal disease. It begins by defining biomarkers and explaining their advantages over traditional diagnostic methods. It then explores various categories of biomarkers, including microbiological markers like bacterial species and their products, as well as immune and inflammatory markers like cytokines. Specific biomarkers that have shown promise are discussed, such as GCF levels of PGE2, AST, and IgG subclasses. The document also notes challenges with biomarkers, like the polymicrobial nature of periodontal disease making it difficult to choose single bacterial species markers. Overall, the document provides a comprehensive overview of the types of biomarkers studied for periodontal disease and their potential for diagnosis and monitoring disease activity.
This document discusses aggressive periodontitis, including its definition, classification, clinical characteristics, diagnostic criteria, and treatment modalities. Aggressive periodontitis is defined as a rare, severe form of periodontitis characterized by early onset and familial aggregation. It can be localized or generalized. Treatment involves nonsurgical and surgical therapies like scaling and root planing as well as adjunctive systemic or local antibiotics. Maintaining frequent periodontal maintenance visits is important for long-term disease control.
AAP 2017 CLASSIFICATION OF PERIODONTAL DISEASE PART 1Babu Mitzvah
This document outlines the proceedings of a world workshop on classifying periodontal and peri-implant diseases and conditions. It discusses the need to update the 1999 classification system to current understanding. The outline covers periodontal health, gingival diseases, periodontitis, peri-implant diseases and key changes. Specifically, it defines periodontal health as having less than 10% bleeding sites and no probing depths over 3mm. It also discusses categories for periodontal health with an intact versus reduced periodontium, such as for successfully treated periodontitis patients.
Classification of Diseases & Conditions Affecting the Periodontium.pdfssuseraf61fb
This document discusses the classification of periodontal diseases and conditions over time. It describes four major attempts at classification between 1989-2017 based on criteria like etiology, histopathology, and genetics. The 1989 classification categorized periodontitis into prepubertal, juvenile, and adult types. The 1993 classification grouped periodontitis into adult and early onset types. The 1999 classification revised categories to include chronic, aggressive, and necrotizing periodontitis as well as periodontitis associated with systemic diseases. The 2017 classification framework characterized periodontitis based on multidimensional staging and grading that can be adapted over time with new evidence.
1, Klasifikasi Newman and Carranza's Clinical Periodontology E-Book.pdfisaurasanger1
This document discusses the classification of periodontal diseases and conditions affecting the periodontium. It begins with an outline of the topics to be covered, including gingival diseases, periodontitis, necrotizing periodontal diseases, and other conditions. The classification system presented is based on the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. Key aspects of the classification include distinguishing between gingivitis and periodontitis based on the extent of tissue involvement, and classifying periodontitis based on factors like severity and rate of progression. An updated 2018 classification from the AAP and EFP is also mentioned. The document then discusses the various categories of gingival and periodontal diseases in more detail
1, Klasifikasi Newman and Carranza's Clinical Periodontology E-Book.pdfisaurasanger1
This document discusses the classification of periodontal diseases and conditions affecting the periodontium. It begins with an outline of the key topics to be covered, including gingival diseases, periodontitis, necrotizing periodontal diseases, and developmental conditions. The classification system presented is based on the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. It categorizes diseases based on factors like extent, severity, progression, and localization. An updated 2018 classification from the AAP and EFP aims to address shortcomings like diagnostic inaccuracies. The document then examines the classifications and characteristics of various gingival diseases and conditions in more detail.
This document outlines the process and factors involved in diagnosing and determining the prognosis of periodontal diseases. Diagnosis involves a thorough medical and dental history, clinical examination including probing, radiographs, and other tests to determine the type, extent, severity and cause of periodontal disease present. The prognosis takes into account disease severity and extent, oral hygiene ability, systemic factors like smoking, genetic risks, and anatomic and restorative challenges that could impact treatment outcomes. Prognosis can range from excellent to hopeless depending on these various clinical factors.
This document discusses supportive periodontal treatment (SPT). It outlines the goals and phases of periodontal treatment, including preliminary, non-surgical, surgical, restorative, and maintenance phases. SPT, also called periodontal maintenance therapy, involves procedures performed at regular intervals to help patients maintain oral health after initial periodontal treatment. The document emphasizes that SPT is important to prevent recurrence of periodontal disease by supporting patients' efforts to control infections through regular professional cleanings and monitoring. Compliance with the SPT recall system and maintaining good oral hygiene are also highlighted as important factors that influence disease progression risk.
