1. The document discusses desquamative lesions of the gingiva, which describes red, painful, glazed gingiva that may be a manifestation of mucocutaneous conditions like lichen planus.
2. It provides a classification and overview of various diseases that can clinically present as desquamative gingivitis, including lichen planus, pemphigoid, and pemphigus vulgaris.
3. Diagnosis of desquamative gingivitis involves clinical examination, biopsy, microscopy, and immunofluorescence to arrive at a final diagnosis, as desquamative gingivitis is not a
The document summarizes the key phases and techniques involved in nonsurgical periodontal therapy (NSPT). It discusses the goals of NSPT to eliminate pathogens and halt disease progression. Techniques include scaling and root planing to remove calculus, contaminated cementum, and bacterial toxins. Studies found that aggressive root planing is not needed and that clinical improvements result from scaling alone or with root planing. The effects of NSPT on subgingival microflora and selection of instrumentation techniques are also summarized.
This document discusses dental splints, including their definition, rationale, requirements, classifications, indications, and contraindications. It notes that splints are used to immobilize and stabilize mobile or loose teeth. They help reduce tooth mobility, distribute forces evenly, preserve arch integrity, and provide psychological benefits. Splints are classified based on duration, materials used, and location. They are indicated when tooth mobility impairs function or comfort, while contraindications include poor oral hygiene or insufficient firm teeth for stabilization. The document reviews different splint designs and their advantages of stabilizing teeth, but also notes disadvantages like hindering oral hygiene.
This document discusses chemically modified tetracyclines (CMTs), a group of drugs developed from tetracyclines that lack antimicrobial properties but retain anti-collagenase activity. CMTs have several potential benefits, including inhibiting matrix metalloproteinases (MMPs), reducing proinflammatory mediators, inhibiting bone resorption, and scavenging reactive oxygen species. While CMTs show promise for treating conditions like periodontitis, they have not been fully approved for human use due concerns around excessive MMP suppression and other side effects.
This document provides an overview of periodontal dressings. It discusses the history of dressings from the early 20th century use of eugenol-containing dressings to the development of non-eugenol dressings. The ideal properties and types of dressings are described, including eugenol, non-eugenol, and those containing neither zinc oxide nor eugenol. Modifications to dressings through the addition of substances like chlorhexidine to improve antimicrobial activity are also summarized. The document concludes by stating that while dressings provide wound protection, mouthwashes are now preferred for their antimicrobial effects during healing.
This document discusses the effects of endogenous sex hormones on the periodontium. It begins by explaining that hormones play an important role in homeostasis of the periodontium and can influence periodontal conditions. It then examines the specific effects of androgens, estrogens, progesterone, and how these hormones may impact the periodontium during puberty and the menstrual cycle. The document concludes by stating that periodontal manifestations can occur when there is an imbalance in these sex hormones.
This document discusses root surface biomodification for periodontitis treatment. It begins with an introduction to root surface changes from periodontitis, including structural, chemical, and cytotoxic changes. It then discusses the historical background of root biomodification and defines important terms. The document outlines various methods of root biomodification, including mechanical, chemical, and physical approaches. It provides details on specific chemical agents used like citric acid and their proposed mechanisms of action in facilitating periodontal regeneration.
1. A periodontal splint is an appliance used to stabilize mobile teeth and promote healing. It prevents mobility during chewing and allows non-mobile teeth to heal faster.
2. Splints are classified based on the period of use, material type, and location on teeth. Common splints include direct bonding resins, intracoronal wires, and bite guards.
3. Principles of splinting include including healthy teeth, splinting around the arch, and ensuring proper plaque control and occlusion. Splints distribute forces and are indicated to stabilize mobility and trauma, but can hamper hygiene and unevenly distribute forces if not fabricated properly.
Host modulation therapy aims to reduce tissue destruction and stabilize the periodontium by modifying the host response. The document discusses several targets of host modulation therapy including:
1. Modulation of arachidonic acid metabolites like NSAIDs, selective COX-2 inhibitors, lipoxins, and omega-3 fatty acids.
2. Modulation of bone remodeling using bisphosphonates and osteoprotegerin which inhibit osteoclast activity and bone resorption.
3. Modulation of matrix metalloproteinases using tetracyclines, chemically modified tetracyclines, and endogenous inhibitors like TIMPs.
The document provides details on the rationale, history, targets,
The document summarizes the key phases and techniques involved in nonsurgical periodontal therapy (NSPT). It discusses the goals of NSPT to eliminate pathogens and halt disease progression. Techniques include scaling and root planing to remove calculus, contaminated cementum, and bacterial toxins. Studies found that aggressive root planing is not needed and that clinical improvements result from scaling alone or with root planing. The effects of NSPT on subgingival microflora and selection of instrumentation techniques are also summarized.
This document discusses dental splints, including their definition, rationale, requirements, classifications, indications, and contraindications. It notes that splints are used to immobilize and stabilize mobile or loose teeth. They help reduce tooth mobility, distribute forces evenly, preserve arch integrity, and provide psychological benefits. Splints are classified based on duration, materials used, and location. They are indicated when tooth mobility impairs function or comfort, while contraindications include poor oral hygiene or insufficient firm teeth for stabilization. The document reviews different splint designs and their advantages of stabilizing teeth, but also notes disadvantages like hindering oral hygiene.
This document discusses chemically modified tetracyclines (CMTs), a group of drugs developed from tetracyclines that lack antimicrobial properties but retain anti-collagenase activity. CMTs have several potential benefits, including inhibiting matrix metalloproteinases (MMPs), reducing proinflammatory mediators, inhibiting bone resorption, and scavenging reactive oxygen species. While CMTs show promise for treating conditions like periodontitis, they have not been fully approved for human use due concerns around excessive MMP suppression and other side effects.
This document provides an overview of periodontal dressings. It discusses the history of dressings from the early 20th century use of eugenol-containing dressings to the development of non-eugenol dressings. The ideal properties and types of dressings are described, including eugenol, non-eugenol, and those containing neither zinc oxide nor eugenol. Modifications to dressings through the addition of substances like chlorhexidine to improve antimicrobial activity are also summarized. The document concludes by stating that while dressings provide wound protection, mouthwashes are now preferred for their antimicrobial effects during healing.
This document discusses the effects of endogenous sex hormones on the periodontium. It begins by explaining that hormones play an important role in homeostasis of the periodontium and can influence periodontal conditions. It then examines the specific effects of androgens, estrogens, progesterone, and how these hormones may impact the periodontium during puberty and the menstrual cycle. The document concludes by stating that periodontal manifestations can occur when there is an imbalance in these sex hormones.
This document discusses root surface biomodification for periodontitis treatment. It begins with an introduction to root surface changes from periodontitis, including structural, chemical, and cytotoxic changes. It then discusses the historical background of root biomodification and defines important terms. The document outlines various methods of root biomodification, including mechanical, chemical, and physical approaches. It provides details on specific chemical agents used like citric acid and their proposed mechanisms of action in facilitating periodontal regeneration.
1. A periodontal splint is an appliance used to stabilize mobile teeth and promote healing. It prevents mobility during chewing and allows non-mobile teeth to heal faster.
2. Splints are classified based on the period of use, material type, and location on teeth. Common splints include direct bonding resins, intracoronal wires, and bite guards.
3. Principles of splinting include including healthy teeth, splinting around the arch, and ensuring proper plaque control and occlusion. Splints distribute forces and are indicated to stabilize mobility and trauma, but can hamper hygiene and unevenly distribute forces if not fabricated properly.
Host modulation therapy aims to reduce tissue destruction and stabilize the periodontium by modifying the host response. The document discusses several targets of host modulation therapy including:
1. Modulation of arachidonic acid metabolites like NSAIDs, selective COX-2 inhibitors, lipoxins, and omega-3 fatty acids.
