This document discusses Necrotizing Ulcerative Gingivitis (NUG), also known as trench mouth. It defines NUG as a microbial disease of the gingiva caused by an impaired host response. Key clinical features include necrosis of gingival tissue and pain. Diagnosis is based on these clinical findings and microscopic examination. Management involves reducing the microbial load, removing necrotic tissue, treating any systemic conditions, and supportive periodontal therapy. Prognosis is generally good with treatment but recurrence is possible without ongoing maintenance of oral hygiene.
This document provides an overview of pulp and periapical pathologies. It begins by defining the dental pulp and pulpitis. It then covers causes of pulp disease including physical, chemical, and bacterial factors. It classifies pulp disease and discusses factors affecting the pulp response. It details the pathways of bacterial invasion of the pulp and describes different types of reversible and irreversible pulpitis. It also discusses chronic hyperplastic pulpitis, gangrenous necrosis of the pulp, and diseases of the periapical tissues like acute and chronic apical periodontitis and periapical abscess.
Juvenile periodontitis is a type of periodontitis that occurs in otherwise healthy individuals under 30 years old. It is characterized by rapid attachment and bone loss. There are two types: localized juvenile periodontitis, which is destructive to the first molars and incisors, and generalized juvenile periodontitis, which affects at least three teeth besides the first molars and incisors. Both types are caused by specific microorganisms like Actinobacillus actinomycetemcomitans and have features like deep pockets despite minimal plaque. Treatment involves scaling, root planing, antibiotics, and sometimes surgery.
This document discusses the clinical features of gingivitis. It begins by defining gingivitis as inflammation of the gingiva and describes how plaque bacteria can damage gingival tissues. It then covers the different types of gingivitis based on duration and distribution. Key signs of gingivitis that are discussed include gingival bleeding, color changes, changes in consistency, size, surface texture, position and contour. Specific conditions like gingival recession are also explained in terms of definition, classification, etiology and clinical significance.
One of the most painful but easy-to-treat dental emergencies is a dry socket.
• Dry socket symptoms are experienced after a tooth extraction.
• This condition requires follow-up care by the doctor who performed the surgery, an oral surgeon or a dentist who is familiar with how to treat it.
For more information, contact :-
Dr Sachdeva's Dental Aesthetic And Implant Institute,
I 101, Ashok Vihar Phase 1, Delhi- 110052
Contact us at
• Phone : +919818894041,01142464041
• Our Websites:
• www.sachdevadentalcare.com
• www.dentalclinicindelhi.com
• www.dentalimplantindia.co.in
• www.dentalcoursesdelhi.com
• www.facialaestheticsdelhi.com
#drysocket #management #thirdmolarextraction #extractioncomplications
This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.
This document discusses different types of pulpitis and periapical inflammation. It defines pulpitis as inflammation of the dental pulp that can be acute or chronic. Acute pulpitis is further divided into reversible and irreversible types based on whether the inflammation is localized or involves the entire pulp. Chronic pulpitis can be closed or open (hyperplastic). Periapical inflammation ranges from granulomas and cysts to abscesses. Diagnosis involves x-rays and pulp testing to evaluate the pulp chamber and periapical region. Treatment depends on the specific condition but may include removal of irritants, root canals, drainage or extraction.
This document discusses Necrotizing Ulcerative Gingivitis (NUG), also known as trench mouth. It defines NUG as a microbial disease of the gingiva caused by an impaired host response. Key clinical features include necrosis of gingival tissue and pain. Diagnosis is based on these clinical findings and microscopic examination. Management involves reducing the microbial load, removing necrotic tissue, treating any systemic conditions, and supportive periodontal therapy. Prognosis is generally good with treatment but recurrence is possible without ongoing maintenance of oral hygiene.
This document provides an overview of pulp and periapical pathologies. It begins by defining the dental pulp and pulpitis. It then covers causes of pulp disease including physical, chemical, and bacterial factors. It classifies pulp disease and discusses factors affecting the pulp response. It details the pathways of bacterial invasion of the pulp and describes different types of reversible and irreversible pulpitis. It also discusses chronic hyperplastic pulpitis, gangrenous necrosis of the pulp, and diseases of the periapical tissues like acute and chronic apical periodontitis and periapical abscess.
Juvenile periodontitis is a type of periodontitis that occurs in otherwise healthy individuals under 30 years old. It is characterized by rapid attachment and bone loss. There are two types: localized juvenile periodontitis, which is destructive to the first molars and incisors, and generalized juvenile periodontitis, which affects at least three teeth besides the first molars and incisors. Both types are caused by specific microorganisms like Actinobacillus actinomycetemcomitans and have features like deep pockets despite minimal plaque. Treatment involves scaling, root planing, antibiotics, and sometimes surgery.
This document discusses the clinical features of gingivitis. It begins by defining gingivitis as inflammation of the gingiva and describes how plaque bacteria can damage gingival tissues. It then covers the different types of gingivitis based on duration and distribution. Key signs of gingivitis that are discussed include gingival bleeding, color changes, changes in consistency, size, surface texture, position and contour. Specific conditions like gingival recession are also explained in terms of definition, classification, etiology and clinical significance.
One of the most painful but easy-to-treat dental emergencies is a dry socket.
• Dry socket symptoms are experienced after a tooth extraction.
• This condition requires follow-up care by the doctor who performed the surgery, an oral surgeon or a dentist who is familiar with how to treat it.
For more information, contact :-
Dr Sachdeva's Dental Aesthetic And Implant Institute,
I 101, Ashok Vihar Phase 1, Delhi- 110052
Contact us at
• Phone : +919818894041,01142464041
• Our Websites:
• www.sachdevadentalcare.com
• www.dentalclinicindelhi.com
• www.dentalimplantindia.co.in
• www.dentalcoursesdelhi.com
• www.facialaestheticsdelhi.com
#drysocket #management #thirdmolarextraction #extractioncomplications
This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.
