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Periodontal diseases

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Periodontal diseases

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Periodontal diseases

  1. 1. Periodontal Diseases Dr. Deepak Kumar Gupta
  2. 2. Syllabus • Anatomy of Periodontium • Pellicle • Calculus • Halitosis • Gingivitis • Gingival enlargements • Periodontitis
  3. 3. The Periodontium comprises:- • Gingiva • Periodontal Ligament (PDL) • Root Cementum • Alveolar Bone
  4. 4. The main function of the periodontium is to attach the tooth to the bone tissues of the jaws and to maintain integrity of the surface of the masticatory mucosa of the oral cavity
  5. 5. Pellicle • Thin deposit formed shortly after eruption on the exposed surface of teeth • Usually invisible and is probably of no pathologic significance • Reformed within minutes of polishing and fully formed in 30 minutes • Reaches its mature thickness of 0.1–0.8 microns within 24 hours.
  6. 6. Pellicle • Brown pigment - presence of tannins • pellicle frequently penetrates into the enamel, especially on the proximal surfaces of the teeth • histochemistry and the electron histochemistry indicated that pellicles are of salivary origin – mucoproteins or glycoproteins – Primary amino acid groups and 1:2 glycol groups
  7. 7. Dental Stains • Pigmented deposits on the tooth surface • It may be either extrinsic or intrinsic • oral flora in many cases contains chromogenic microorganisms • Intrinsic stain: incorporated into tooth structure. Ex: porphyria, erythroblastosis fetalis and tetracycline therapy
  8. 8. Stain from Smoking • collection of tobacco tars and resins • yellowish-brown to black deposit • light brown, powdery deposit : occasional cigarette • dense black tarry deposit: heavy smokers • harmless to the teeth, although it should be removed – Esthetics – nidus for calculus – or have a mild, irritating effect on the gingiva • If the dentin is exposed as in older patients by attrition, the staining may be severe
  9. 9. Stain from Smoking
  10. 10. Brown Stain • thin, brown, delicate pellicle like structure that occurs on the teeth • composed of salivary mucin • closely adjacent to the orifices of the salivary gland ducts tends to confirm its relation to saliva. • Mesenteric line – delicate pigmented dental plaque – brown or black dots that coalesce to form a thin, dark line on the enamel at the cervical margin of the tooth – Its presence often associated with a relative freedom from dental caries
  11. 11. Brown Stain
  12. 12. Black Stain • Thin, black deposit - children and adults • Narrow line or band, just above the free gingiva • Not associated with smoking • Chromogenic microorganisms, although none has been identified or cultured from adult stains • Black stain on primary teeth is associated with a low incidence of dental caries – Actinomyces species
  13. 13. Black Stain
  14. 14. Green Stain • mostly children, usually a heavy gray-green stain • especially prominent on the gingival third of the maxillary anterior teeth • soft or ‘furry’ and is difficult to remove • association with the enamel cuticle • No chromogenic microorganism • remnants of Nasmyth’s membrane, possibly by blood pigments
  15. 15. Green Stain
  16. 16. Orange Stain • light, thin deposit of a material of brick red or orange color • Cause of this stain is not known • But it is also believed to be due to pigment- producing microorganisms • Easily removed, • No apparent significance and may or may not recur.
  17. 17. Orange Stain
  18. 18. Halitosis • Oral malodor, fetor oris, fetor ex ore • unpleasant or foul odor exhaled while breathing or talking • most common reasons for seeking dental aid • It may be transient or persistent • Transient: Present in all for some time – Fasting, – Eating certain foods such as garlic, onions, fish – Obesity – Smoking – Alcohol consumption. • Persistent: some for all time • Because the mouth is dry and inactive during the night: usually worse upon awakening (morning breath)
  19. 19. Etiology • Causes of halitosis may be local or extraoral • Local causes – tongue and gingival sulcus - retention of food debris on and between the teeth – unclean prostheses – diseased states like chronic periodontitis, dental caries, abscesses, and dry socket. • Extraoral causes – Respiratory tract infections – Hepatic disorders – Excretion through breath of metabolites – Sweet odor of diabetes, – Alcoholic breath – Uremic breath of kidney diseases
  20. 20. Pathogenesis • Proteins retained in the mouth are broken down by the anaerobic bacteria into amino acids • This is further broken down to produce volatile sulfur compounds namely – Hydrogen sulfide – Methyl mercaptan • Detecting or diagnosing – Organoleptic measurement – Sulfide monitoring – Gas chromatography
  21. 21. Pseudo-halitosis or Halitophobic • No halitosis may be present in spite of their complaint of oral malodor – Causes include chemosensory dysfunction like taste – olfactory dysfunction – psychosomatic factor.