2. Modulation of bone remodeling using bisphosphonates and osteoprotegerin which inhibit osteoclast activity and bone resorption.
3. Modulation of matrix metalloproteinases using tetracyclines, chemically modified tetracyclines, and endogenous inhibitors like TIMPs.
The document provides details on the rationale, history, targets,
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.
This document summarizes the effects of hormones on periodontal tissues throughout a woman's life. During puberty, increased sex hormones lead to higher levels of gram-negative bacteria and gingivitis. In pregnancy, hormones cause gingival enlargement and increased inflammation. Menopause brings thinning tissues, dry mouth, bone loss and increased risk of periodontal disease. Oral contraceptives also increase gingival inflammation through hormonal effects. Proper oral hygiene and treatment are important for managing periodontal health at all stages of a woman's life.
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.
The document discusses factors responsible for failures in periodontal therapy. It identifies failures that can occur during the pre-therapeutic, therapeutic, and post-therapeutic phases of treatment. Pre-therapeutic failures include incorrect patient selection, incomplete diagnosis, and improper prognosis. Therapeutic failures involve issues with nonsurgical treatments like scaling and root planing as well as surgical procedures. Post-therapeutic failures relate to inadequate maintenance by the patient after treatment. Both dentist and patient-related factors can contribute to failures at each treatment phase.
This document defines and outlines common iatrogenic (treatment-caused) factors that can contribute to periodontal disease. It discusses 10 main factors: overhanging or subgingival restoration margins, poor restoration contours, materials and procedures, partial denture design, malocclusion, orthodontic therapy, impacted tooth extractions, habits like toothbrushing, chemical injuries, radiation therapy, and laser use complications. Each factor is described in terms of how it can disrupt plaque control and the periodontal environment, leading to issues like gingivitis, recession, and bone loss. Prevention methods are also outlined.
Periodontitis is caused by bacterial infection of the gums that triggers an inflammatory host response. Bacteria form biofilms in the gingival crevice. This elicits production of inflammatory molecules like IL-1β and TNF-α by immune cells. In susceptible individuals, inflammation is excessive and causes tissue destruction and bone loss. As bone loss progresses, periodontal pockets deepen, increasing pathogen load and further inflammation.
Supportive periodontal therapy (SPT) involves long-term maintenance programs following active periodontal treatment to maintain periodontal health. SPT involves periodic examination, motivation and instrumentation of sites showing inflammation, treatment of reinfected sites, and polishing. It begins after active treatment and is aimed at preventing recurrence through early detection of disease. The frequency of SPT visits depends on the patient's periodontal risk assessment but generally occurs every 3-4 months. It can be performed by general dentists or specialists depending on the extent of original periodontal destruction. Adjunctive use of antimicrobials may also be included in SPT.
This document discusses the role of viruses in periodontal diseases. It begins by introducing viruses and their structure. It then discusses several important virus families and examples of viruses that can cause oral infections, including herpesviruses like HSV-1, EBV, CMV; papillomaviruses; and picornaviruses. The document reviews the prevalence of herpesviruses detected in samples from patients with gingivitis, aggressive periodontitis, chronic periodontitis, and provides theories on how viruses like CMV may contribute to the pathogenesis of diseases like localized juvenile periodontitis.
The document discusses the role of occlusion in periodontal disease. It defines occlusion and classifies occlusion types. It explores the biological basis of occlusal function and the relationship between occlusal disharmony and periodontal disease. Occlusal trauma from hyperfunction, hypofunction, and parafunctions like bruxism can impact periodontal tissues. The document outlines methods for clinical diagnosis and developing treatment plans involving occlusal therapy, adjustment, and splinting to address occlusal factors and support periodontal treatment.
Surgical v/s Non surgical periodontal therapy Achi Joshi
Both surgical and nonsurgical therapy produced improvement in the periodontal health.
Treatment approach was based on the comfort level of the practitioner.
In the late 60’s and continuing into the 70’s and 80’s, many series of longitudinal studies were conducted, aimed to document the immediate and most importantly long term clinical results following several types of periodontal therapy.
This document provides an overview of desquamative gingivitis (DG), a clinical sign characterized by redness and scaling of the gingiva. It discusses the various diseases that can present as DG, including lichen planus, pemphigus, pemphigoid, linear IgA disease, and lupus erythematosus. It outlines the diagnostic process and significance of DG, noting that the associated disorders can impact oral health and require systemic treatment with corticosteroids or immunosuppressants, increasing risk of complications. Proper diagnosis of the underlying condition is important for effective management of DG lesions and systemic disease.
Scaling and root planing (SRP) is a non-surgical treatment for periodontitis that aims to remove dental plaque and calculus from tooth surfaces. It involves scaling to remove deposits and root planing to smooth root surfaces. The goals are to eliminate periodontitis by removing irritants and restoring a healthy environment for tissue healing. The long-term effectiveness depends on factors like patient compliance, disease severity, and anatomical challenges. Overhanging restorations can interfere with cleaning and disturb the ecological balance, allowing disease-causing bacteria to proliferate.
This document discusses periodontal vaccines and their potential role in preventing periodontal disease. It provides background on periodontal disease, outlines key periodontal pathogens like Porphyromonas gingivalis and Actinomyces actinomycetemcomitans, and summarizes different vaccine approaches - including active immunization using whole cells/subunits/peptides, passive immunization using monoclonal antibodies or plantibodies, and genetic immunization using plasmid or viral vectors. While animal studies show promise, translating vaccine efficacy to humans and clinical use remains challenging due to the complex multifactorial nature of periodontal disease. Future research opportunities include multispecies vaccines targeting multiple pathogens and genomic approaches.
The document discusses furcation involvement and its management. It begins with an introduction that defines furcation and notes that its presence indicates advanced periodontitis with poor prognosis. It then covers etiology, diagnosis, classification, anatomy, and other factors related to furcation involvement. For treatment, it discusses non-surgical options like scaling and root planing for early defects. For more advanced defects, surgical therapies like furcation plasty, tunnel preparation, root resection, and extraction may be used. The prognosis depends on the degree of furcation involvement and response to treatment.
This document discusses the anatomy, measurement, and clinical significance of the attached gingiva. It notes that the attached gingiva extends from the base of the gingival sulcus to the mucogingival junction. The normal width is 3-4.5mm in the maxillary anterior region but narrower in other areas. Inadequate width can facilitate subgingival plaque formation. Methods to measure width and increase width through surgery are described. The importance of keratinized, attached tissue for resisting mechanical irritation and stabilizing the gingival margin is emphasized.
Certains medications have been associated with gingival enlargement.
the seminar gives a complete analysis of etilogy and pathogenesis involved in digo as well as sequlae of it
Full Mouth Disinfection (FMD) is a treatment approach that involves scaling and root planing of all teeth in one or two visits to eliminate periodontal pathogens. The goals of FMD are to prevent reinfection of treated sites by untreated sites or other oral niches harboring pathogens. FMD originally included scaling, root planing, chlorhexidine treatment, and prolonged chlorhexidine use. Over time, variations have been developed including replacing chlorhexidine, supplementing with antibiotics or probiotics, and combining with photodynamic therapy. FMD aims to provide more effective periodontal treatment than the standard approach of scaling and root planing in quadrants over multiple visits.
The document discusses the Cumulative Interceptive Supportive Therapy (CIST) protocol for treating peri-implant mucositis and peri-implantitis. The CIST protocol is a 4-step approach using increasing levels of antibacterial treatment and potentially regenerative surgery. Step A involves plaque removal and patient education. Step B adds local antiseptics. Step C adds systemic or local antibiotics. Step D uses regenerative treatments like bone grafting or resective treatments like defect osteoplasty if previous steps fail to resolve bone loss. The document also mentions promising results using laser-assisted peri-implantitis treatment to remove pathogens.