This document discusses different types of pulpitis and periapical inflammation. It defines pulpitis as inflammation of the dental pulp that can be acute or chronic. Acute pulpitis is further divided into reversible and irreversible types based on whether the inflammation is localized or involves the entire pulp. Chronic pulpitis can be closed or open (hyperplastic). Periapical inflammation ranges from granulomas and cysts to abscesses. Diagnosis involves x-rays and pulp testing to evaluate the pulp chamber and periapical region. Treatment depends on the specific condition but may include removal of irritants, root canals, drainage or extraction.
This document discusses prognosis in periodontal disease. Prognosis is the prediction of the probable course and outcome of a disease based on knowledge of pathogenesis and risk factors. It is determined before treatment based on disease characteristics and previous experience. Prognosis can be excellent, good, fair, poor, questionable or hopeless depending on factors like bone loss, furcation involvement, and patient compliance. Systemic factors like smoking and diabetes can affect prognosis. Anatomical root characteristics also influence prognosis. The relationship between diagnosis and prognosis is discussed.
Tooth mobility refers to loose teeth that can move within their sockets. It is classified on a scale of 0 to 3 based on the degree of horizontal and vertical movement. Physiologic mobility of about 0.25mm is normal, while pathologic mobility over 1mm indicates loose teeth from periodontal disease or trauma. Periodontal disease is a primary cause as it leads to loss of attachment and bone supporting the teeth. Treatment involves splinting loose teeth together, replacing missing teeth, and correcting occlusal surfaces to reduce excessive forces. For advanced periodontal cases, extraction may be necessary.
This document discusses pin-retained amalgam restorations for teeth with extensive caries or fractures. It describes the advantages as conserving tooth structure and providing increased resistance and retention compared to cast restorations. Potential disadvantages include dentinal microfractures, microleakage, and decreased amalgam strength. Factors that affect pin retention such as pin type, size, orientation, and number are examined. Guidelines for cavity preparation and pin placement based on tooth anatomy and pulp location are provided. Common problems and their solutions are also outlined.
This document discusses various classifications and types of periapical diseases including symptomatic and asymptomatic apical periodontitis, acute alveolar abscess, phoenix abscess, persistent apical periodontitis, chronic alveolar abscess, radicular cyst, condensing osteitis, and different types of external and internal root resorption. It provides definitions, causes, symptoms, diagnostic features and treatment options for each condition.
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
The document defines and classifies different types of gingival enlargement based on etiology and pathologic changes. It describes inflammatory enlargement including chronic, acute, and drug-induced types. It also covers enlargements associated with systemic diseases, neoplastic enlargements including benign and malignant tumors, and false enlargements. Grading systems and detailed clinical, histological, and radiographic features are provided for many conditions.
Gingival enlargement, also known as gingival overgrowth, has several potential causes including inflammatory, drug-induced, and systemic conditions. It is classified based on etiology and pathology. Inflammatory enlargement is caused by prolonged bacterial plaque exposure and poor oral hygiene. Drug-induced enlargement can be caused by medications like anticonvulsants, immunosuppressants, and calcium channel blockers. Systemic conditions like pregnancy, leukemia, and granulomatous diseases can also cause gingival enlargement. Treatment depends on the specific cause but may include nonsurgical approaches like improved plaque control or surgical procedures like gingivectomy.
Pericoronitis refers to inflammation around the crown of an unerupted tooth. It most commonly occurs with the mandibular third molar and can be acute, subacute, or chronic. Acute pericoronitis presents as a red, swollen, painful lesion that may cause fever and lymphadenitis. Treatment involves antibiotics and flushing the area for mild cases or flap removal for persistent symptoms to prevent recurrence. The decision to retain or extract the tooth depends on its stage of eruption, position, and likelihood of further eruption without complications.
This document summarizes diseases of the periodontium. The periodontium comprises the gingiva, periodontal ligament, root cementum, and alveolar bone. It attaches the tooth to the jaw bone and maintains the integrity of the oral mucosa. Necrotizing ulcerative gingivitis is a specific type of gingivitis characterized by pain, interdental ulceration, and bleeding. It is caused by an endogenous polymicrobial infection facilitated by factors like stress, smoking, and poor nutrition. Treatment involves cleaning, scaling, antibiotics, and surgical procedures to restore tissue contours. Gingival enlargement causes an increase in gingival size, overfilling interproximal spaces and protr
This document discusses the causes, progression, and presentation of various periapical and periodontal infections and abscesses. It describes how untreated pulpitis can lead to periodontitis as bacteria spread through the root canal. Acute traumatic periodontitis is usually temporary and caused by occlusal trauma or dental procedures. Persistent irritation can lead to chronic periapical periodontitis characterized by bone resorption and granulation tissue formation. Abscesses may develop from these infections and spread in various directions depending on anatomical structures, presenting as facial swelling, palatal abscesses, or submandibular involvement in severe cases like Ludwig's angina.
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
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
This presentation specifically deals with the maxillary and mandibular Major connectors used in a cast partial denture. it also mentions the uses, advantages and disadvantages of each,
The document discusses different types of cysts that can occur in the oral and maxillofacial region. It defines cysts and classifies them based on their origin and location. It provides details on the pathogenesis, clinical features, radiographic appearance and histology of specific cysts such as dentigerous cysts and odontogenic keratocysts. Dentigerous cysts are defined as cysts originating from the separation of the dental follicle from around the crown of an unerupted tooth. Odontogenic keratocysts are distinctive cysts that arise from cell rests of the dental lamina and have more aggressive behavior than other cysts. Complications of cysts include recurrence, development of
1. Gingival recession is the exposure of root surface caused by an apical shift in gingival position. It can be classified as visible, hidden, localized, or generalized.
2. Miller and Atkin & Sullivan classified gingival recession defects based on their location and amount of bone loss. Common causes of recession include age, faulty brushing technique, tooth malposition, gingival inflammation, abnormal frenal attachment, and masochistic habits.
3. Recession can be treated non-surgically through modifying risks or surgically through pedicle or free soft tissue grafts to cover exposed root surfaces and reduce sensitivity.
The document defines and describes periodontal pockets. It notes that periodontal pockets can be classified based on their location relative to the alveolar bone as either suprabony or infrabony. Suprabony pockets have bone loss horizontally while infrabony pockets have bone loss vertically. The document also discusses the pathogenesis of pocket formation, clinical features, histopathology, and diagnosis and probing of periodontal pockets.