  22. 22. CLASSIFICATION OF PERIODONTAL DISEASE • Gingival diseases – Plaque induced gingival disease – Nonplaque induced gingival lesions • Chronic periodontitis – Localized – Generalized • Aggressive periodontitis – Localized – Generalized • Periodontitis as a manifestation of systemic disease • Necrotizing periodontal disease – Necrotizing ulcerative gingivitis (NUG) – Necrotizing ulcerative periodontitis (NUP) • Abscesses of periodontium – Gingival abscess – Periodontal abscess – Pericoronal abscess • Periodontitis associated with endodontic lesions – Endodotic – periodontal lesion – Periodontal – endodontic lesion – Combined lesion • Developmental or acquired deformities and conditions – Localized tooth related factors that predispose to plaque induced gingival diseases or periodontitis – Mucogingival deformities and conditions around teeth – Mucogingival deformities and conditions on edentulous ridges • Occlusal trauma
  23. 23. GINGIVAL DISEASES • Broadly classified into dental plaque induced and non-plaque induced • Plaque induced – Local factors – Systemic Factors: affected by local factors modified by the specific systemic factors of the host
  24. 24. Plaque induced Local factors • Microorganisms • Calculus • Food impaction • Faulty or irritating restorations or appliances • Mouth breathing • Tooth malposition Systemic factors • Nutritional deficiencies • Drug action • Endocrine changes associated with puberty, pregnancy, menstrual cycle, and diabetes mellitus • Allergy • Heredity • Psychic phenomena • Specific granulomatous infections • Neutrophil dysfunction • Immunopathies
  25. 25. Microorganisms • Biofilm or plaque: many varieties of oral microorganisms • Most commonly, on the nonself-cleansing areas of the teeth, particularly below the cervical convexity of the crown and in the cervical areas • Early Disease – Cocci, various types of bacilli, fusiform organisms, spirochetes – complex and heterogeneous – Actinomyces group - dominant genus in the supragingival plaque. • Advanced periodontitis: amoebas and trichomonads
  26. 26. Microorganisms • Homeostatic Mechanisms – Plaque and plaque-derived endotoxins – Act as irritants or antigens in both nonspecific acute inflammatory responses and immune mechanisms of defense • Many destructive enzymes released by PMNs and numerous tissue destructive lymphokines and lymphotoxins elaborated by B- or T lymphocytes – Collagenase : PMNs and lymphocytes – other lysosomal enzyme secretions – Lysosomal acid hydrolases: macrophages – Lymphotoxin-mediated cytotoxins – Osteoclast-activating factor (OAF)
  27. 27. Microorganisms • Specific microorganisms sometimes cause an inflammatory reaction of the gingiva, although the clinical appearance may be entirely nonspecific – Monilial or a tuberculous – Herpes simplex virus – Fusospirochetal organisms: necrotizing ulcerative gingivitis – Streptococcal and staphylococcal gingivitis
  28. 28. Calculus • whether in a supragingival or a subgingival: causes irritation of the contracting gingival tissue • This irritation is probably caused by the byproducts of the microorganisms • Although the mechanical friction resulting from the hard, rough surface of the calculus may also play a role.
  29. 29. Food Impaction and General Oral Neglect • Impaction of food and the accumulation of debris on the teeth • Irritation of the gingiva by toxins of microorganisms growing in this medium • The degradation of food debris may also prove irritating to the gingival tissues.
  30. 30. Faulty or Irritating Restorations or Appliances • Faulty restorations: irritants to gingival tissues and thereby induce gingivitis. • Overhanging margins of proximal restorations – directly irritate the gingiva – allow the collection of food debris and organisms that further injure these tissues • Improperly contoured restorations: food packing or abnormal excursions of food against the gingiva during mastication • Prosthetic or orthodontic appliances: impinging on the gingival tissues - pressure and of the trapping of food and microorganisms
  31. 31. Mouth Breathing • Drying of the oral mucous membrane - causes gingival irritation with accompanying inflammation or sometimes hyperplasia – mouth breathing – excessive environmental heat – excessive smoking
  32. 32. Tooth Malposition • Teeth which have erupted or which have been moved out of physiologic occlusion • Repeatedly subjected to abnormal forces during mastication • Very susceptible to the development of periodontal disease • Calculus may be deposited on the lingual surface of such a tooth • Bacteria attack the tissue around this tooth - inflamed and may recede • Teeth in labial positions have less osseous coverage over their radicular surface - more susceptible to trauma from toothbrushing and other local irritations • Abnormally high frenal attachments also contribute to gingival recession
  33. 33. Chemical or Drug Application • Many drugs are potentially capable of inducing gingivitis, particularly an acute gingivitis • Direct local or systemic irritating action • For example: phenol, silver nitrate, volatile oils, or aspirin • Others, such as dilantin sodium, produce gingival changes when administered systemically • Beside this there are numerous drugs which causes gingival irritation
  34. 34. Chemical or Drug Application • Plasma cell gingivitis: unusual type of gingivostomatitis • Mainly caused by allergic reaction to some component of chewing gum • Beside this it may be caused by hypersensitivity, allergy, endocrine disease, specific infection
  35. 35. Nutritional Disturbances • Nutritional imbalance is frequently manifested in changes in the gingiva and deeper underlying periodontium • It is sufficient to point out that adequate intake, absorption and utilization of the various vitamins, minerals and other foodstuffs are essential to the maintenance of a normal periodontium.