This document discusses gingival pigmentation from a historical, physiological, and clinical perspective. It begins by covering the historical descriptions of pigmentation in various populations dating back to the early 1900s. It then describes the structure and function of melanocytes and melanin, as well as the genetic, hormonal, and environmental factors that regulate melanin synthesis. The document classifies different types of pigmentation and pigmented lesions that can occur in the oral mucosa. Finally, it reviews various surgical and non-surgical methods that can be used to depigmentate abnormal gingival pigmentation.
Oral mucosal lesions in denture wearersAamir Godil
The document discusses oral mucosal lesions that can occur in denture wearers. It describes several types of denture-related mucosal lesions (DMLs) such as traumatic ulcers, denture-induced stomatitis, and denture hyperplasia. It also discusses non-denture related lesions including fissured tongue and lichen planus. A statistical analysis found the most common DMLs were traumatic ulcers and denture stomatitis. Complete denture wearers had higher rates of DMLs while partial denture wearers saw more stomatitis. The document provides details on clinical presentation and management of several specific oral lesions.
Case history is one of the most important step before planning and starting patient's treatment. It gives an overall picture of the patient's current and past dental status and his attitude towards treatment outcomes. It also gives the clinician the idea about the affordibility of the patient for the treatment so that alternate treatment options can be provided. It creates a initial good rapport between the clinician and the patient.
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.
This document summarizes the effects of hormones on periodontal tissues throughout a woman's life. During puberty, increased sex hormones lead to higher levels of gram-negative bacteria and gingivitis. In pregnancy, hormones cause gingival enlargement and increased inflammation. Menopause brings thinning tissues, dry mouth, bone loss and increased risk of periodontal disease. Oral contraceptives also increase gingival inflammation through hormonal effects. Proper oral hygiene and treatment are important for managing periodontal health at all stages of a woman's life.
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.
The document discusses factors responsible for failures in periodontal therapy. It identifies failures that can occur during the pre-therapeutic, therapeutic, and post-therapeutic phases of treatment. Pre-therapeutic failures include incorrect patient selection, incomplete diagnosis, and improper prognosis. Therapeutic failures involve issues with nonsurgical treatments like scaling and root planing as well as surgical procedures. Post-therapeutic failures relate to inadequate maintenance by the patient after treatment. Both dentist and patient-related factors can contribute to failures at each treatment phase.
This document defines and outlines common iatrogenic (treatment-caused) factors that can contribute to periodontal disease. It discusses 10 main factors: overhanging or subgingival restoration margins, poor restoration contours, materials and procedures, partial denture design, malocclusion, orthodontic therapy, impacted tooth extractions, habits like toothbrushing, chemical injuries, radiation therapy, and laser use complications. Each factor is described in terms of how it can disrupt plaque control and the periodontal environment, leading to issues like gingivitis, recession, and bone loss. Prevention methods are also outlined.
Periodontitis is caused by bacterial infection of the gums that triggers an inflammatory host response. Bacteria form biofilms in the gingival crevice. This elicits production of inflammatory molecules like IL-1β and TNF-α by immune cells. In susceptible individuals, inflammation is excessive and causes tissue destruction and bone loss. As bone loss progresses, periodontal pockets deepen, increasing pathogen load and further inflammation.
Supportive periodontal therapy (SPT) involves long-term maintenance programs following active periodontal treatment to maintain periodontal health. SPT involves periodic examination, motivation and instrumentation of sites showing inflammation, treatment of reinfected sites, and polishing. It begins after active treatment and is aimed at preventing recurrence through early detection of disease. The frequency of SPT visits depends on the patient's periodontal risk assessment but generally occurs every 3-4 months. It can be performed by general dentists or specialists depending on the extent of original periodontal destruction. Adjunctive use of antimicrobials may also be included in SPT.
This document discusses the role of viruses in periodontal diseases. It begins by introducing viruses and their structure. It then discusses several important virus families and examples of viruses that can cause oral infections, including herpesviruses like HSV-1, EBV, CMV; papillomaviruses; and picornaviruses. The document reviews the prevalence of herpesviruses detected in samples from patients with gingivitis, aggressive periodontitis, chronic periodontitis, and provides theories on how viruses like CMV may contribute to the pathogenesis of diseases like localized juvenile periodontitis.
The document discusses the role of occlusion in periodontal disease. It defines occlusion and classifies occlusion types. It explores the biological basis of occlusal function and the relationship between occlusal disharmony and periodontal disease. Occlusal trauma from hyperfunction, hypofunction, and parafunctions like bruxism can impact periodontal tissues. The document outlines methods for clinical diagnosis and developing treatment plans involving occlusal therapy, adjustment, and splinting to address occlusal factors and support periodontal treatment.
Surgical v/s Non surgical periodontal therapy Achi Joshi
Both surgical and nonsurgical therapy produced improvement in the periodontal health.
Treatment approach was based on the comfort level of the practitioner.
In the late 60’s and continuing into the 70’s and 80’s, many series of longitudinal studies were conducted, aimed to document the immediate and most importantly long term clinical results following several types of periodontal therapy.
This document provides an overview of desquamative gingivitis (DG), a clinical sign characterized by redness and scaling of the gingiva. It discusses the various diseases that can present as DG, including lichen planus, pemphigus, pemphigoid, linear IgA disease, and lupus erythematosus. It outlines the diagnostic process and significance of DG, noting that the associated disorders can impact oral health and require systemic treatment with corticosteroids or immunosuppressants, increasing risk of complications. Proper diagnosis of the underlying condition is important for effective management of DG lesions and systemic disease.
Scaling and root planing (SRP) is a non-surgical treatment for periodontitis that aims to remove dental plaque and calculus from tooth surfaces. It involves scaling to remove deposits and root planing to smooth root surfaces. The goals are to eliminate periodontitis by removing irritants and restoring a healthy environment for tissue healing. The long-term effectiveness depends on factors like patient compliance, disease severity, and anatomical challenges. Overhanging restorations can interfere with cleaning and disturb the ecological balance, allowing disease-causing bacteria to proliferate.
This document discusses periodontal vaccines and their potential role in preventing periodontal disease. It provides background on periodontal disease, outlines key periodontal pathogens like Porphyromonas gingivalis and Actinomyces actinomycetemcomitans, and summarizes different vaccine approaches - including active immunization using whole cells/subunits/peptides, passive immunization using monoclonal antibodies or plantibodies, and genetic immunization using plasmid or viral vectors. While animal studies show promise, translating vaccine efficacy to humans and clinical use remains challenging due to the complex multifactorial nature of periodontal disease. Future research opportunities include multispecies vaccines targeting multiple pathogens and genomic approaches.
The document discusses furcation involvement and its management. It begins with an introduction that defines furcation and notes that its presence indicates advanced periodontitis with poor prognosis. It then covers etiology, diagnosis, classification, anatomy, and other factors related to furcation involvement. For treatment, it discusses non-surgical options like scaling and root planing for early defects. For more advanced defects, surgical therapies like furcation plasty, tunnel preparation, root resection, and extraction may be used. The prognosis depends on the degree of furcation involvement and response to treatment.
This document discusses the anatomy, measurement, and clinical significance of the attached gingiva. It notes that the attached gingiva extends from the base of the gingival sulcus to the mucogingival junction. The normal width is 3-4.5mm in the maxillary anterior region but narrower in other areas. Inadequate width can facilitate subgingival plaque formation. Methods to measure width and increase width through surgery are described. The importance of keratinized, attached tissue for resisting mechanical irritation and stabilizing the gingival margin is emphasized.