- Trauma from occlusion occurs when occlusal forces exceed the adaptive capacity of the periodontium, causing injury. It can be acute or chronic.
- The magnitude, direction, duration, and frequency of forces impact the periodontium's ability to adapt. Excessive pressure or tension can damage tissues.
- Primary trauma from occlusion is caused by changes in occlusal forces, while secondary trauma occurs when reduced bone support impairs the tissues' resistance to normal forces.
- The periodontium responds to trauma in three stages - injury, repair through new tissue formation, and adaptive remodeling to better withstand forces. Trauma can cause reversible damage if forces are reduced, or lead to irreversible injury if
Classification of periodontal diseasesEnas Elgendy
This document classifies periodontal diseases into two main categories: gingivitis and periodontitis. Gingivitis is further divided into plaque-induced gingivitis and non-plaque induced gingivitis. Periodontitis is classified as chronic periodontitis, aggressive periodontitis, periodontitis as a manifestation of systemic diseases, and several other types. The document provides detailed descriptions and examples for each category and type of periodontal disease.
The document discusses anatomical landmarks that are visible on radiographs of the teeth and jaws. It describes radiolucent and radiopaque structures of the tooth and surrounding bone, including the pulp, periodontal ligament space, enamel, dentin, cementum, lamina dura, alveolar bone and crest. It also lists radiolucent and radiopaque landmarks of the maxilla and mandible, such as the maxillary sinus, nasal fossa, mandibular canal, mental foramen and rami. The document is intended to familiarize dental students with normal anatomical structures seen on dental radiographs.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
This document provides an overview of chronic periodontitis. It discusses the introduction, history, prevalence, etiology, pathogenesis, clinical features, models of disease progression, microbiological and immunological considerations, and risk factors of chronic periodontitis. Chronic periodontitis is a complex polymicrobial infection that results from an imbalance between pathogenic bacteria in plaque and the host immune response. It begins as plaque-induced gingivitis and progresses to the destruction of connective tissue and alveolar bone through periods of activity and remission, leading to pocket formation and potential tooth loss over time if left untreated. Systemic and environmental risk factors like smoking can increase the risk and rate of disease progression.
This document discusses chronic periodontitis, the most common form of periodontitis. It is defined as an infectious disease resulting in inflammation and destruction of the tissues supporting the teeth. The key clinical features are plaque, gingivitis, attachment loss, bone loss, and inflammation. Chronic periodontitis is considered a site-specific disease where inflammation and bone loss occur at specific sites due to local plaque accumulation. The severity is classified as slight, moderate, or severe based on the amount of attachment loss. Risk factors include poor plaque control, systemic diseases, environmental/behavioral factors like smoking, and genetics. Treatment involves improving oral hygiene, nonsurgical treatments like scaling and root planing, and sometimes surgery.
This document discusses prognosis in periodontal disease. Prognosis is the prediction of the probable course and outcome of a disease based on knowledge of pathogenesis and risk factors. It is determined before treatment based on disease characteristics and previous experience. Prognosis can be excellent, good, fair, poor, questionable or hopeless depending on factors like bone loss, furcation involvement, and patient compliance. Systemic factors like smoking and diabetes can affect prognosis. Anatomical root characteristics also influence prognosis. The relationship between diagnosis and prognosis is discussed.
Tooth mobility refers to loose teeth that can move within their sockets. It is classified on a scale of 0 to 3 based on the degree of horizontal and vertical movement. Physiologic mobility of about 0.25mm is normal, while pathologic mobility over 1mm indicates loose teeth from periodontal disease or trauma. Periodontal disease is a primary cause as it leads to loss of attachment and bone supporting the teeth. Treatment involves splinting loose teeth together, replacing missing teeth, and correcting occlusal surfaces to reduce excessive forces. For advanced periodontal cases, extraction may be necessary.
This document discusses pin-retained amalgam restorations for teeth with extensive caries or fractures. It describes the advantages as conserving tooth structure and providing increased resistance and retention compared to cast restorations. Potential disadvantages include dentinal microfractures, microleakage, and decreased amalgam strength. Factors that affect pin retention such as pin type, size, orientation, and number are examined. Guidelines for cavity preparation and pin placement based on tooth anatomy and pulp location are provided. Common problems and their solutions are also outlined.
This document discusses various classifications and types of periapical diseases including symptomatic and asymptomatic apical periodontitis, acute alveolar abscess, phoenix abscess, persistent apical periodontitis, chronic alveolar abscess, radicular cyst, condensing osteitis, and different types of external and internal root resorption. It provides definitions, causes, symptoms, diagnostic features and treatment options for each condition.
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
The document defines and classifies different types of gingival enlargement based on etiology and pathologic changes. It describes inflammatory enlargement including chronic, acute, and drug-induced types. It also covers enlargements associated with systemic diseases, neoplastic enlargements including benign and malignant tumors, and false enlargements. Grading systems and detailed clinical, histological, and radiographic features are provided for many conditions.
Gingival enlargement, also known as gingival overgrowth, has several potential causes including inflammatory, drug-induced, and systemic conditions. It is classified based on etiology and pathology. Inflammatory enlargement is caused by prolonged bacterial plaque exposure and poor oral hygiene. Drug-induced enlargement can be caused by medications like anticonvulsants, immunosuppressants, and calcium channel blockers. Systemic conditions like pregnancy, leukemia, and granulomatous diseases can also cause gingival enlargement. Treatment depends on the specific cause but may include nonsurgical approaches like improved plaque control or surgical procedures like gingivectomy.
Pericoronitis refers to inflammation around the crown of an unerupted tooth. It most commonly occurs with the mandibular third molar and can be acute, subacute, or chronic. Acute pericoronitis presents as a red, swollen, painful lesion that may cause fever and lymphadenitis. Treatment involves antibiotics and flushing the area for mild cases or flap removal for persistent symptoms to prevent recurrence. The decision to retain or extract the tooth depends on its stage of eruption, position, and likelihood of further eruption without complications.