  36. 36. Pregnancy • Pregnancy gingivitis – smooth, shiny, deeply reddened marginal gingiva with frequent focal enlargement – intense hyperemia of the interdental papilla • Pregnancy tumor: single tumor like mass histologically identical with the pyogenic granuloma • Pregnancy induces a hypersensitive response to a mild injury • clinically nonspecific in appearance: near the end of the first trimester • may regress or even completely disappear at the termination of the pregnancy.
  37. 37. Diabetes Mellitus • Repeatedly reported in association with severe periodontal disease, especially in younger people. • Uncontrolled diabetes is a specific cause of severe periodontal disease - metabolic processes are affected – resistance to infection or trauma – effectiveness of the healing process: cellular carbohydrate metabolism • Beside this there are gingival angiopathy • PAS-positive, • diastase-resistant thickening of vessel walls • hyalinization of vessel walls • sometimes luminal obliteration
  38. 38. Other Endocrine Dysfunctions • Puberty gingivitis: frequency in puberty – gingiva appears hyperemic and edematous – many adolescents are chronic mouth-breathers as a result of lymphoid hyperplasia of the tonsils and adenoids has suggested that the endocrine basis is relatively unimportant • Gingivitis associated with menstruation has been reported by many - phenomenon is rare.
  39. 39. Psychiatric disturbances • significantly greater in psychiatric patients • Significant differences in severity were noted proportional to degree of anxiety • Severity of periodontal disease decreased significantly in both normal and psychiatric groups as the educational level of the patient increased
  40. 40. Incidence • Periodontal disease is worldwide in distribution • no age group (except in very young infants) in which it does not occur • Although all races are affected, there is some difference in incidence between different races and different countries. • 80% at age 13–15, to 95% at age 60 • An interestingly significant reduction in incidence of gingival disease to 62% occurred in the late teens and early 20s – End of puberty – Social factors, greater emphasis on oral hygiene and esthetics than they had previously • Men were affected more frequently than women
  41. 41. Clinical Features • Acute gingivitis is painful uncommon lesion with sudden onset and shorter duration • In gingivitis the inflammation is limited only to the gingiva without underlying attachment loss • It may be localized or generalized • Although all forms of periodontitis are preceded with gingivitis, it is not necessarily progress to periodontitis all the time.
  42. 42. Clinical Features • Marginal gingivitis: involving only the marginal gingiva • Papillary gingivitis: interdental papilla • Traumatic crescent – hyperemia and swelling of the marginal gingiva are confined to a localized area of the gingiva – affected area sometimes assumes a crescent shape
  43. 43. Clinical Features • Diffuse gingivitis: marginal gingiva, attached gingiva and interdental papilla • Chronic gingivitis: slight alterations in the color of the free or marginal gingiva from a light to a deeper hue of pink, progressing to red or reddish blue • Early feature of gingivitis – Bleeding from the gingival sulcus following even mild irritation such as tooth brushing or probing – Edema: slight swelling of the gingiva and loss of stippling
  44. 44. Clinical Features • Lately interdental papillae becomes bulbous – more debris with increased bacterial accumulations – more gingival irritation which goes on • Chronic hyperplastic gingivitis: marked enlargement due to edema and fibrosis as a result of chronic inflammation • Advanced chronic gingivitis: Suppuration of the gingiva, manifested by the ability to express pus from the gingival sulcus by pressure
  45. 45. Radiographic Features • Chronic gingivitis, in which the inflammation is limited strictly to the gingiva, does not manifest changes in the underlying bone • When bony changes become evident, the condition is termed ‘periodontitis’.