Certains medications have been associated with gingival enlargement.
the seminar gives a complete analysis of etilogy and pathogenesis involved in digo as well as sequlae of it
Full Mouth Disinfection (FMD) is a treatment approach that involves scaling and root planing of all teeth in one or two visits to eliminate periodontal pathogens. The goals of FMD are to prevent reinfection of treated sites by untreated sites or other oral niches harboring pathogens. FMD originally included scaling, root planing, chlorhexidine treatment, and prolonged chlorhexidine use. Over time, variations have been developed including replacing chlorhexidine, supplementing with antibiotics or probiotics, and combining with photodynamic therapy. FMD aims to provide more effective periodontal treatment than the standard approach of scaling and root planing in quadrants over multiple visits.
The document discusses the Cumulative Interceptive Supportive Therapy (CIST) protocol for treating peri-implant mucositis and peri-implantitis. The CIST protocol is a 4-step approach using increasing levels of antibacterial treatment and potentially regenerative surgery. Step A involves plaque removal and patient education. Step B adds local antiseptics. Step C adds systemic or local antibiotics. Step D uses regenerative treatments like bone grafting or resective treatments like defect osteoplasty if previous steps fail to resolve bone loss. The document also mentions promising results using laser-assisted peri-implantitis treatment to remove pathogens.
This document discusses gingival pigmentation from a historical, physiological, and clinical perspective. It begins by covering the historical descriptions of pigmentation in various populations dating back to the early 1900s. It then describes the structure and function of melanocytes and melanin, as well as the genetic, hormonal, and environmental factors that regulate melanin synthesis. The document classifies different types of pigmentation and pigmented lesions that can occur in the oral mucosa. Finally, it reviews various surgical and non-surgical methods that can be used to depigmentate abnormal gingival pigmentation.
Oral mucosal lesions in denture wearersAamir Godil
The document discusses oral mucosal lesions that can occur in denture wearers. It describes several types of denture-related mucosal lesions (DMLs) such as traumatic ulcers, denture-induced stomatitis, and denture hyperplasia. It also discusses non-denture related lesions including fissured tongue and lichen planus. A statistical analysis found the most common DMLs were traumatic ulcers and denture stomatitis. Complete denture wearers had higher rates of DMLs while partial denture wearers saw more stomatitis. The document provides details on clinical presentation and management of several specific oral lesions.
Case history is one of the most important step before planning and starting patient's treatment. It gives an overall picture of the patient's current and past dental status and his attitude towards treatment outcomes. It also gives the clinician the idea about the affordibility of the patient for the treatment so that alternate treatment options can be provided. It creates a initial good rapport between the clinician and the patient.
Lichen planus is a chronic inflammatory skin and mucous membrane disease characterized by violaceous papules that may form plaques. Oral lichen planus commonly presents as striae - sharply defined white lacy patterns - but can also be erosive, atrophic, or bullous. CD8 T cells trigger apoptosis of oral epithelial cells. Treatment aims to reduce symptoms, resolve lesions, and prevent oral squamous cell carcinoma through topical corticosteroids, systemic medications, surgery or laser, with complications including infection and malignant transformation requiring careful long-term follow-up.
Necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitisyeahlifehai
This document provides an overview of necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP). It discusses the history and epidemiology of these conditions, describing outbreaks among military troops. Clinically, NUG presents as ulcerated and necrotic gingival tissue with characteristic punched out lesions. Untreated, it can progress to involve the underlying bone as NUP. Predisposing factors include poor oral hygiene, preexisting gingivitis, smoking, nutritional deficiencies, systemic illnesses, fatigue, stress and immunodeficiencies. Microorganisms play a role in conjunction with an impaired host response.
Leukoplakia can be defined as a “white patch” or “plaque” in the oral cavity, which cannot be scrapped off and which cannot be characterized clinically or pathologically as any other disease.
This excludes lesions such as lichen planus, candidiasis, leukoedema, white spongy nevus, and obvious frictional keratosis.
The term leukoplakia should be used to recognise white plaques of questionable risk having excluded (other) known diseases or disorders that carry no risk for cancer-WHO 2005.
This PowerPoint presentation demonstrate a useful review of Oral candidiosis, including its different types, clinical presentations, differential diagnosis, and treatment options.
Trench mouth, sometimes called acute necrotizing ulcerative gingivitis (ANUG), is a severe gum infection that spreads quickly. It is typified by the abrupt onset of significant bleeding, ulceration, and gum discomfort; these symptoms are frequently accompanied by a very bad breath odor. ANUG is frequently linked to immunosuppression, smoking, stress, and poor dental hygiene. Young individuals are usually affected by the illness, which if neglected can result in severe tissue loss. It is crucial to have prompt dental care, such as expert cleaning and antibiotic treatments, in order to control ANUG and stop subsequent issues.
Chronic periodontitis is a slowly progressive infectious disease that results in inflammation of the supporting tissues of the teeth and bone loss. It is caused by an extension of gingival inflammation into deeper periodontal tissues due to plaque accumulation. Key characteristics include a localized or generalized onset at any age, usually in adults, with periods of rapid progression possible. Treatment involves non-surgical procedures like scaling, root planing, and curettage as well as surgical procedures like pocket reduction surgery to correct anatomical defects. Prognosis depends on factors like patient compliance, systemic involvement, disease severity, and status of remaining teeth.
This document provides information on oral lichen planus (OLP), including its definition, epidemiology, etiology, clinical presentations, management, and treatment. OLP is a common chronic inflammatory mucocutaneous disorder that typically affects the oral mucosa. Clinically, it presents as reticular, papular, plaque-like, atrophic, or erosive lesions. Management involves observation, stopping smoking, topical corticosteroids, immunosuppressants, and maintaining good oral hygiene. While there is no cure for OLP, treatment aims to reduce symptoms and potentially lower cancer risk.
Chronic periodontitis is characterized by inflammation within the supporting tissues of the teeth and progressive bone and attachment loss. It is caused by an extension of gingival inflammation into deeper periodontal tissues due to plaque accumulation. Key features include bleeding gums, deepening pockets between teeth and gums, and recession or loss of bone. Treatment involves nonsurgical procedures like scaling and root planing to remove plaque and tartar, as well as potential surgical procedures to reduce deep pockets and regenerate lost bone if nonsurgical methods are not fully effective. Prognosis depends on factors like severity, systemic involvement, remaining teeth and compliance with treatment and maintenance.
Periodontal therapy involves the diagnosis and treatment of plaque-associated diseases as well as non-plaque related conditions like desquamative gingivitis. Desquamative gingivitis presents as erythema, desquamation, and ulceration of the gingiva and can be caused by conditions like lichen planus, pemphigoid, and pemphigus vulgaris. The pathogenesis involves autoimmune responses against epithelial antigens that disrupt cellular junctions and cause separation of the epithelium from the underlying connective tissue. Management consists of treating the underlying cause, improving oral hygiene, and using topical or systemic corticosteroids.
Hereditary white lesions include leukoedema, white sponge nevus, hereditary benign intraepithelial dyskeratosis, and dyskeratosis congenita. Reactive and inflammatory white lesions include linea alba, frictional keratosis caused by mechanical irritation such as dentures, and traumatic keratosis that resolves upon removal of the irritant.