This document summarizes diseases of the periodontium. The periodontium comprises the gingiva, periodontal ligament, root cementum, and alveolar bone. It attaches the tooth to the jaw bone and maintains the integrity of the oral mucosa. Necrotizing ulcerative gingivitis is a specific type of gingivitis characterized by pain, interdental ulceration, and bleeding. It is caused by an endogenous polymicrobial infection facilitated by factors like stress, smoking, and poor nutrition. Treatment involves cleaning, scaling, antibiotics, and surgical procedures to restore tissue contours. Gingival enlargement causes an increase in gingival size, overfilling interproximal spaces and protr
This document discusses the causes, progression, and presentation of various periapical and periodontal infections and abscesses. It describes how untreated pulpitis can lead to periodontitis as bacteria spread through the root canal. Acute traumatic periodontitis is usually temporary and caused by occlusal trauma or dental procedures. Persistent irritation can lead to chronic periapical periodontitis characterized by bone resorption and granulation tissue formation. Abscesses may develop from these infections and spread in various directions depending on anatomical structures, presenting as facial swelling, palatal abscesses, or submandibular involvement in severe cases like Ludwig's angina.
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
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
This presentation specifically deals with the maxillary and mandibular Major connectors used in a cast partial denture. it also mentions the uses, advantages and disadvantages of each,
The document discusses different types of cysts that can occur in the oral and maxillofacial region. It defines cysts and classifies them based on their origin and location. It provides details on the pathogenesis, clinical features, radiographic appearance and histology of specific cysts such as dentigerous cysts and odontogenic keratocysts. Dentigerous cysts are defined as cysts originating from the separation of the dental follicle from around the crown of an unerupted tooth. Odontogenic keratocysts are distinctive cysts that arise from cell rests of the dental lamina and have more aggressive behavior than other cysts. Complications of cysts include recurrence, development of
1. Gingival recession is the exposure of root surface caused by an apical shift in gingival position. It can be classified as visible, hidden, localized, or generalized.
2. Miller and Atkin & Sullivan classified gingival recession defects based on their location and amount of bone loss. Common causes of recession include age, faulty brushing technique, tooth malposition, gingival inflammation, abnormal frenal attachment, and masochistic habits.
3. Recession can be treated non-surgically through modifying risks or surgically through pedicle or free soft tissue grafts to cover exposed root surfaces and reduce sensitivity.
The document defines and describes periodontal pockets. It notes that periodontal pockets can be classified based on their location relative to the alveolar bone as either suprabony or infrabony. Suprabony pockets have bone loss horizontally while infrabony pockets have bone loss vertically. The document also discusses the pathogenesis of pocket formation, clinical features, histopathology, and diagnosis and probing of periodontal pockets.
- Trauma from occlusion occurs when occlusal forces exceed the adaptive capacity of the periodontium, causing injury. It can be acute or chronic.
- The magnitude, direction, duration, and frequency of forces impact the periodontium's ability to adapt. Excessive pressure or tension can damage tissues.
- Primary trauma from occlusion is caused by changes in occlusal forces, while secondary trauma occurs when reduced bone support impairs the tissues' resistance to normal forces.
- The periodontium responds to trauma in three stages - injury, repair through new tissue formation, and adaptive remodeling to better withstand forces. Trauma can cause reversible damage if forces are reduced, or lead to irreversible injury if
Classification of periodontal diseasesEnas Elgendy
This document classifies periodontal diseases into two main categories: gingivitis and periodontitis. Gingivitis is further divided into plaque-induced gingivitis and non-plaque induced gingivitis. Periodontitis is classified as chronic periodontitis, aggressive periodontitis, periodontitis as a manifestation of systemic diseases, and several other types. The document provides detailed descriptions and examples for each category and type of periodontal disease.
The document discusses anatomical landmarks that are visible on radiographs of the teeth and jaws. It describes radiolucent and radiopaque structures of the tooth and surrounding bone, including the pulp, periodontal ligament space, enamel, dentin, cementum, lamina dura, alveolar bone and crest. It also lists radiolucent and radiopaque landmarks of the maxilla and mandible, such as the maxillary sinus, nasal fossa, mandibular canal, mental foramen and rami. The document is intended to familiarize dental students with normal anatomical structures seen on dental radiographs.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
This document provides an overview of chronic periodontitis. It discusses the introduction, history, prevalence, etiology, pathogenesis, clinical features, models of disease progression, microbiological and immunological considerations, and risk factors of chronic periodontitis. Chronic periodontitis is a complex polymicrobial infection that results from an imbalance between pathogenic bacteria in plaque and the host immune response. It begins as plaque-induced gingivitis and progresses to the destruction of connective tissue and alveolar bone through periods of activity and remission, leading to pocket formation and potential tooth loss over time if left untreated. Systemic and environmental risk factors like smoking can increase the risk and rate of disease progression.
This document discusses chronic periodontitis, the most common form of periodontitis. It is defined as an infectious disease resulting in inflammation and destruction of the tissues supporting the teeth. The key clinical features are plaque, gingivitis, attachment loss, bone loss, and inflammation. Chronic periodontitis is considered a site-specific disease where inflammation and bone loss occur at specific sites due to local plaque accumulation. The severity is classified as slight, moderate, or severe based on the amount of attachment loss. Risk factors include poor plaque control, systemic diseases, environmental/behavioral factors like smoking, and genetics. Treatment involves improving oral hygiene, nonsurgical treatments like scaling and root planing, and sometimes surgery.
Chronic periodontitis is an inflammatory disease that causes the destruction of the tissues that support the teeth. It is caused by bacterial plaque accumulating at and below the gumline. The disease is characterized by pocket formation, attachment loss, and bone loss. It is usually slowly progressive and can range from mild to severe. Diagnosis involves measuring pocket depths, attachment levels, bleeding, and bone loss visible on radiographs. Risk factors include poor oral hygiene, smoking, diabetes, and genetic factors. Treatment aims to eliminate plaque and bacteria through nonsurgical methods like scaling and root planing or sometimes surgical procedures to reduce pocket depths and regenerate lost tissues.
classification of periodontal diseasesfiza shameem
The document categorizes and describes various types of periodontal diseases including:
- Chronic periodontitis, which is common in adults and progresses slowly, and can be localized or generalized.