  46. 46. Histologic Features • Gingiva in chronic gingivitis – connective Infiltration of tissue by varying numbers of lymphocytes, monocytes, and plasma cells – Polymorphonuclear leukocytes are occasionally noted, particularly beneath the crevicular epithelium. • Crevicular epithelium: irregular and is frequently ulcerated • Increased blood supply in CT • Hyperemia, edema, and hemorrhage may be present. • PDL, nor the crest of the alveolar bone is disturbed • Except free gingival group may be involved sometime
  47. 47. Histologic Features • Junctional Epithelium – weak point to the oral environment – collection of PMN and lymphocytes are always found • Glycogen content of the granular and spinous layers of the epithelium increases as the intensity of the underlying inflammation increases • Mast cells: contains increased granules of sulfonated mucopolysaccharide • Alkaline phosphatase activity increases
  48. 48. Histologic Features • No remarkable differences were found in nucleic acid distribution between normal and inflamed gingiva – However concentration of RNA is lower in all cells of the crevicular epithelium and in the marginal epithelium • The reaction is absent or very weak in the epithelial lining of the gingival sulci and periodontal pockets and in the epithelial attachment
  49. 49. Treatment and Prognosis • Most cases of chronic gingivitis are due to local irritation • If the irritants are removed at this stage, the inflammation will disappear within a matter of hours or a few days, leaving no permanent damage • So irritants should be removed as early as possible followed by good oral hygiene practise.
  50. 50. Treatment and Prognosis • Mechanical removal of plaque aided by chemical plaque control measures such as using mouthwashes containing chlorhexidine, listerine or triclosan • If there is poor response to good local therapy, then there may be risk of systemic etiology • Non-plaque induced gingival diseases may have different etiology and have characteristic clinical presentation • These groups of gingival diseases include specific bacterial, viral, and fungal infections, gingival manifestations of certain dermatoses.
  51. 51. Necrotizing Gingivostomatitis (NG)
  52. 52. Necrotizing Gingivostomatitis (NG) • It commonly includes Necrotizing ulcerative gingivitis (NUG), Necrotizing Ulcerative Periodontitis (NUP), and Necrotizing stomatitis • Share many clinical and etiological characteristics • The spectrum of NG ranges from necrotizing gingivitis to cancrum oris
  53. 53. Necrotizing Gingivostomatitis (NG) • Predisposing factors – emotional stress, – Immunosuppression – HIV infection – Smoking – Malnutrition – Pre-existing gingivitis. • Diagnosis - marker for immune deterioration in HIV- seropositive patients • NUP & NUG shares many of the clinical and etiologic characteristics except the former has known systemic disease or immune dysfunction and attachment loss
  54. 54. Necrotizing Ulcerative Gingivitis (NUG) • Also known as Vincent’s infection • Trench mouth • Acute ulceromembranous gingivitis • Phagedenic gingivitis • Fusospirochetal gingivitis • Acute ulcerative gingivitis
  55. 55. Necrotizing Ulcerative Gingivitis (NUG) • Specific type of gingivitis with characteristic signs and symptoms • Disease manifests as both acute and recurrent (subacute) phases • inflammatory condition involves primarily the free gingival margin, the crest of the gingiva, and the interdental papillae • When it spreads to to the soft palate and tonsillar areas: Vincent’s angina • Diagnostic triad: Pain, interdental ulceration, and gingival bleeding
  56. 56. Epidemiology • Frequently occurs in an epidemic pattern • Groups of persons in close contact, especially those living under similar conditions • Apparent during World War I, term ‘trench mouth’: troops in the trenches • Similar sporadic outbreaks also occurred during World War II • Relatively uncommon in developed countries nowadays • Global increase associated with HIV infection.