Oral inflammatory lesions include aphthous ulcers, herpes simplex virus infections, and oral candidiasis. Aphthous ulcers are painful but self-limiting, while herpes simplex virus causes vesicles that rupture and heal without scarring. Oral candidiasis occurs when the oral microbiota is altered. Proliferative lesions like fibromas and pyogenic granulomas are reactive lesions of the oral mucosa. Leukoplakia and erythroplakia are pre-neoplastic lesions, with erythroplakia carrying a greater risk of malignant transformation. Oral squamous cell carcinoma is the most common oral cancer, often associated with tobacco and alcohol
This document outlines the components and process of taking a thorough case history for a dental patient. It discusses gathering information on the chief complaint, medical history, examination of extraoral and intraoral soft tissues and hard tissues, diagnosing swellings or ulcers, developing provisional and differential diagnoses, ordering relevant investigations like radiographs or biopsies, reaching a final diagnosis, and citing references. The case history is a planned conversation to understand a patient's symptoms and concerns to determine their illness and mental state.
Chronic Periodontitis- the malaise of populationAshokKp4
Chronic periodontitis is an infectious disease that results in inflammation of the supporting tissues of the teeth and progressive bone and attachment loss. It is caused by an extension of gingival inflammation into deeper periodontal tissues due to plaque accumulation. It is characterized by localized or generalized pockets, bleeding, attachment loss, and bone loss. The extent and severity can range from slight to severe. Treatment involves non-surgical procedures like scaling and root planing as well as surgical procedures depending on the severity. Prognosis depends on factors like patient compliance, systemic involvement, severity of the condition, and status of individual teeth.
Allergic and Immunologic Diseases of the Oral Cavity.pptxDr.Shubham Patel
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This document discusses several controversies in periodontics. It addresses debates around the classification of periodontal diseases, factors involved in periodontal pathogenesis like invasiveness of bacteria and the role of the periodontal epithelium. It also examines controversies in diagnosing periodontal diseases and determining an accurate prognosis. Additionally, it looks at debates around treatments like gingival curettage, tooth mobility and splinting, one stage full-mouth disinfection versus quadrant SRP, and whether results are comparable between non-surgical and surgical periodontal therapy. The document acknowledges that while knowledge has improved, some controversies remain due to limitations in present diagnostic methods and incomplete understanding of periodontal pathology.
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1. Inducible nitric oxide synthase (iNOS) is involved in inflammatory processes by synthesizing nitric oxide (NO) in response to stimuli like cytokines.
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B-cells play a central role in the humoral immune response by differentiating into antibody-secreting plasma cells upon activation. They can be activated through T-cell dependent or independent pathways to produce high or low affinity antibodies, respectively. In periodontal diseases, B-cells are involved in the host immune response against the bacterial biofilm and help control infection through antibody production. Their fate in periodontal diseases includes differentiation into plasma cells or memory B-cells to provide long-lasting immunity. B-cells also participate in periodontal bone resorption through antibody-mediated mechanisms.
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3. Linear IgA disease
Dermatitis herpetiformis
Lupus erythematous
Erythema multiforme
7. Drug eruptions
8. Conditions mimicking desquamative gingivitis
9. Conclusion
10. Reference
4. Introduction
Desquamative gingivitis is a clinical term to describe red, painful,
glazed and friable gingivae which may be a manifestation of some
mucocutaneous conditions such as lichen planus or the
vesiculobullous disorders.
The systemic involvement of desquamative gingivitis with oral and
extra-oral manifestations can cause high morbidity and occasionally
lethal complications.
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders– a review.
Aust dent j 2003;48:206-2011.
5. History
Coined in 1932 - Prinz to describe a peculiar condition characterized
by intense erythema, desquamation, and ulceration of the free and
attached gingiva.
McCarthy and colleagues (1960) concluded that desquamative
gingivitis was not a specific disease entity but a gingival response
associated with a variety of conditions.
Glickman and Smulow, 1964- DG is not a definitive diagnosis due to
it is a clinical association with several disorders.
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative Gingivitis:
Review of the Literature and Clinical Guide for Dental Undergraduates. J int oral health 2015;7:88-92.
6. Classification
1) Dermatoses
a) Cicatricial pemphigoid
b) Pemphigus
c) Lichen Planus
d) Erythema Multiforme
e) Lupus Erythematosis
f) Linear IgA disease
2) Hormonal influence
a) Estrogen deficiency following oophorectomy & post
menopausal women
b) Testosterone imbalance
c) Hypothyroidism
7. 3) Abnormal response to irritation
4) Chronic infection
a) Tuberculosis
b) Chronic candidiasis
c) Histoplasmosis
5) Aging
6) Idiopathic
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative
Gingivitis: Review of the Literature and Clinical Guide for Dental Undergraduates. J int oral
health 2015;7:88-92.
8. Chronic desquamative gingivitis
Widespread desquamation and/or erosion of the buccal side of
attached gingiva of anterior teeth.
Can be confined to a limited multiple areas.
These lesions can be more extensive gingival lesions with oral/and
or extra-oral involvement, in the primary phases or in disease
recurrence.
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative Gingivitis:
Review of the Literature and Clinical Guide for Dental Undergraduates. J int oral health 2015;7:88-92.
9. • Long standing disease of indefinite duration with periods of
remission and exacerbation, which may terminate spontaneously
after months or years of involvement.
• Varies in appearance in different areas of the mouth and at different
times in the same patient.
Glickman I, Smulow JB. Chronic Desquamative Gingivitis - Its Nature and Treatment. In:
Clinical Periodontology.1:W. B. Saunders Company;1964:397-405.
10. Epidemiology:
Peak incidence – fourth and fifth decade.
Female predilection- 80%.
Approximately, 50% of the lesions are localized to gingiva,
although in some cases intraoral as well as extraoral sites may be
involved.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
11. According to Nisengard et al (1981, 1987) :
Approx. 75% of
desquamative
lesions are
dermatological
diseases.
95%- cicatricial
pemphigoid and
lichen planus.
25%- either
idiopathic or
associated with an
endocrine
imbalance, aging,
chronic infection or
abnormal response
to bacterial plaque.
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders– a review.
Aust dent j 2003;48:206-2011.
12. Clinical features-
Mild form :
Diffuse erythema.
Condition is painless
Age: 17 – 23 years
Common in females.
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders– a review.
Aust dent j 2003;48:206-2011.
13. Moderate form:
Patchy distribution of bright red and gray areas.
Surface is smooth and shiny and soft in consistency.
Slight pitting on pressure.
Nicolsky’s sign +ve
Remainder of the mucosa is also extremely smooth ad shiny.
Age: 30 – 40 years.
C/o of burning sensation and sensitivity to thermal changes.
14. Severe form:
• Scattered, irregularly shaped areas -striking red appearance.
• grayish blue areas giving an overall speckled appearance.
• Surface epithelium - shredded and friable and can be peeled
off in small patches.
• Areas of involvement seem to shift to different locations on
the gingiva.
• Patient cannot tolerate coarse food, condiments or
temperature changes.
• Constant dry and burning sensation throughout the oral
cavity,
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders– a review.
Aust dent j 2003;48:206-2011.
15. Diagnosis
Desquamative gingivitis is only a clinical term and not a diagnosis
per se.
Once the presence of this condition is determined, a series of
investigations are used to arrive at final diagnosis.
Clinical examination
Biopsy
Microscopic Examination
Immunofluorescence
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative
Gingivitis: Review of the Literature and Clinical Guide for Dental Undergraduates. J int oral
health 2015;7:88-92.
16. Management
Depends on:
1) Practitioner's experience,
2) Systemic impact of the disease, and
3) Systemic complications of the medications.
Once oral treatment is provided, periodic evaluation is needed to
monitor the response of the patient.
Initially, evaluation is done at 2 to 4 weeks after beginning of the
treatment
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
17. Diseases clinically presenting as Desquamative
gingivitis
1. Lichen planus
• Characterized by the presence of cutaneous violaceous papules
that may coalesce to form plaques.