- Aggressive periodontitis, which affects younger individuals and progresses rapidly. It can be localized or generalized.
- Periodontitis as a manifestation of systemic diseases such as hematological or genetic disorders.
- Developmental or acquired deformities and conditions that can modify or predispose individuals to plaque-induced gingivitis or periodontitis.
This document provides an overview of abscesses of the periodontium, specifically focusing on periodontal abscesses. It defines a periodontal abscess and classifies them based on location, course, number, affected tissue, and cause. Periodontal abscesses are most prevalent in molar sites and those with pre-existing periodontal pockets. They can be caused by factors like untreated periodontitis, foreign bodies, or changes after periodontal procedures or antibiotics. The pathogenesis involves bacterial entry triggering an inflammatory response that leads to tissue destruction and pus formation.
This document provides an overview of periodontal abscesses. It defines a periodontal abscess as a localized collection of pus within the periodontal tissues. Periodontal abscesses are classified based on duration, number, location and etiology. The main causes are periodontitis, trauma from foreign objects, and certain dental procedures. Microbiologically, periodontal abscesses involve anaerobic bacteria normally found in the oral cavity like P. gingivalis, P. intermedia and F. nucleatum. Clinical features include pain, swelling and exudate from the gingiva. Management involves incision and drainage of the acute lesion along with antibiotics and treatment of the underlying condition like scaling or surgery.
This document discusses several conditions that can affect the gingiva including necrotizing ulcerative gingivitis (NUG), primary herpetic gingivostomatitis, and recurrent aphthous stomatitis. NUG is a painful inflammatory disease affecting the gingiva caused by spirochetes and fusiform bacteria. It is characterized by ulcers and can cause bad breath and increased salivation. Treatment involves antibiotics, rinsing with hydrogen peroxide, and improving oral hygiene. Primary herpetic gingivostomatitis is caused by the herpes simplex virus and produces gingival lesions and sores. It typically resolves within 7-10 days with top
The document summarizes research into the relationship between chronic periodontitis (gum disease) and coronary heart disease (CHD). It first outlines the hypothesis that periodontitis can be statistically and mechanically linked to CHD. It then reviews literature showing a statistical association between dental infections and heart attacks. Studies found higher rates of gum issues in heart patients versus controls. Additional research demonstrated that the bacteria P. gingivalis accelerated atherosclerosis in mice. The conclusion is that periodontitis may be a better predictor of heart disease risk than traditional CHD risk factors.
Acute necrotising ulcerative gingivitis is a rare condition characterized by necrosis of the gingiva and interdental papillae. It frequently occurs during times of stress and poor oral hygiene. The condition is caused by fusiform bacillus and Borrelia vincentii bacteria. Clinically, the gingiva becomes painful and develops punched-out ulcers. It can spread to other oral tissues and rarely the skin, causing further complications.
classification of periodontal diseasesneeti shinde
The document provides an overview of the historical development of classification systems for periodontal diseases from the 1870s to present. It discusses early systems based on clinical characteristics and concepts of classical pathology and the current dominant paradigm of periodontal diseases having an infectious etiology. The American Academy of Periodontology classification from 1999 is summarized, categorizing diseases as gingival diseases, chronic periodontitis, aggressive periodontitis, periodontitis as a manifestation of systemic diseases, and necrotizing periodontal diseases.
Federación Odontológica del Perú
IX Jornada Anual
Auditorio del Colegio Odontológico del Perù
Conferencia: Abscesos Periodontales
Prof. Dr. Ricardo Benza Bedoya
This document summarizes various acute periodontal conditions, including abscesses of the periodontium (gingival, periodontal, pericoronal), necrotizing periodontal diseases (necrotizing ulcerative gingivitis, necrotizing ulcerative periodontitis), gingival diseases of viral origin (primary herpetic gingivostomatitis, recurrent oral herpes), recurrent aphthous stomatitis, and allergic reactions in the oral cavity. Treatment options focus on drainage, debridement, antimicrobials, pain control, and identifying/eliminating predisposing factors or allergens. Comprehensive evaluation and follow-up are important after resolution of acute
This document discusses early onset periodontitis, which comprises rare, severe, and rapidly progressive forms of periodontitis characterized by an early age of onset and familial aggregation. It describes several types including prepubertal, juvenile, and rapidly progressive periodontitis. Localized juvenile periodontitis is highlighted, which clinically presents with deep probing depths, attachment loss, and radiographic bone loss localized to first molars and incisors in otherwise healthy teenagers, despite minimal plaque and gingivitis. Treatment involves nonsurgical and surgical approaches along with antibiotic therapy.
The document discusses the historical development and current classification of periodontal diseases. It outlines several past classification systems from the 19th century based on clinical characteristics to more recent systems from the late 20th century incorporating etiology and pathogenesis. The current 1999 classification system from the International Workshop for a Classification of Periodontal Diseases and Conditions is explained in detail, categorizing diseases based on factors like plaque-induced vs. non-plaque induced gingival diseases, chronic vs. aggressive periodontitis, and periodontitis as a manifestation of systemic diseases.
This document discusses acute gingival infections, including primary herpetic gingivostomatitis, necrotizing ulcerative gingivitis (NUG), and pericoronitis. NUG is characterized by necrosis and sloughing of gingival tissues due to an impaired host response allowing pathogenic bacteria to invade. Clinically, it presents with crater-like gingival ulcers, pseudomembranes, pain, and systemic symptoms. The etiology involves both specific bacteria like fusospirochetal complexes and an underlying host immunosuppression. Treatment focuses on improving nutrition, antibiotics, and palliative care. Differential diagnosis includes herpes, desquamative gingivitis,
Dr. Eirini Georgiou from PerioExperts.
Periodontal disease refers to the periodontal tissues that surround, bind and support the teeth into their socket. These tissues are the gums, the jaw bone, the cementum of the root and the periodontal ligament. In healthy circumstances the gums are light pink, do not bleed and are firmly attached to the tooth, like a nice frame around a picture painting.