  57. 57. Epidemiology • Not a contagious infection: similar predisposing conditions among the members of the group • At any age, but is more common among young and middle-aged adults • In developing countries, it is seen almost exclusively in children, related to poverty and malnutrition
  58. 58. Etiology • Endogenous, polymicrobial infection causing destructive inflammation due to the coexistence of several predisposing factors • Fusiform bacillus and Borrelia vincentii (a spirochete): present in small numbers in the healthy gingival flora • fusiforms, and filamentous organisms are also found. • number of factors disturb the host-parasite relationship, facilitating overgrowth of the organisms of the fuso-spirochaetal complex • increase in IgG and IgM antibody titers to spirochetes and increased IgG titers to Bacteroides melaninogenicus
  59. 59. Etiology • Vibrio and coccal forms as important agents in the etiology of this disease • B. intermedius and Bacteroides melaninogenicus: motile gram negative anaerobic bacillus another causative agent
  60. 60. Predisposing Factors • Psychological stress plays an important role - increased frequency of the disease in people in the military services • Other predisposing factors include – Immunosuppression – Smoking – upper respiratory tract infection, – local trauma, – poor nutritional status – poor oral hygiene. • HIV-positive persons suffer from a severe form of disease ultimately HIV associated periodontitis
  61. 61. Predisposing Factors • highest incidence occurring between October and February: respiratory infections and exanthemas are at their peak • lowest incidence occurring in July and August • deficient in vitamin C and B complex
  62. 62. Clinical Features • Painful, hyperemic gingiva and sharply punched- out crater like erosions of the interdental papillae of sudden onset • Ulcerated remnants of the papillae and the free gingiva bleed when touched • Become covered by a grayish green, necrotic pseudomembrane • Ulceration tends to spread and may eventually involve all gingival margins • It begins rather commonly at a single isolated focus, with a rapid onset
  63. 63. Clinical Features • A fetid odor ultimately develops that is extremely unpleasant. • The patient almost always c/o an inability to eat because of the severe gingival pain and the tendency for gingival bleeding • pain is that of a superficial ‘pressure.’ • The patient usually suffers from headache, malaise, and a low-grade fever • Excessive salivation with the presence of a metallic taste to the saliva is often noted • regional lymphadenopathy is usually present.
  64. 64. Clinical Features • In advanced and more serious cases, there may be generalized or systemic manifestations – Leukocytosis – gastrointestinal disturbances – Tachycardia. • After the NUG is cured, the crests of the interdental papillae, which have been destroyed leaving a hollowed-out area – constitute an area which retains debris and microorganisms – serve as an ‘incubation zone.’
  65. 65. Bacteriologic Examination • Smears of material from the gingiva – fusiform bacilli (genus Fusobacterium or Fusiformis) – oral spirochete (Borrelia vincentii), – various other spirochetes, – filamentous organisms, – vibrios, – Cocci – desquamated epithelial cells – varying numbers of polymorphonuclear leukocytes • Relative numbers of MCO present vary with the stage of the disease • Secondary invaders being more prominent in the later phases as well as in the subacute form of necrotizing ulcerative gingivitis
  66. 66. Diagnosis • Diagnosis based on smear studies is hazardous because of the nonspecific findings • Although the presence of the disease can often be confirmed when vast numbers of the spirochete and fusiform bacteria are seen • It may be also present in ‘normal mouths,’ acute herpetic gingivostomatitis, simple pericoronitis, marginal gingivitis and chronic gingivitis • final diagnosis is made clinically
  67. 67. Histologic Features • M/s of the gingiva: acute gingivitis with extensive necrosis • Surface epithelium is ulcerated and replaced – Thick fibrinous exudate – Pseudomembrane, containing many PMN and MCO • Lack of keratinization of the gingival tissues • CT is infiltrated by dense numbers of PMN and shows an intense hyperemia • Microscopic picture is an entirely nonspecific one
  68. 68. Histologic Features • Vast numbers of both spirochetes and fusiform bacilli are found on the surface of the living tissue in and beneath the necrotic pseudomembrane • Both forms have also been reported as invading viable tissues to variable depths below the surface
  69. 69. Treatment • Superficial cleansing in the early acute stage with – Chlorhexidine – Diluted hydrogen peroxide – or Warm Saltwater • This is followed by thorough scaling and polishing • Topical anesthetics may be required to reduce the pain during this procedure • In many such cases, prompt regression of the disease results even without medication • If not use of antibiotics coupled with local treatment
  70. 70. Treatment • Usually NUG subside in 48 hours with adequate treatment • Sometimes there may be – Considerable destruction of tissue, involving the interdental papillae and marginal gingiva – Leading to punched-out appearance of the interproximal gingiva – And the apparent gingival recession even after the regression of the disease • Recontouring of gingival papillae is usually required – proper use of round toothpicks – or gingivoplasty
  71. 71. Prognosis • Treatment cannot be considered complete until the gingival tissue contours almost normal. • High recurrence rate • Occasional serious sequelae such as gangrenous stomatitis or noma, septicemia and toxemia • Even death have also been reported following this disease
  72. 72. Desquamative Gingivitis • Not a disease entity but a clinical term • unique condition of the gingiva characterized by intense redness and desquamation of the surface epithelium • Inflammation of unknown etiology • Also called ‘gingivosis’
  73. 73. Desquamative Gingivitis
  74. 74. Etiology • Causative factors to be: – Certain dermatoses – Hormonal influences – Abnormal responses to irritation – Chronic infections – Idiopathic
  75. 75. Etiology • The most important dermatoses presenting oral findings categorized as a desquamative gingivitis – Cicatricial pemphigoid (benign mucous membrane pemphigoid) – Pemphigus – Lichen planus – Epidermolysis bullosa – Systemic lupus Erythematosus – Linear IgA disease
  76. 76. Gingival Abscess • Acute, localized, and painful lesion of sudden onset • caused by sudden forceful penetration of any foreign objects – bristle of a toothbrush – An apple core • carry bacteria deep into the gingival tissue
  77. 77. Gingival Abscess
  78. 78. Clinical Features • It is usually limited to the marginal gingiva • Initially it appears as reddish swelling with a smooth and shiny surface. • Within hours, it becomes fluctuant and exhibits pointing and through which pus discharges
  79. 79. Histologic Features • Connective tissue shows – vascular engorgement – edema and formation of abscess cavity – surrounded by a diffused collection of PMN • Epithelium exhibits secondary changes – intra- and inter-cellular edema – microabscess formation – sometimes ulceration.