• Immunologically mediated muco-cutaneous disorder- T cells
play a central role.
Surface covered by characteristic, very fine grayish white lines
called Wickham’s striae.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
18. White papules and striae on tongue
White striations on lower lip
Neville BW, Damm DD. Dermatological disease. In: Colour Atlas of Clinical Oral
Pathology.2:BC Decker;2003: 425-466.
19. Skin lesions - flexor surfaces of wrist and forearms.
ORAL MANIFESTATIONS:-
• Radiating white or gray, velvety, thread-like papules in a
linear, annular or retiform arrangement forming typical lacy,
reticular patches, rings and streaks over the buccal mucosa,
lips, tongue and palate.
• Vesicle and bulla formation.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
21. A triad of lichen planus, diabetes mellitus and vascular
hypertension-GRINSPAN SYNDROME
Immunologically mediated - host T lymphocytes play a
central role.
0.1 - 4% of the population
Female : Male – 2:1
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
22. Forms of lichen planus :-
• Bullous :- Raised fluid filled blisters
• Erosive form- when bullae rupture; eroded or frankly ulcerated
lesions –irregular in size and shape and appear as raw, painful areas.;
characteristic radiating striae noted on the periphery of lesions.
• Atrophic form – smooth, red, poorly defined areas, often but not
always with peripheral striae present.
• Hypertrophic form- well –circumscribed, elevated white lesion
resembling leukoplakia
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
24. Histological features
• Hyper parakeratosis or hyper orthokeratosis
• Thickening of the granular layer
• Acanthosis with intercellular edema of the spinous cells
• Saw tooth appearance of rete pegs.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
25.
26. Pullon et al (1969)
• Irregularity of
nuclear membrane
• Increased
thickening and
granularity of
epithelial
tonofibrils
27. • Necrosis or liquefaction degeneration of the basal layer
• Infiltration of lymphocytes and occasionally plasma cells.
• Colloid bodies– present mostly in spinous and basal cell layers-
APPEAR as round , eosinophilic globules probably representing
degenerated epithelial cells or phagocytosed epithelial cell
remnants within macrophages.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
28. Differential diagnosis
Lupus erythematosus
Chronic ulcerative stomatitis
Cicatricial pemphigoid- if white striation are absent.
Pemphigus vulgaris
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
29. Mild cases:
Delivery of therapeutic agent can be enhanced with use of vacuum-formed custom trays.
Rx: Lidex (0.05% fluocinonide) gel
Disp: One tube 1.5 g
Sig: Apply to affected area pc and hs.
Monitoring patient's oral cavity is warranted because candidiasis may develop after a
few weeks of topical steroid use; concomitant use of antifungal may be necessary.
Rx: Nystatin oral pastilles (100,000 IU)
Disp: 60 pastilles
Sig: Dissolve in mouth bid, then expectorate for 30 consecutive days.
30. Recalcitrant cases:
Rx: Protopic (0.1% tacrolimus) ointment
Disp: One tube 15 gm
Sig: Apply to affected area bid.
Severe or refractory cases:
Refer to dermatologist for management with systemic corticosteroids.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
31. 2. Pemphigoid
Cutaneous, immune-mediated, subepithelial bullous diseases
characterized by separation of the basement membrane zone
Types of pemphigoid:-
1. Bullous pemphigoid
2. Cicatricial pemphigoid
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
32. BULLOUS PEMPHIGOID
• Chronic, autoimmune, subepidermal, bullous disease with tense
bullae that rupture and become flaccid in the skin
• Oral involvement- 1/3 cases
• Age- elderly (over 60 yrs)
34. Cutaneous lesions-
• Begin as generalized non specific rash, commonly on the limbs,
which appears urticarial or eczematous- which may persist for
several weeks to months before appearance of vesiculobullous
lesions
• Abdomen may also be affected
• Bullae are thick walled and remain intact for longer- don’t
necessarily rupture.
35. Oral manifestations:
• Vesicles and areas of erosion and ulceration.
• Gingival lesions similar to cicatricial pemphigoid- generally
involves most of gingival mucosa- exceedingly painful.
• Gingival tissues erythematous and desquamate even on minor
friction.
• Vesicles and ultimately erosions appear on gingiva and even on
buccal mucosa, palate, floor of mouth and tongue.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
36. Histologically,
No acantholysis
Subepithelial vesicles
Epithelium separation
Two major antigenic determinants
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
37. Treatment
Etiology unknown- control signs and symptoms.
Primary Rx –moderate dose of systemic prednisone.
Steroid sparing strategies (Prednisone + immunomodulator drugs)
used when steroids have to be used in large doses or steroids
alone not affective.
Local lesions- topical steroids.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
38. Mucous membrane pemphigoid (cicatricial pemphigoid)
• Chronic, vesiculobullous autoimmune disorder of unknown cause.
• Predominant in women (5th decade of life).
• Rarely reported in children.
• Involvement- oral cavity, conjunctiva, mucosa of nose, vagina,
rectum, esophagus, and urethra; 20% cases skin involved.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
39. Oral lesions
Areas of erythema, desquamation, ulceration
Bullae - thick walled
Healing - 3 weeks or longer
Ocular lesions
Adhesions of eyelids to eyeball
Adhesions at edges of eyelids
Small vesicular lesions on conjunctiva – eventually produces
scarring, corneal damage and blindness.
44. If acantholysis is present – pemphigus
Acantholysis is absent – pemphigoid.
EM- onset is acute
labial involvement is severe
gingiva is not affected.
45. Epidermolysis bullosa –
When biopsy is treated with salts,
separation of dermis and epidermis occurs
If the basement membrane immunoprotein is towards
epidermal side- pemphigoid
If towards dermal side – epidermolysis bullosa
46. Mild cases:
Rx: Lidex (0.05% fluocinonide) gel
Disp: One tube 1.5 g
Sig: Apply to affected area pc and hs.
Rx: Temovate (0.05% clobetasol propionate)
Disp: One tube 1.5 g
Sig: Apply to affected area qid.
Severe or refractory cases:
Refer to a dermatologist for management with prednisone
(20-30 mg/day); concomitant use of azathioprine may be needed; dapsone,
sulfonamide, and
tetracycline are other alternatives.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
47. 3. Pemphigus Vulgaris
• Group of autoimmune bullous disorders that produce cutaneous
and/or mucous membrane blisters.
• Most common of pemphigus disease - pemphigus vulgaris,
pemphigus foliaceous, pemphigus vegetans, and pemphigus
erythematosus
• Lethal chronic condition.
• Predilection in women(after 4th decade of life)
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
48. ETIOLOGY:
Mostly idiopathic
Drug-induced:- penicillamine and captopril (reversible)
Paraneoplastic pemphigus- genetically distinct from pemphigus-
associated with underlying malignancies.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
49. ORAL LESIONS:-
60% of the patients oral lesion is the 1st sign and may herald
dermatological lesion by a year or more.
Range from small vesicles to large bullae.
Rupture of bullae leads to extensive areas of ulceration.
Any area of oral cavity involved, Oral lesions confine less often to
gingival tissues
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
50. Paraneoplastic pemphigus-
crusting of lips
Erosive lesions on buccal mucosa
Multiple and coalescent areas
of ulceration are covered by
pseudomembranes of necrotic
epithelium.
51. Histopathology:
Intraepithelial vesiculation begins as microscopic alteration and
gradually results in a grossly visible, fluid filled bulla
Occasionally – entire superficial layers of epithelium lost, leaving
only basal cells attached to underlying lamina propria-
TOMBSTONE appearance of epithelial cells.
Acantholysis characterized by round rather than polyhedral
epithelial cells- intercellular bridges are lost& nuclei are large and
hyperchromatic.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
52. Mild to moderate chronic inflammatory infiltrate in underlying
connective tissue.