Periodontitis is a chronic, slowly progressing disease which mainly results in the destruction of tooth supporting apparatus. Earlier it was classified as Chronic and Aggressive periodontitis with different clinical features and etiology. Current classification ( 2017) of periodontal disease involves periodontitis with is further divided into 4 stages and 3 grades depending on severity and rate of disease progression respectively. Diabetes meelitus and smoking are the validated risk factors for the progression of periodontitis.
DETERMINATION OF PROGNOSIS IN PERIODONTICS.pptxKanchanMane4
The document discusses the determination and classification of periodontal prognosis. Prognosis is made based on specific disease information, risk factors, and treatment history. It is classified as good, fair, poor, questionable or hopeless. Factors like attachment loss, bone loss, furcation involvement, and mobility affect individual tooth prognosis, while age, medical history and oral hygiene impact overall prognosis. A provisional prognosis allows reevaluation after initial treatment. Smoking, genetics and stress influence prognosis. Prognosis of specific diseases like chronic periodontitis and aggressive periodontitis are discussed. Reevaluation after treatment can update the original prognosis.
The document provides an overview of chronic periodontitis, including its definition, classification, etiology, clinical features, disease progression, risk factors, diagnosis, and treatment. It discusses how chronic periodontitis is caused by an inflammatory response to bacterial plaque biofilm and is influenced by both local and systemic risk factors. Key points include that it is a slowly progressive disease involving loss of attachment and bone, and that risk is increased by factors like smoking, diabetes, genetic predispositions, and a prior history of periodontitis.
This document outlines the new 2018 classification of periodontal and peri-implant diseases and conditions presented at the World Workshop. It defines periodontal health and introduces a new classification that stages periodontitis based on severity and grades it based on progression rate. Gingivitis is classified by extent of bleeding. Peri-implant diseases of mucositis and periimplantitis are also defined. Other conditions discussed include necrotizing periodontal diseases, endo-perio lesions, mucogingival conditions, and effects of systemic diseases and trauma.
Latest Classification of Periodontal disease..pptxMumtaz Ali
1. The document presents information on the classification of periodontal diseases from the World Workshop on Classification of Periodontal and Peri-implant Diseases and Conditions held in 2017.
2. The new classification updates and improves upon the 1999 classification. It includes categories for periodontal health, gingival diseases and conditions, periodontitis in four stages, peri-implant diseases and conditions, and periodontal manifestations of systemic diseases.
3. Periodontitis is now graded on a scale of A to C based on severity and risk factors to allow for a more personalized approach to diagnosis and treatment.
Supportive periodontal therapy (SPT) involves regular maintenance visits after initial treatment for periodontal disease to prevent recurrence. The goals of SPT are to prevent further loss of attachment and tooth loss through monitoring the dentition. Key parts of SPT include examining the patient, providing re-instruction on oral hygiene, instrumenting reinfected sites, and polishing teeth while applying fluoride. Regular visits every 3-6 months are typically recommended, with more frequent visits for higher-risk patients. Failure to comply with SPT risks recurrence of periodontal disease due to a buildup of plaque and bacteria.
Aggressive periodontitis is a rare, severe form of periodontitis characterized by rapid attachment and bone loss. It is defined by early onset, familial aggregation, and microbial features including elevated levels of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis. Treatment involves non-surgical therapy such as scaling and root planing along with adjunctive antibiotic therapy targeting the causative bacteria. If non-surgical therapy is insufficient, surgical treatment may also be used in combination with antibiotics to gain access to deep pockets and remove infected tissue. The goals of treatment are to eliminate the pathogenic bacteria, arrest disease progression, and regenerate lost periodontal structures.
This document discusses supportive periodontal therapy (SPT), which involves maintenance care after initial treatment for periodontal disease. SPT is important for preventing recurrence of the disease and further tooth/bone loss. Long-term studies show that without SPT, periodontal disease often progresses again. The goals of SPT are to maintain periodontal health and reduce future tooth loss through regular cleanings and evaluation. Key aspects of SPT include subgingival plaque removal, risk assessment, and motivating patients to continue proper oral hygiene between visits. SPT has been shown to successfully maintain periodontal health for many years when done correctly.