  80. 80. Treatment • Spontaneous rupture is common • The invading foreign material, if any, will be usually expelled along with the pus
  81. 81. Pericoronitis • inflammatory lesion occurring around the impacted or partially erupted tooth • Incomplete eruption of the tooth provides a large stagnation area for food debris under the gingival flap. • This becomes infected easily and results in inflammation of the pericoronal flap • It exhibits chronic inflammation for a long period • If the debris and bacteria are deeply entrapped, an abscess may form which is called a pericoronal abscess. • It is a mixed infection and various bacteria of the dental plaque (particularly anaerobes)
  82. 82. Pericoronitis
  83. 83. Pericoronitis
  84. 84. Clinical Features • Mandibular third molar is the commonly involved tooth. • Pain and swelling of the pericoronal tissue around the affected tooth • difficulty in chewing, and difficulty in opening the mouth • mildly ill with fever, malaise, and regional lymphadenopathy
  85. 85. Histologic Features • Epithelium of the pericoronal flap show – Hyperplasia – intercellular edema – leukocytic infiltration • Underlying connective tissue exhibits • increased vascularity, • dense diffused infiltration with lymphocytes, and plasma cells • varying number of PMN
  86. 86. Management • Entrapped food debris must be removed. • When the upper tooth is involved, it should be grounded or extracted if it is malposed • Radiograph helps in assessing the position of the involved tooth. • If impacted, the tooth must be removed. • And if it is in a favorable position, surgical removal of the pericoronal flap is advocated after acute symptoms subside. • The administration of antibiotics helps to relieve the symptoms and prevents the spread of infection to the adjacent tissue spaces
  87. 87. Gingival Enlargement
  88. 88. Gingival Enlargement • increase in the size of the gingiva so that soft tissue overfills the interproximal spaces • Balloons out over the teeth and protrudes into the oral cavity • May be localized to one papilla • Or may involve several or all of the gingival papillae throughout the mouth
  89. 89. Gingival Enlargement • The enlargement is usually more prominent on the labial and buccal surfaces, • although it does occasionally develop in the lingual gingiva. • It does not involve the vestibular mucosa • not to be confused with overgrowths of bone, or exostoses, noted occasionally on the alveolar bone,
  90. 90. Etiology • It can be classified based on etiologic factors and pathologic changes as follows: – Inflammatory gingival enlargement – Drug induced gingival enlargement – Enlargement associated with systemic factors – Conditioned enlargement – Enlargements due to systemic diseases – Idiopathic gingival enlargement – Neoplastic enlargement – False enlargement
  91. 91. Inflammatory Enlargement • Local irritation: poor oral hygiene, accumulation of dental calculus or mouth breathing • Host tissue response to dental plaque accumulation. • Clinical Features – Gingivae are soft edematous, – hyperemic or erythematosus – sensitive to touch - bleed easily – glossy, nonstippled surface • Histological Features – Hyperemia edema – Lymphocytic infiltration – proliferation of the fibrous CT of the gingiva
  92. 92. Inflammatory Enlargement Inflammatory gingival enlargement due to local collection of plaque
  93. 93. Drug-induced Gingival Enlargement • Anticonvulsants: Diphenylhydantoin (dilantin sodium), valproic acid, methsuximide, and succinimides • Immune suppressants: Cyclosporine • Calcium channel blockers: nifedipine, nitrendipine and verapamil • Hydantoins: ethotoin and mephenytoin • Phenytoin – stimulates proliferation of fibroblast-like cell in tissue culture – decreases the collagen degradation
  94. 94. Drug-induced Gingival Enlargement Enlargement of the gingiva in an epileptic patient receiving dilantin sodium
  95. 95. Drug-induced Gingival Enlargement Gingival enlargement in a patient receiving nifedipine
  96. 96. Drug-induced Gingival Enlargement • Clinical Features – Begins painlessly – Involving one or two interdental papillae – Increased stippling and ultimately a roughened or pebbled surface with lobulations – gingival tissues are dense, resilient, and insensitive – show little or no tendency to bleed