Periodontal disease can affect all people regardless age, but as age progresses the incidence of infection increases. It is estimated that in US 80% of people over 45 years old suffer from periodontal disease. Although periodontal disease is nowadays the main cause of tooth loss in adults, early diagnosis and preventive therapy, provide effective treatment.
Recently, periodontal disease is associated with the onset of cardiovascular problems, diabetes melitus, or premature birth and underweight babies, and morbid obesity. Therefore, the preservation and restoration of periodontal health is directly related to the conservation and restoration of general health.
Periodontal examintation,diagnosis and prognosisSaeed Bajafar
This document discusses the main concerns of a periodontal patient, including symptoms like bleeding, pain, swelling and bad breath. It examines factors contributing to conditions like gingivitis and periodontal disease. The objectives are to identify systemic factors, note medical conditions requiring precautions during treatment, and check for transmissible diseases. A thorough periodontal exam evaluates plaque, calculus, probing depth, mobility and other dental health factors to fully diagnose the patient's condition and determine an appropriate treatment plan and prognosis.
The periodontal pocket is a pathologically deepened sulcus that is a key feature of periodontal disease. It develops as plaque causes gingival inflammation that leads to migration of the junctional epithelium and destruction of supporting tissues. Pockets are classified by morphology as gingival pockets from enlarged gingiva or periodontal pockets from true tissue loss, and by number of tooth surfaces involved. Periodontal pockets contain bacteria and experience cycles of activity and quiescence that further deepen the pocket and destroy bone and connective tissue.
Periodontal disease is a chronic bacterial infection that affects the gums and bone supporting the teeth. It ranges from gingivitis, a reversible early stage marked by red, swollen gums, to periodontitis, a more advanced stage involving irreversible bone and tissue destruction. Risk factors include smoking, diabetes, genetics, and certain medications. Symptoms include bad breath, bleeding gums, and loose teeth. Treatment involves deep cleaning below the gumline, antibiotics, and sometimes surgery to regenerate lost bone and tissue. Regular cleanings and proper brushing and flossing can help prevent periodontal disease.
Chronic periodontitis is an infectious disease that causes inflammation of the tissues supporting the teeth and progressive bone and attachment loss. It typically affects people aged 30-35 and causes variable pocket depths and bone loss patterns, including horizontal and vertical loss. Symptoms may include pain, sensitivity, and food impaction. Risk factors include poor oral hygiene, smoking, diabetes, and genetic factors. Treatment involves improving oral hygiene, nonsurgical therapies like scaling and root planing, and sometimes surgery.
Chronic periodontitis is the most common form of periodontitis and is characterized by microbial biofilm formation, periodontal inflammation, and attachment and bone loss. It is diagnosed based on clinical attachment level assessment and radiographs showing bone loss. Risk factors include local factors like plaque and calculus that retain bacteria, and systemic factors like diabetes which impair the immune response and increase the severity of periodontitis. The condition progresses slowly over time with increased attachment and bone loss with age.
Chronic periodontitis is an infectious disease resulting in inflammation with in supporting tissues of the teeth, progressive attachment loss and bone loss. With all emerging technologies, a successful diagnosis and treatment will only be achieved through open sharing of ideas, research findings and thorough testing .
Chronic periodontitis is an inflammatory disease that causes the destruction of the tissues that support the teeth. It is caused by bacterial plaque accumulating at and below the gumline. It is characterized by pocket formation, attachment loss, and bone loss. The disease progresses slowly over time and is generally classified as slight, moderate, or severe depending on the amount of attachment loss. A clinical diagnosis involves measuring pocket depths and looking for signs of inflammation, recession, and bone loss. Radiographs can also help assess bone level changes over time. Risk factors include poor oral hygiene, smoking, diabetes, and genetic factors. Treatment involves nonsurgical debridement or surgical procedures to reduce pockets and regenerate lost tissues.
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 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.
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.
This document discusses the epidemiology of periodontal disease. It begins by defining key terms like periodontitis, gingivitis, dental plaque, and calculus. It then discusses the prevalence and distribution of periodontal diseases globally and over age, noting that over 70% of adults worldwide have some degree of gingivitis or periodontitis. While gingivitis and calculus tend to be more prevalent and severe in low-income countries, the prevalence of severe periodontitis shows fewer global differences. The document also outlines methods used for measuring and classifying periodontal diseases in epidemiological studies.
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.
Chronic periodontitis is the most common form of periodontitis. It is characterized as a slow progressing, chronic inflammatory disease caused by bacterial plaque that leads to progressive loss of attachment and bone. If left untreated, chronic periodontitis can cause deep pockets, furcation involvement, tooth mobility, and eventual tooth loss. Risk factors include poor oral hygiene, pre-existing periodontitis, systemic diseases like diabetes, smoking, and genetic factors. Treatment involves nonsurgical and surgical therapies aimed at reducing the bacterial load and regenerating lost tissues through improved plaque control.
Chronic periodontitis is an inflammatory disease that causes the destruction of tissues that support the teeth. It is caused by an accumulation of plaque and calculus on the teeth over time. It is characterized by pocket formation, attachment loss, and bone loss. Risk factors include smoking, diabetes, and certain bacteria. The disease progresses slowly through periods of destruction and remission. Treatment involves plaque control, scaling and root planing to reduce bacteria and inflammation.
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 discusses aggressive periodontitis, a rare and severe form of periodontitis. It is characterized by early onset, rapid progression, and familial aggregation. There are two main types: localized aggressive periodontitis, which mainly affects first molars and incisors, and generalized aggressive periodontitis, which affects at least three teeth across the mouth. Risk factors include certain bacteria like Aggregatibacter actinomycetemcomitans, genetic factors, and immune system abnormalities. The document provides details on the clinical features, causes, and differences between the chronic and aggressive forms of periodontitis.