Immunofluorescence-
Intercellular deposits in epithelium
( IgG in most; C3 in some) of perilesional mucosa
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
55. 4. Chronic ulcerative gingivitis
Condition presents with chronic oral ulcerations
Predilection for women(4th decade)
Erosions and ulcerations in oral cavity- few cases with
Cutaneous lesions
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
56. ORAL LESIONS
Painful, solitary small blisters and erosions with surrounding
Erythema – mainly on gingiva and lateral border of the tongue
Hard palate may also present similar lesions.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
57. Chronic and ulcerative lesions
Erythema and ulceration of gingiva
Neville BW, Damm DD. Dermatological disease. In: Colour Atlas of Clinical Oral
Pathology.2:BC Decker;2003: 425-466.
58. Histopathology
Hyperkeratosis, acanthosis, and liquefaction of the basal layer,
areas of subepithelial clefting
underlying lamina propria – lymphohistiocytic chronic infiltrate in
a band like configuration.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
59. Immunofluorescence :-
Direct (normal and perilesional tissues) –
IgG with a speckled pattern - basal cell layer of the normal
epithelium.
Fibrin deposits at the epithelial- connective tissue interface.
DIAGNOSIS
Direct and Indirect Immunofluorescence required to arrive at
correct diagnosis
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
60. Nuclear deposits of IgG prominent in basal cell layer,
fades toward the superficial layer.
Neville BW, Damm DD. Dermatological disease. In: Colour Atlas of Clinical Oral
Pathology.2:BC Decker;2003: 425-466.
61. For mild cases- Lidex gel (0.05% flucinonide), applied to affected area qid. Temovate
(0.05% clobetasol propionate), apply to affected area qid.
For severe cases, a high dose of systemic corticosteroids is needed to achieve remission.
Reduction of the corticosteroid dose results in relapse of the lesions.
Hydroxychloroquine sulfate at a dosage of 200 to 400 mg per day seems to be the treatment
of choice to produce complete, long-lasting remission.
However, a long-term follow-up study demonstrated that combined therapy (small doses of
corticosteroids and chloroquine) may be required, because the initial good response to
chloroquine ceases after several months or even years of treatment .
Treatment:
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
62. 5. Linear IgA disease
Uncommon mucocutaneous disorder with predilection in women
Clinical features:
Pruritic vesiculobullous rash during middle to late age
plaques or crops with an annular presentation surrounded by a peripheral
rim of blisters .
skin of upper and lower trunk, shoulders, groin and lower limbs- face and
perineum may also be affected.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
63. Oral lesions ( mucosal involvement in 50-100% of cases)
• Vesicles
• Painful ulcerations or erosions
• Erosive gingivitis/chelitis
• Hard and soft palate commonly affected → tonsillar pillars, buccal
mucosa, tongue and gingiva
• Occasionally oral lesion only manifestation for several years
before cutaneous lesions
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
66. Treatment
• Combinations of dapsones and sulfones
• Small amounts of prednisone (10 - 30 mg/ day)
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
67. 6. Dermatitis herpetiformis
Dermatitis herpetiformis is a chronic condition that usually
develops in young adults (ages 20-30 years).
Slight predilection for men.
Dermatitis herpetiformis is a cutaneous manifestation of celiac
disease.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
68. Etiology of celiac disease is obscure; however, tissue
transglutaminase seems to be the predominant autoantigen in the
intestine, skin, and sometimes mucosae.
Gluten enteropathy can be severe in about two thirds of patients
and mild or subclinical in the remaining third.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
69. Clinical features:
bilateral
symmetric pruritic papules or vesicles
primarily restricted to the extensor surfaces of the extremities.
In severe cases, patients may complain of dysphagia, weakness, diarrhea,
and weight loss.
clusters of vesicles or papules arise on the skin.
These vesicles or papules eventually resolve and are followed by
hyperpigmentation of the skin, which ultimately wanes.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
70. Oral lesions
presence of painful ulcerations preceded by the collapse of
ephemeral vesicles or bullae.
Histopathology:
Focal aggregates of neutrophils and eosinophils among deposits of
fibrin at the apices of the dermal pegs.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
71. Immunoflurescence:
Direct immunofluorescence - IgA and C3 are present at the dermal
papillary apices.
Although no circulating autoantibodies to epithelial basement
membrane are present in dermatitis herpetiformis, almost 80% of
patients have antiendomysial and gliadin antibodies.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
72. Treatment:
A gluten-free diet is essential in the treatment.
Oral dapsone to alleviate oral symptoms.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
73. 7. Lupus erythematous
An autoimmue disease
has three different clinical presentations :
1. Systemic
2. Chronic cutaneous
3. Subacute cutaneous
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
74. Systemic lupus erythematous
female predilection (10:1 female:male)
affects vital organs such as kidney, heart, skin as well as mucosa.
Oral lesions (36% of SLE patients) - ulcerative or lichen planus -
like
Tendency to bleed, surrounded by red halo
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
75. Cutaneous lesions:
rash on the malar area with a butterfly distribution.
Oral lesions:
Usually ulcerative
In about 4% of patients- hyperkeratotic plaque reminiscent of
lichen planus appear on buccal mucosa and palate.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
76. Erythema on bridge of the nose with a “butterfly” pattern
Neville BW, Damm DD. Dermatological disease. In: Colour Atlas of Clinical Oral
Pathology.2:BC Decker;2003: 425-466.
77. Direct immunofluorescence:
Perilesional and normal tissue
Ig and C3 deposits at the dermal-epidermal interface.
Antinuclear antibodies- 95% of cases.
DNA and extractable nuclear antigens (ENA) antibodies – 50%
cases.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
78. Chronic cutaneous lupus erythematous
No systemic signs or symptoms
Lesions limited to skin or mucosal surfaces.
Skin lesions- discoid lupus erythematous (DLE)
DLE-
Chronic scarring, atrophy producing lesions that may develop into
hyperpigmentation or hypopigmentation of healing area
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
79. Oral lesions-
Lichen-planus like lesions.
Palate and buccal mucosa
Gingiva maybe affected and clinically present as desquamative
gingivitis.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
80. Intense erythema with ulceration is bordered
by white radial line
Speckled erythematous lesion with radiating white striae
•Multiple facial lesions with irregular
hyperpigmented borders.
•Central scarring with cutaneous
atrophy
81. Direct immunofluorescence-
Reveals immunoglobulins and C3 deposits at the dermal-epidermal
junction of the lesional or perilesional tissue but not in normal
tissue.
This seems to differentiate SIE from DLL.
Indirect immunofluorescence
ANAs in more than 95% of patients,
DNA- and INA-circulating antibodies are present in more than
50%.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
82. Histopathology:
hyperkeratosis or parakeratosis,
Alternated acanthosis and atrophy, and
hydropic degeneration of the basal layer of the epithelium.
lamina propria exhibits a chronic inflammatory cell infiltrate
similar to that observed in lichen planus.
a more diffuse and deeper inflammatory infiltrate with a
perivascular pattern is seen.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
83. Subacute cutaneous lupus erythematous
have a characteristic cutaneous lesion that has similarities to DLE
but lacks the development of scarring and atrophy.
arthritis/arthralgia, low-grade fever, malaise, and myalgia may
present in up to 50% of SCLE patients.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
84. Direct immunofluorescence:
immununoglobulins and C3 deposits at the dermal-epidermal junction in
60% of cases
granular IgG deposits in the cytoplasm of basal cells in 30%.
About 80% of patients have Ro (SSA) antibodies to nuclear antigens,
whereas
25% to 30% have La (SSB) antibodies to nuclear antigens.