Chronic periodontitis is an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss. It is no more a separate entity, as earlier it had Aggressive periodontitis as a differential diagnosis. According to the New Classification from the 2017 World Workshop on Periodontal and Peri- Implant Disease and Conditions, it is now classified further into stages and grades under Periodontitis.
Periodontal diseases Classifications and treatmentsRiad Mahmud
Prof. Dr. Md. Zahid Hossain, Division of Periodontology, Department of Preventive Dental Sciences, College of Dentistry, Najran University, Saudi Arabia.Former Professor of Periodontology, City Dental College, Dhaka
STAGING AND GRADING IN PERIODONTITIS.pptxsamanvibadri1
This document discusses the 2017 classification of periodontal and peri-implant diseases. It begins with introducing classifications and their importance. It then discusses the historical aspects and limitations of previous classifications from 1999. The highlights of the new 2017 classification are presented, which was developed by an international workshop with 130 experts. The new classification has four main categories: I) Periodontal health, gingivitis and gingival conditions, II) Periodontitis, III) Necrotizing periodontal diseases, and IV) Periodontitis as a manifestation of systemic diseases. Key aspects of the new classification are staging and grading of periodontitis to better aid in diagnosis, prognosis and treatment planning.
Risk factors for periodontal disease can be divided into modifiable risk factors like smoking and diabetes, and non-modifiable risk determinants like genetics. The development of periodontitis depends on both the specific bacteria involved and an individual's risk factor profile. Major risk factors include smoking, diabetes, stress, certain drugs, systemic diseases, and nutrition. Genetics, socioeconomic status, and gender can also influence risk. A thorough patient history is important to identify all relevant risk factors to guide treatment planning and prognosis.
This presentation focusses on definition, history, goals and objectives of SPT, patient compliance, ways to improve patient's compliance, parts of SPT, SPT in daily practice, classification of post treatment patients, AAP Guidelines for periodontist and dentist and studies related to SPT.
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.
The document discusses tissue engineering and its application in periodontal regeneration. It describes the key elements of tissue engineering which include progenitor/stem cells, scaffolds, and signaling molecules. It discusses various sources of progenitor cells for periodontal tissues, methods of scaffold fabrication, and growth factors used to enhance regeneration such as PDGF and BMPs. Studies evaluating the efficacy of different scaffold-growth factor combinations for achieving periodontal regeneration are also mentioned.
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
This document provides an overview of trauma from occlusion including:
- Definitions from various dental organizations
- Etiology and types of occlusal forces that can cause trauma
- Historical perspectives on the study of occlusion and trauma
- Terminologies used to describe occlusal trauma
- Stages of tissue response to excessive occlusal forces
- Signs and symptoms of trauma from occlusion
- Classification systems for trauma from occlusion
- Examination and diagnosis techniques
- Radiographic signs of trauma
- Debate around reversibility of traumatic occlusion
- Considerations for trauma around dental implants
- Treatment approaches including occlusal adjustments and splinting
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Classification 2017 part 1
1. CLASSIFICATION OF PERIODONTAL AND PERI-IMPLANT DISEASE
& CONDITION-2017
Dr. BEENA VIJAYAN PARVATHY
1st YEAR POST GRADUATE
Dept of Periodontics and Implantology
2. Introduction
Landmarks in periodontal classification
Need for classification
Classification 1989 – with limitation
Classification 1993 – with limitation
Classification 1999 – changes made from 1989
classification and its limitation
Consensus report 2017classification
Classification 2017
Key features in 2017 classification
Gingival and periodontal health – induced and reduced
periodontium
Gingivitis – biofilm induced
Gingivitis – non biofilm induced
Conclusion
References
CONTENTS
3. INTRODUCTION
A classification scheme for periodontal and peri-implant diseases and conditions is
necessary for clinicians to
Properly diagnose and treat patients
Scientists to investigate etiology, pathogenesis, natural history, and treatment
of the diseases and conditions
Clinicians to design appropriate therapeutic strategies
Developing framework to study the etiopathogenesis.