  97. 97. ENLARGEMENT ASSOCIATED WITH SYSTEMIC FACTORS • Conditioned Enlargement – Hormonal Enlargement: Pregnancy and Puberty – Allergic Enlargement – Nutritional Enlargement
  98. 98. Hormonal Enlargement: Puberty • Inflammatory gingival enlargement often occurs at puberty, both in men and women • endocrine imbalance at this particular stage of the patient’s development. • Or because oral care is poor at this age: local irritation associated with eruption of teeth, and/or nutrition may be inadequate • Thus, the enlargement may be only indirectly associated with an endocrine disturbance
  99. 99. Hormonal Enlargement: Pregnancy • Gingival enlargement of the inflammatory type during pregnancy • This proliferation may be due to – disturbed nutrition, – poor oral hygiene, • Increased levels of estrogen and progesterone in pregnancy • vascular permeability: leads to gingival edema • altered inflammatory response to dental plaque
  100. 100. Hormonal Enlargement: Pregnancy • Pregnancy gingivitis: also called as ‘gingivitis in pregnancy’or ‘pregnancy tumor,’ • Microscopic studies resemble Pyogenic granuloma – Increased vascularity, – multiplication of fibroblasts, – Edema – infiltration of leukocytes into the gingiva
  101. 101. Allergic Enlargement: Plasma Cell Gingivitis • Also called as Atypical gingivitis, plasma cell gingivostomatitis • arises as a hypersensitive reaction to a component of chewing gum, dentifrices, or some of the dietary components • Commonly presents – mild marginal gingival enlargement, sometimes extending to involve the attached gingiva – more prevalent in young women – initial symptom is soreness of the mouth, which is intensified by hot or spicy food
  102. 102. Plasma Cell Gingivitis
  103. 103. Allergic Enlargement: Plasma Cell Gingivitis • In severe cases, extends to buccal and vestibular mucosa. – Gingiva appears swollen, – erythematous, – friable with loss of stippling • The involvement of other oral tissues like the tongue and lips is common • They appear atrophic, dry, and exhibit cracks or fissures
  104. 104. Plasma Cell Gingivitis - Histologic Features • Surface epithelium is hyperplastic, shows intracellular edema, and micro abscesses • Connective tissue – densely infiltrated with chronic inflammatory cells – predominantly a polyclonal mixture of plasma cells • Marked vascular dilatation with severe thinning of epithelium over the connective tissue pegs
  105. 105. Treatment and Prognosis • Possible allergens should be identified • Careful study of the patient’s history and eliminated • Topical and systemic steroids give good results
  106. 106. Nutritional Enlargement: Vitamin C Deficiency • Spongy, bleeding gums of scurvy, tender, swollen, and edematous • Gingival sulci are often filled with partially clotted blood • Crests of the interdental papillae are red or purple • Sometimes ulceration and necrosis of the papillae as infection becomes superimposed upon the susceptible tissues • Hemorrhages following slight trauma to other parts of the body
  107. 107. Nutritional Enlargement: Vitamin C Deficiency • Enlargement is essentially a conditioned response to bacterial plaque. • Combined effect of vitamin C deficiency and inflammation produces this enlargement. • Treatment: improvement of oral hygiene and administration of vitamin C
  108. 108. ENLARGEMENT DUE TO SYSTEMIC DISEASES • Leukemia • Granulomatous Diseases • Regional Enteritis (Crohn’s Disease) • Idiopathic Gingival Enlargement • Neoplastic enlargements • False enlargements
  109. 109. Leukemia • Early finding in acute monocytic, lymphocytic or myelocytic leukemia • Leukemic enlargement may be diffused or marginal, localized or generalized • Gingiva appears shiny, bluish red, soft, edematous, easily compressible, tender, and frequently ulcerated • No signs of stippling • gingivae are usually inflamed, owing to local infection • occasionally a necrotizing ulcerative gingivitis develops
  110. 110. Leukemia • Histology – gingival tissues are packed with immature leukocytes – specific type depending on the nature of the leukemia – These abnormal white blood cells are unable to perform their defensive function – Capillaries are engorged – connective tissue is edematous.