Rheumatoid factor (RF) is positive in about 30%
ANA is positive
Antiribonucleoprotein (anti-RNP) antibodies to nuclear antigens.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
86. Treatment:
For patients resistant to topical therapy, systemic antimalarial drugs may be used.
For CCLE, topical steroids are effective to manage the cutaneous and oral lesions.
immunosuppressive drugs such as cytotoxic agents (cyclophosphamide and azathioprine)
and plasmapheresis alone or with steroids are useful.
For severe systemic organ involvement, moderate to high doses of prednisone are
effective.
For arthritis and mild pleuritis, a nonsteroidal antiintlammatory drug (NSAID) or
hydroxychloroquine is used.
Cutaneous rashes are treated with topical steroids, sunscreens, and hvdroxvciiloroquine.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
88. Male predilection
Symmetric distribution of macules, papules or vesicles
Etiology:
Mycoplasma
infection
Herpes simplex
infection
Drug reactions
89. •Hemorrhagic crusting of the vermillion border of lips common;
• Presence of crusting important in arriving at diagnosis
•Target or iris lesions with central clearing
•Multiple, large, shallow painful ulcers with an erythematous
borders
•Lesions –so painful that chewing and swallowing is impaired
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
90. Large, shallow and painful ulcers
involving the buccal and labial mucosa
Bull’s eye appearance
Neville BW, Damm DD. Dermatological disease. In: Colour Atlas of Clinical Oral
Pathology.2:BC Decker;2003: 425-466.
91. Steven Johnsons Syndrome
• Severe bullous form
• Abrupt occurrence of fever, malaise, photophobia and eruptions of
oral mucosa, genitilia and skin
• Oral lesions → rupture → surfaces covered with thick white or
yellow exudate
• Lips - ulceration with bloody crusting
• ANUG
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
92. Hemorrhagic and crusting of lips
and nostrils
Ulcers of oral mucosa
Neville BW, Damm DD. Dermatological disease. In: Colour Atlas of Clinical Oral
Pathology.2:BC Decker;2003: 425-466.
93. Histopathology:
• Liquefaction degeneration of upper epithelium and intraepithelial
microvesicles but without acantholysis
• Pseudoepitheliomatous hyperplasia and necrotic keratinocytes
• Degenerative changes- basement membrane
• Dense inflammatory cell infiltrate at the junction of epithelium and
lamina propria, which becomes indistinct.
• Edema of the lamina propria, vascular dilation, and congestion are
also present.
94. Treatment
• No specific Rx, some cases resolve spontaneously
• bullous or ulcerative lesions require intervention-
Mild symptoms- systemic and local antihistamines topical
anesthetics and debridement of lesions with an oxygenating agent.
Intravenous human Ig (high dose)
Severe symptoms- corticosteroids- but its use is not completely
accepted
95. Drug eruptions
Eruptions in the oral cavity resulting from sensitivity to drugs that
have been taken by mouth or parenterally are termed stomatitis
medicamentosa.
The local reaction from the use of a medicament in the oral cavity
(e.g., aspirin burn, stomatitis resulting from topical penicillin) is
referred to as stomatitis venenata or contact stomatitis.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
96. Drug eruptions in the oral cavity are
multiform.
Vesicular and bullous lesions occur most
often,
But pigmented or nonpigmented macular
lesions are also frequently observed.
Erosions, often followed by deep ulceration
with purpuric lesions, may also occur.
The lesions are seen in different areas of the
oral cavity, with the gingiva often affected.
97. Reported with the use of tartar control toothpaste.
Pyrophosphates and flavoring agents have been identified as the
main causative agents of this unusual condition
Oral reactions to cinnamon compounds (cinnamon oil, cinnamic
acid, cinnamic aldehyde) used to mask the taste of pyrophosphates in
tartar control toothpaste induce an intense erythema of the attached
gingival tissues characteristic of plasma cell gingivitis.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.
98. Plasma cell gingivitis-
Band of moderate to severe inflammation
Neville BW, Damm DD. Dermatological disease. In: Colour Atlas of Clinical Oral
Pathology.2:BC Decker;2003: 425-466.
99. Diagnosis and treatment:
A thorough clinical history usually discloses the source of the
gingival disturbance.
Elimination of the offending agent (e.g., tartar control toothpaste)
leads to resolution of the gingival lesions within a week.
Challenge with the offending agent leads to recurrence of the oral
lesions.
If removal of offending agent is not possible, topical
corticosteroids and topical tacrolimus are used.
101. 1. consciously and intentionally produced injuries without a clear
motive, although, guilt, seeking sympathy, or monetary
compensation may be the driving force behind this abnormal
behavior.
2. Graft-versus-host disease occur in recipients of allogenic bone
marrow transplants, whose oral lesions may occasionally
resemble desquamative gingivitis
102. Wegener's granulomatosis is a systemic disease that may initially
present with striking alterations that are confined to the gingival
tissues. Classically, the gingival tissues exhibit erythema and
enlargement and are typically described as "strawberry gums”.
103. Foreign body gingivitis is clinically characterized by red or red and
white chronic lesions that may be painful and are reminiscent of
desquamative gingivitis.
women in the fifth decade of life.
Microscopic analysis reveals small (<5 pm in diameter) foreign
bodies
chronic inflammatory cell response that may exhibit granulomatous
and lichenoid characteristics.
109. Conclusion
Desquamative gingivitis can be mistaken for plaque induced
gingivitis and this can lead to delayed diagnosis and inappropriate
treatment of serious dermatological diseases such as pemphigoid or
pemphigus.
Correct identification of these conditions entails taking a careful
history and performing a thorough intra-oral examination, biopsy
and referral to an appropriate specialist.
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders– a review.
Aust dent j 2003;48:206-2011.
110. Reference
1. Newmann, Takei, Klokkevold et al. Desquamative gingivits. In:
Carranza’s Clinical Periodontology.11:Elsevier;2011:152-170.
2. Neville BW, Damm DD. Dermatological disease. In: Colour Atlas
of Clinical Oral Pathology.2:BC Decker;2003: 425-466.
3. Robinson NA, Wray D. Desquamative gingivitis: A sign of
mucocutaneous disorders– a review. Aust dent j 2003;48:206-2011.
111. 4. Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The
Differential Diagnosis of Desquamative Gingivitis: Review of the
Literature and Clinical Guide for Dental Undergraduates. J int oral
health 2015;7:88-92.
5. Glickman I, Smulow JB. Chronic Desquamative Gingivitis - Its
Nature and Treatment. In: Clinical Periodontology.1:W. B.
Saunders Company;1964: 397-405.
Editor's Notes
Erosive- extensive erythema with a patchy distribution , may present as focal or diffuse hemmorrhage
Reticular- keratotic- raised white lesions, present as papule, linear, reticular or plaquelike
Hyperkeratosis, basal cell degeneration, lymphocytic exocytosis, bandlike infiltration of lymphocytes in lamina propria, saw tooth rete peg
Fibrin deposits along the basement membrane of the epithelium exhibit a shaggy configuration
Clusters of cytoid body exhibit igM in lamina propria
Pc- after meals
Hs-at bedtime
Symblepharon- adhesion of eyelid to eyeball
Ankyloblepharon- adhesion of edges of the eyelids
Seperation of epithelium from the subjacent connective tissue (subepithelial clefting)
Intact basement membrane
C3 deposit confined along the basement membrane
Typical intraepithelial clefting with "tombstone" appearance of basal cells, which remain attached to subjacent basement membrane and fibrous connective tissue. Acantholysis of epithelial cells with formation of "Tzanck" cells is seen in the intraepithelial cleft.
igG deposits seen in keratinocytes of the stratifeid squamous epithelium.