This seminar summarizes the proceedings of the World Workshop on the
Classification of Periodontal and Peri-implant Diseases and Conditions; along with
drawbacks of older classifications and need for newer one.
5. NEED FOR CLASSIFICATION
Classification systems are not rigid or fixed entities
Every classification system has to be evolved based on understanding of disease at
the time the classifications were proposed.
The classifications are needed to be modified periodically based on CURRENT
THINKING and KNOWLEDGE
6. REVISITING CLASSIFICATION OF
PERIODONTAL DISEASES
Periodontal disease
classifications went from
1977
2 categories
1986
4 categories
1989
1999
8 categories
(Gingival diseases classified)
5 categories
(The category of Periodontitis associated with
systemic disease)
7. Classification 1989 – Limitation
OVERLAPPING AMONG CATEGORIES
ABSENCE OF GINGIVAL DISEASE COMPONENT
INAPPROPRIATE EMPHASIS ON AGE & ONSET
OF DISEASE & RATE OF PROGRESSION
UNCLEAR CLASSIFICATION CRITERIA
A
B
C
D
IMPACT OF SYSTEMIC DISEASE ON
PERIODONTAL TISSUES UNEXPLAINED
10. AAP & European classification schemes were amended in 1999 WWP -with these
changes
•Gingival disease category introduced
•“Adult Periodontitis” replaced by “Chronic
Periodontitis” ( “Refractory” category removed )
•“Early onset periodontitis” replaced by “Aggressive
periodontitis”
•Impact of systemic diseases/conditions
expanded and defined
•“Necrotizing Periodontal Diseases” introduced
•Periodontal abscess & Endo- Perio lesions added
•A category of developmental & acquired lesions
introduced
LIMITATIONS
Etiology
Multiple appointment –to diagnose
Absence of implantology
Risk factors –smoking & diabetes not included.
11. AAP convened a World Workshop in 2017 to address problems
associated with 1999 classification
12. OUTLINE TO 2017
CLASSIFICATION 2015 PREPARATION STARTED
BY EFP AND AAP IN CHICAGO FROM NOV 9 TO 11
FORMED 4 WORK GROUPS & GAVE CASE
DEFINITIONS
FINALLY THEY PUT FORWARD 19 REVIEW PAPERS
( BASED ON 4 CONSENSUS REPORT )
13. Periodontal diseases and Conditions
Periodontal health,
Gingival diseases
and Conditions
Periodontal
health &
Gingival
health
Gingivitis:
Dental
Biofilm –
Induced
Gingival
diseases:
Non-
Dental
Biofilm-
Induced
Periodontitis
Necrotizing
Periodontal
diseases
Periodontitis
as a
manifestatio
n of
systemic
disease
Other conditions affecting the
periodontium
Systemic
diseases or
conditions
affecting
the
periodontal
supporting
tissues
Periodontal
abscess &
Endodontic
-
Periodontal
lesions
Mucogingival
deformities &
conditions
Traumatic
occlusal
forces
Tooth &
Prosthesis
related
factors
14.
15. Key features of 2017 classification
DEFINITIONS
Case definitions, Definition of Gingival and periodontal health
STAGES
Severity & Complexity
STAGE 1 to STAGE 4
GRADING
Rate of progression
Grade A, B ,C
Classification of Periimplant diseases and conditions
Re categorization of various forms of periodontitis
16. Term plaque induced replaced by dental biofilm induced
Systemic risk factors – smoking , hyperglycemia , hematological condition, nutritional factor ,
were added
Mycobacterium tuberculosis – added to specific infection
Specific infections –disscused in detail
17. Terminology
Case Definitions
Case definitions are guidelines that should be applied using sound clinical judgement to arrive at the most appropriate
clinical diagnosis.
Clinical periodontal health
Is defined as no bleeding on probing and no anatomical loss of periodontal structures.
Gingivitis
Is defined as a nonspecific inflammatory reaction to a nonspecific accumulation of plaque that is confined to the
gingival tissue, with no underlying destruction of the attachment apparatus.
Periodontitis
Covers the major plaque‐associated periodontal diseases, and treatment outcomes are expected to be either
periodontal disease stability or periodontal disease remission/control.
Periodontal disease stability
It is defined as a state in which the periodontitis has been successfully treated and clinical signs of the disease do not
appear to worsen in extent or severity despite the presence of a reduced periodontium.