This document discusses various direct sequelae that can be caused by wearing removable dentures, including mucosal reactions, oral galvanic currents, altered taste perception, burning mouth syndrome, gagging, residual ridge reduction, periodontal disease of abutment teeth, and caries of abutment teeth. It focuses on denture stomatitis, providing classifications, causes, diagnostic methods, and management approaches. Predisposing factors, treatment with antifungals, and preventive measures are described. Other conditions addressed include flabby ridge, denture irritation hyperplasia, fibroepithelial polyp, traumatic ulcers, and burning mouth syndrome. Causes, diagnostic steps, and management of these conditions are
Chronic periodontitis is an infectious disease that results in inflammation of the tissues supporting the teeth and progressive bone and attachment loss. It is caused mainly by plaque and can be localized, affecting less than 30% of sites, or generalized, affecting more than 30% of sites. Risk factors include diabetes, smoking, poor oral hygiene, and a genetic predisposition. Symptoms include bleeding gums, loose teeth, and pain. Diagnosis is based on clinical signs of inflammation, pocket formation, attachment and bone loss seen during examination and on radiographs.
Chronic periodontitis is the most common form of periodontitis, characterized by a slowly progressive inflammation and destruction of the tissues surrounding the teeth. It is caused by an excessive host response to bacterial plaque accumulated at and below the gumline. Symptoms include bleeding gums, deepening pockets between teeth, and loose or mobile teeth. The disease progresses gradually over time as plaque accumulates. Risk factors include a prior history of periodontitis, poor plaque control, diabetes, smoking, stress, and certain genetic factors.
Chronic periodontitis is a slowly progressing infectious disease resulting in inflammation of the supporting tissues of the teeth and progressive bone and attachment loss. It is caused by bacterial plaque accumulation at the gumline. Key characteristics include site-specific or generalized bone and attachment loss, commensurate with plaque levels and modified by systemic and environmental risk factors like smoking and diabetes. The disease progresses in an episodic, intermittent manner with periods of rapid tissue destruction. Risk factors include prior history of periodontitis, specific pathogenic bacteria like P. gingivalis, local factors like calculus, and environmental factors like smoking which impair the host response.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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.
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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).
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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4. The Periodontal Disease Classification System of the
American Academy of Periodontology (AAP), 1999
I. Gingival Diseases
A. Dental plaque-induced gingival diseases
B. Non-plaque-induced gingival lesions
II. Chronic Periodontitis (slight: 1-2 mm CAL; moderate: 3-4 mm CAL;
severe: > 5 mm CAL)
A. Localized ( < 30% of sites are involved)
B. Generalized (> 30% of sites are involved)
III. Aggressive Periodontitis
A. Localized ( < 30% of sites are involved)
B. Generalized (> 30% of sites are involved)
IV. Periodontitis as a Manifestation of Systemic Diseases
A. Associated with hematological disorders
B. Associated with genetic disorders
C. Not otherwise specified
5. .
V. Necrotizing Periodontal Diseases
A. Necrotizing ulcerative gingivitis
B. Necrotizing ulcerative periodontitis
VI. Abscesses of the Periodontium
A. Gingival abscess
B. Periodontal abscess
C. Pericoronal abscess
VII. Periodontitis Associated With Endodontic Lesions
A. Combined periodontic-endodontic lesions
VIII. Developmental or Acquired Deformities and
Conditions
A. Localized tooth-related factors that modify or
predispose to plaque-induced gingival
diseases/periodontitis
B. Mucogingival deformities and conditions around
teeth
C .Mucogingival deformities and conditions on
edentulous ridges
D. Occlusal trauma
6. INTRODUCTION
Chronic periodontitis, formerly known as adult
periodontitis or chronic adult periodontitis, is the
most prevalent form of periodontitis.
It is generally considered to be a slowly
progressing disease.
Although chronic periodontitis is most frequently
observed in adults, it can occur in children and
adolescents in response to chronic plaque and
calculus accumulation.
7. DEFINITION
Chronic periodontitis has been defined
as “an infectious disease resulting in
inflammation with in supporting tissues
of the teeth, progressive attachment loss
and bone loss”.
8. Major clinical and etiologic
characteristics of the disease:
1. Microbial plaque formation.
2. Periodontal inflammation, and
3. Loss of attachment and alveolar bone.
9.
10. PREVALENCE
Effects both sexes equally.
Increases with age.
Age associated disease not age related and
occurs depending on disease duration.
11. CLINICAL FEATURES
Most prevalent in adults but can occur
in children and adolescents.(age‐35+yrs)
Supragingival and subgingival plaque
accumulation (frequently associated with
calculus)
Gingival inflammation
Pocket formation
Loss of periodontal attachment
Occasional suppuration
Poor oral hygiene – gingiva is typically
may be slightly to moderately swollen
12. .
Color- pale red to magenta
Consistency – soft or firm
Surface topography – loss of
stippling
Blunted or rolled gingival margin
Flattened or cratered papillae.
Tooth mobility.
Furcation involvement.
Spontaneous gingival bleeding.
Pocket depths are variable and
both suprabony and intrabony
pockets can be found.
13. Attachment loss with and without deep
periodontal pocket.
Pocket depths are variable, and both horizontal
and vertical bone loss can be found.
14. Furcation involvement in the molars
are common in advance cases of
chronic periodontitis.
Tooth mobility often appears in
advanced cases when bone loss has
been considerable.
15. SYMPTOMS
Bleeding gums during brushing or eating
Increasing spacing between teeth as a result of tooth movement
Loose teeth
Usually painless, but sometimes localized dull pain radiating deep
into the jaw
Sensitivity to heat, cold, or both due to exposed roots
Food impaction
Halitosis
Gingival tenderness or itching
16. TYPES
DISEASE DISTRIBUTION
Chronic periodontitis is considered to be as “site
specific disease”
Inflammation, pockets, attachment loss and bone
loss are due to direct site-specific effects of sub-
gingival plaque accumulation as a result of this
local effect, attachment loss and pockets may
occur.
It may occur on one surface of the tooth while the
other surface remain normal.
17. In addition to being site specific, chronic
periodontitis may be described as:
Localized:
Periodontitis is considered localized when <30% of the
sites assessed in oral cavity demonstrate attachment loss
and bone loss.
Generalized:
Periodontitis is considered generalized when >30% of
the sites assessed demonstrate attachment loss and bone
loss.