Periodontal disease remission/control
It is defined as a period in the course of disease when symptoms become less severe but may not be fully resolved.
18.
19. Gingival Health
Intact Periodontium Reduced Periodontium
Clinical Gingival Health
Pristine Gingival Health
Stable Periodontitis
HEALTH
CAL – YES
PPD < 4mm
BOP <10 % sites
ABL-YES
GINGIVITIS
CAL – YES
PPD < 4mm
BOP >10 % sites
ABL-YES
Non Periodontitis
HEALTH
CAL – YES
PPD < 3mm
BOP <10 % sites
ABL-YES
GINGIVITIS
CAL – YES
PPD < 3mm
BOP >10 % sites
ABL-YES
HEALTH
CAL – NIL
PPD < 3mm
BOP <10 %
sites
ABL-NIL
GINGIVITIS
CAL – NIL
PPD < 3mm
BOP >10 %
sites
ABL-NIL
<10% of sites BOP
No probing depth of 4mm or greater.(≤3mm)
REFERENCE: Trombelli
L,Farina .Plaque-
induced
gingivitis:case
definition and
diagnostic
consideration.J
Periodontal2018
20. Intact Periodontium
Absence of BOP, erythema and edema, patient symptoms and attachment and bone loss. Physiological bone level
range from 1.0 to 3.0mm apical to CEJ.
Clinical gingival health is generally associated with an inflammatory infiltrate and a host response consistent with
homeostasis.
21. Reduced Periodontium
Stable periodontitis patients:
Successfully treated periodontitis patient
Non periodontitis patients:
Eg :- Recession, Crown lengthening
In presence of increased clinical attachment and bone level, successfully treated, stable periodontitis patient remain at
increased risk of recurrent progression.
Reference:
Periodontal health Niklaus P.La:ng; P.Mark Bartold Jclin Periodontal.2018;
45(Suppl20):S9-S16
24. Initiation of gingivitis
By accumulation of dental
plaque
Biofilm( >days /weeks)without
Disruption or removal
Due to loss of symbiosis
between
Biofilm and hosts immune-
inflammatory response.
Development of incipient dysbiosis
25. Gingivitis case can objectively, accurately defined and graded using a BOP score assessed as proportion of
bleeding sites (dichotomous) when stimulated by a standardized dental probe with a controlled force (0.25N)
to the apical end of the sulcus at six sites on all teeth present
LIMITATION
Characteristics of probe
Examiner variability
Patient related factors
Bleeding on Probing , if standardised , is the most relevant indicator of periodontal health
PPD and PAL alone are not indicators of periodontal health or disease rather should be correlated with BOP
Tooth mobility is not a good sign to define health/disease
Radiographs are not good indicators of clinical periodontal health on a reduced periodontium
26. CLASSIFICATION OF DENTAL BIOFILM INDUCED GINGIVITIS AND MODIFYING
FACTORS
Associated with bacterial dental biofilm only
Mediated by Systemic /Local risk factors :-
Systemic condition:
a. Sex steroid hormone
o Puberty
o Menstrual cycle
o Pregnancy
o Oral contraceptives
b. Hyperglycaemia
c. Leukaemia
d. Smoking
e. Malnutrition
Oral factors enhancing plaque accumulation
a. Prominent subgingival plaque accumulation
b. Hyposalivation/Oral dryness
Drug influenced gingival enlargements.
27. Dental Plaque Biofilm-Induced Gingivitis
Inflammatory lesion – resulting from interaction between dental plaque biofilm and host’s
immune inflammatory response.
Inflammation – does not extends to periodontal attachment (cementum , PDL, alveolar bone )
These inflammation confined to gingiva & not extend beyond mucogingival junction
Gingival inflammation on reduced periodontium in a successfully treated periodontitis patient
(recurrent periodontitis cannot be ruled out).
Its reversable by reducing levels of dental plaque at and apical to the gingival margin.
28.
29. Mediated By Systemic Risk
Factors(Modifying)
Sex Steroid Hormone :-
Tissue response within periodontium – modulated by-
o Androgen
o Oestrogen
o Progestins
For endocrinotropic condition: - plaque bacteria and elevated steroid hormone levels – produces gingival
inflammation
PUBERTY:
o Incidence & severity of gingivitis influenced by :-
• Biofilm level
• Dental caries
• Mouth breathing
• Crowding of teeth
• Tooth eruption
o Gingival inflammation in circumpubertal age in both gender – without any increase in plaque level
puberty associated gingivitis
30. MENSTRUAL CYCLE
o Studies shows GCF flow increases by 20% (ovulation).
o Over 75% women – have menstrual cycle induced gingival inflammation
PREGNANCY
o Gingival probing depth increases
o Bleeding on probing/ bleeding on brushing
o GCF flow elevated
ORAL CONTRACEPTIVE
o Gingivitis due to oral contraceptive in premenopausal women is similar
to plaque induced gingivitis
o Current dose of oral contraceptive is less than the original dose .
31. Hyperglycemia
o Gingivitis – consistent feature in type I Diabetes Mellitus in children
o Level of glycaemic control determine the severity of gingival inflammation
Leukemia
o Oral manifestation – in acute leukemia
o Signs of inflammation in gingiva swollen glazed & spongy tissue
red to purple in color
o Gingival bleeding –common sign
o Bleeding due to thrombocytopenia & clotting factor deficiency persist as myelodysplasia-initial sign
32. Smoking
o Major lifestyle related environmental risk factor
o Inhaled cigarette smoke
Capillaries absorb via pulmonary alveolar epithelium
Thus enters systemic circulation
o Direct exposure of inhaled cigarette smoke
To periodontal tissue
Vasoconstriction of periodontal microvasculature & gingival fibrosis
o Plaque accumulation exaggerated in smokers
33. Malnutrition
o Depletion of plasma ascorbic acid (Vit C) have effect on periodontium
o Scurvy (infants from low socio-economic families ,
institutionalized elderly & alcoholic ) developed risk for this condition
compromised antioxidant micronutrient defenses to oxidative stress.
o These effects are similar to plaque induced gingivitis
Mediated By Local/Oral
Factors(Predisposing)
Prominent subgingival plaque accumulation
ANATOMY, SUBGINGIVAL RESTORATIONS
increase plaque accumulation
promote gingivitis
34. HYPOSALIVATION
o Hyposalivation Xerostomia Sjogren's syndrome,
uncontrolled DM ,due to medications like antihistamine ,
decongestants, antidepressant, antihypertensive, Mouth breathing
o Cause dental caries
taste disorders ,
halitosis,
inflammation of mucosa, tongue, gingiva
o Dryness in mouth Plaque control is difficult ,
Gingival inflammation worsen
35. Drug Influenced Gingival Enlargements
o DRUGS LIKE antiepileptic – phenytoin , sodium valproate
calcium channel blockers (nifedipine , verapamil ,
diltiazem , amlodipine, felodipine )
Immunoregulating drugs (cyclosporine)
High dose oral contraceptive
o Enlargement commonly seen in – anterior teeth region
o Prevalence in younger individuals
o Onset within 3months of use
o First observed at papilla
o No attachment loss or tooth mortality
o With or without bone loss
Phenytoin Induced
Nifedipine Induced
Cyclosporine Induced
37. GENETIC/DEVELOPMENTAL DISORDERS
Hereditary Gingival Fibromatosis
Generalised fibrous gingival enlargement
Rare disease
Genetic basis –mutation of son of sevenless gene
SPECIFIC INFECTION
Bacterial Origin:
Necrotising Periodontal Disease:
Common term encomposing NG,NP,NS
FLORA contain-treponema spp., selenomonas spp., fusobacterium spp., prevotella intermedia
Ulceration with central necrosis of papilla-tissue destruction-forms crater.
Associated condition –smoking, stress, poor nutrition, HIV, poor oral hygiene
Others
• Gonorrhoeaª- Fiery red mucosa, white pseudomembrane with or without symptoms.
• Syphilis- Ulceration(fiery red,edematous,painful mucosa ), chancres(asymptomatic),inflamed gingiva.