The pattern of bone loss in chronic periodontitis can be
vertical or horizontal.
21. MILD PERIODONTITIS
1 to 2 mm CAL
MODERATE PERIODONTITIS
3 to 4 mm CAL
SEVERE PERIODONTITIS
≥ 5 mm CAL
DISEASE SEVERITY
Severity can be categorized on the basis of the amount of Clinical
attachment loss (CAL) as follows:
25. DISEASE PROGRESSION
The rate of disease progression is usually slow but
may be modified by systemic and/or environmental
and behavioral factors.
Chronic periodontitis does not progress at an equal
rate in all affected sites throughout the mouth.
More rapidly progressive lesions occur:
1. Interproximal areas
2. Areas of greater plaque accumulation
3. Inaccessibility to plaque control measures
(e.g., furcation areas, overhanging margins, sites of
malposed teeth, or areas of food impaction)
26.
27. Clinical Diagnosis
Inflammation of the marginal gingiva
extent to the attached gingiva.
Clinical attachment loss.
Radiographs(in case of bone loss).
28. Widening of PDL space
Loss of corticated interdental crestal margin
Localised or generalized loss of alveolar supporting bone.
Blunting of the alveolar crest due to beginning of bone resorption
RADIOGRAPHIC
FEATURES
29. RADIOGRAPHIC
FEATURES
Pattern of bone loss may
be :
Vertical,
Horizontal,
Vertical bone loss is
usually associated with
intra bony pocket
formation.
Horizontal bone loss is
usually associated with
supra bony pockets.
30. RISK FACTORS FOR DISEASE
•Prior History of Periodontitis
•Local Factors
•Systemic Factors
•Environmental and Behavioral Factors
•Genetic Factors
Risk factor - is a characteristic, an aspect of behavior, or an environmental
exposure that is associated with destructive periodontitis
31. Prior History Of Periodontitis
Although not a true risk factor for disease but rather a
disease predictor, a prior history of periodontitis puts
patients at greater risk for developing further loss of
attachment and bone, given a challenge from bacterial
plaque accumulation.
Patient present with persistent gingivitis or
periodontitis with pocketing, attachment loss, and
bone loss ,may continue to lose periodontal support if
not successfully treated.
32. LOCAL FACTORS
Plaque and plaque retentive factors.
Microbiological Factors
Causative organisms of chronic periodontitis are:
• Porphyromonas gingivalis (P. gingivalis)
• Prevotella intermedia (P. intermedia)
• Treponema denticola
• Capnocytophaga
• A.actinomycetemcomitans (A.a)
• Eikenella corrodens (E. corrodens)
• Campylobacter rectus (C. rectus)
Viruses including cytomegalo , Epstein Barr, Papilloma and
herpes simplex have been proposed to play a role in the
etiology of periodontal diseases, possibly by changing the host
response to the local subgingival microbiota.
33. LOCAL FACTORS
Plaque Accumulation
Oral Hygiene
Tooth Malposition
Restoration
Preserve & Quantity of certain bacteria
Host defences
Subgingival Restoration
Environment
Calculus, smoking
Connective Tissue destruction
Genetic influence
Inflammation
Periodontopathic bacteria
Smoking, Calculus
Loss of Attachment
M
O
D
I
F
Y
I
N
G
F
A
C
T
O
R
S
36. SYSTEMIC FACTORS
Non Genetic
-Smoking is a major risk factor
- Diabetes
-Conditions associated with compromised immune
responses (e.g. HIV)
- Nutritional defects
-Osteoporosis
-Medications that cause drug induced gingival
overgrowth (e.g. some calcium channel blockers,
phenytoin, cyclosporine)
Genetic factors (as yet poorly defined)
37. SMOKING
• Undoubtedly one of the main and most prevalent,
risk factors for chronic periodontitis, risk
calculations suggesting 40% of the cases of chronic
periodontitis may be attributable to smoking.
• It has been estimated that there are 1.1 billlion are
smokers worldwide and 182 million (16.6%) of them
live in India.
41. AGE
Both the prevalence and severity of
periodontal disease increases with age.
Intake of medications,
Decreased immune function, and
Altered nutritional status interaction
42. NUTRITION
Vitamin C or ascorbic acid is essential for the
formation of collagen and intercellular material,
bone and teeth.
↓ phagocytic function of neutrophils and
macrophages
↓ antibody response
↓ cytotoxic T-cell activity
43. OSTEOPOROSIS
It is a disease characterized by low bone mass and deterioration of bone
structure that causes bone fragility and increases the risk of fracture.
Both osteoporosis and periodontal diseases are bone resorptive diseases
Osteoporosis could be a risk factor for the progression of chronic
periodontal disease.
A direct association between skeletal and periodontal disease as
measured by loss of interproximal alveolar bone in postmenopausal
women has been reported.
44. HIV
AIDS epidemics in US suggests HIV positive
patients especially those with AIDS and low
count of T Lymphocytes(CD4 <200 cells/ml)
were at increased risk of chronic periodontitis.
45. TREATMENT
1. NON SURGICAL THERAPY
Initial therapy ( scaling and root planing)
Antimicrobial therapy – as an adjunct to routine
periodontal therapy.
Improvement in oral hygiene.
Instruction, reinforcement, evaluation of plaque
control records.
Removal of all the factors contributing to plaque
accumulation, e.g. correction of ill-fitting
appliances, overcontoured crowns, overhanging
restorations, etc.
46. 2. SURGICAL THERAPY
A variety of surgical treatment modalities may be
appropriate in managing the patient.
1. Pocket elimination procedures.
2. Regenerative therapy:
A. Bone replacement grafts;
B. Guided tissue regeneration;
C. Combined regenerative techniques.
3. Resective therapy:
A. Flaps with or without osseous surgery;
B. Gingivectomy.
47. PROGNOSIS
Slight to moderate periodontitis, the prognosis is
usually good provided , the inflammation can be
controlled through good oral hygiene and the
removal of local plaque retentive factors.
In patients with more severe disease, as
evidenced by furcation involvements and
increasing mobility, or in patients who are
noncompliant with oral hygiene practices, the
prognosis may be downgraded from fair to poor.