38. Viral infection
Coxsackie Virusesª:
Cause- herpangina & HFMD
Primarily seen in children
Occurs in childhood
HSV-1ª & HSV -2ª:
Primarily involve anogenital infection
rarely oral infection
Herpetic Gingivostomatitis:
form vesicles rupture coalesce leave fibrin coated ulcers
Mistaken as aphthous ulcerations
Fungal infection
Candidiasis:
Oral thrush
Erythematous
Plaque like
Nodular
39. INFLAMMATORY & IMMUNE CONDITION
Hypersensitivity Reactions:
o Contact allergyª:
Redness & sometime lichenoid reaction
Due to dental restoration, dentifrices, mouthwash and food
Type IV hypersensitivity reaction
Autoimmune Disease of Skin and Mucous Membrane:
o Pemphigus vulgarisª:
Desquamative gingivitis
Vesiculo-bullous lesion of free and attached gingiva
Intraepithelial bullae
Granulomatous Inflammatory Condition(Orofacial Granulomatosis):
o Crohns diseaseª:
Cobblestone appearance – oral mucosa
Linear ulceration
o Sarcoidosisª:
Gingival swelling
Nodules &Loosening of teeth
Swelling of salivary gland
40. REACTIVE PROCESSES
Epulis:
o Fibrous Epulis
Exophytic smooth surface pink masses- on gingiva
o Calcifying Fibroblastic Granuloma
Pedunculated red or pink mass – derived from interdental papilla
o Pyogenic Granuloma(Vascular Epulis)
Ulcerated , smooth red to pink in color .
•Conditions marked “ª” have associated systemic involvement or are oral manifestations of systemic conditions.
•This helps the other health care providers involved in diagnosis and treatment.
•This kind of patient-centered care has been referred to as Precision Dental Medicine(PDM).
41. Case Definition
Case Definition of Gingivitis in an Intact Periodontium
Localized Gingivitis Generalized Gingivitis
Probing Attachment
Loss
NO NO
Radiographic Bone Loss NO NO
BOP Score ≥10% , ≤30% >30%
Case Definition of Gingivitis in an Reduced Periodontium Without
History of Periodontitis
Localized Gingivitis Generalized Gingivitis
Probing Attachment
Loss
YES YES
Radiographic Bone Loss Possible Possible
Probing Depth (All Sites) ≤3mm ≤3mm
BOP Score ≥10% , ≤30% >30%
42. A female patient of 18yrs with no relevant medical/drug history came with a complaint of pain in gums.
Pt. had
Probing pocket of 2mm in lower anteriors
No Clinical Attachment and bone loss
Bleeding on Probing Score of 28.7%
This gingival condition/case can be diagnosed as localized gingivitis on a intact periodontium.
43. A female patient of 50yrs with no relevant medical/drug history came with a complaint of bleeding gums.
Pt. had
Probing pocket of 2-3mm
With Clinical Attachment and no bone loss
Bleeding on Probing Score of 48.2%
Recession: Present
This gingival condition/case can be diagnosed as generalized gingivitis on a reduced periodontium.
44. This classification aims to provide the right care at the right time.
Classification systems are not rigid and fixed entities.
Every classification system has evolved based on understanding of disease at the time the
classifications were proposed
They are dynamic work in progress that need to be modified periodically based on Current
thinking and Knowledge
New classification in 2017 was made with strongest available scientific evidence
Conclusion
45. REFERENCES
1. Jack G. Catson , Gary Armitage , Panos N. Papapanou , Mariana Sanz Et Al – introduction and key changes from
1999 classification – JCP 2018
1. Trombelli L,Farina .Plaque-induced gingivitis:case definition and diagnostic consideration.J Periodontal2018
;45(Suppl 20):S44–S67.
3. Periodontal health Niklaus P.La:ng; P.Mark Bartold Jclin Periodontal.2018;45(Suppl20):S9-S16.
4. Jack G. Caton, Gary Armitage, Tord Berglundh, Iain L.C. Chapple, Søren Jepsen, Kenneth S. Kornman, Brian L.
Mealey, Panos N. Papapanou, Mariano Sanz, Maurizio S. Tonetti; J Periodontol. 2018;89(Suppl 1):S1–S8.
5. Ilain L.C Chapple , Brain L. Mealey , Thomas E. Van Dyke et al – periodontal health and gingival condition on
intact and reduced periodontium – JCP 2018.
6. Palle Holmstrup , Jacqueline Plemons , Joerg Meyle – Non Dental Plaque Induced Gingival Disease – 2018 JCP