  111. 111. Granulomatous Diseases • Some local and systemic granulomatous diseases may involve the gingiva and present as gingival enlargement – Crohn’s disease – sarcoidosis – Wegner’s granulomatosis – foreign body gingivitis
  112. 112. Regional Enteritis • Also known as Crohn’s Disease • slowly progressive disease of unknown etiology possibly of infective origin • Atypical mycobacteria have been implicated in some cases • all ages, involves both genders equally • Characterized by – Granulomatous – superficial ulcerations of the intestinal tract – frequent fistulas developing onto body surfaces or viscera, or between intestinal loops
  113. 113. Regional Enteritis • Most commonly involved areas are the buccal mucosa: cobblestone appearance • Vestibule: linear and hyperplastic folds, which may mimic denture-induced hyperplasia • Lips: diffusely swollen and indurated • Gingiva and alveolar mucosa: granular erythematous swelling • Palate: multiple ulcers occur
  114. 114. Regional Enteritis • Glossitis may be seen secondary to malabsorption of vitamin B12 • oral lesions may either precede or follow the appearance of the intestinal lesions • commonly show periods of quiescence alternating with exacerbations of the process. • Histological Features: chronic granulomatous disease, reminiscent of sarcoid
  115. 115. Regional Enteritis • Histological Features – fibrosis and a focal dense collection of lymphocytes and plasma cells – Lymph vessels appear dilated – noncaseating granulomas which are typically small, consisting of macrophages, epithelioid cells – ccasional giant cells are seen • Management – Oral lesions resolve when intestinal Crohn’s disease is controlled – oral sulfasalazine – or intralesional injection of corticosteroid gives good results
  116. 116. Idiopathic Gingival Enlargement • Gingival tissues are so diffusely enlarged that the teeth are completely covered • If the enlargement is present before tooth eruption, the dense fibrous tissue may even interfere with or prevent eruption • Also called as ‘fibromatosis’, ‘fibromatosis gingivae,’ ‘elephantiasis gingivae,’ and ‘congenital macrogingiva’ • cause of this developmental enlargement of gingival tissue is not known • It is probably hereditary, being transmitted as an autosomal dominant trait in some instances
  117. 117. Idiopathic Gingival Enlargement • Clinical Features – large masses of firm, – dense, resilient, – insensitive growth that covers the alveolar ridges and extends over the teeth – normal in color – patient complains only of the deformity – gingivae are so enlarged that the lips protrude – fibrous mat of tissue upon which the patient chews may be 25 mm wide and as much as 15 mm thick. • This enlargement may be detected at an early age and in a few cases even at birth • Teeth do not erupt normally because of the dense fibrous tissue.
  118. 118. Idiopathic Gingival Enlargement
  119. 119. Idiopathic Gingival Enlargement • Histological Features – hyperplastic epithelium with elongation of rete ridges – mild hyperkeratosis – underlying stroma is made up almost entirely of dense bundles of mature fibrous tissue with few young fibroblasts present • Management – Surgical removal of the excess fibrous tissue is the only feasible treatment – condition may recur afterwards
  120. 120. Other Cause • Neoplastic enlargements: benign and malignantneoplasms involving the gingiva • False enlargements – due to underlying dental or osseous anomalies – not an abnormality of the gingiva as such.
  121. 121. PERIODONTITIS
  122. 122. PERIODONTITIS • An inflammatory disease of the supporting tissues of the tooth caused by specific MCO or group of specific MCOs, resulting in progressive destruction of the PDL and alveolar bone with pocket formation, recession, or both. • It is classified as – Chronic, – Aggressive, – Manifestation of systemic diseases – Occlusal trauma: Acute periodontitis that results from acute trauma
  123. 123. Chronic Periodontitis • Also known as Periodontoclasia, pyorrhea, pyorrhea alveolaris, Schmutz pyorrhea • most common form of PDL disease and is associated with local irritation • Begins as a marginal gingivitis, which usually progresses, if untreated or improperly treated • Treatment: removal of etiologic factors, both local and systemic, the maintenance of good oral hygiene, and the establishmentof a stable, harmonious articulation free from traumatic interferences.
  124. 124. ETIOLOGY • Local factors – microbial plaque – calculus, – food impactions – irritating margins of fillings • No abnormalities of the immune system seem to appear
  125. 125. Microbiology • Predominantly associated with – Actinobacillus actinomycetemcomitans – Bacteroides forsythus – Porphromonas gingivalis – Prevotella intermedia • Advanced periodontitis – Fusobacterium nucleatum – Bacteroides melaninogenicus – Eikenella corrodens – Bacteroides corrodens – Bacteroides capillosu
  126. 126. Incidence • Rarely before 18 years of age • After 45 years of age almost all subjects show evidence of localized or generalized bone loss. • Incidence of bone loss in men is slightly higher than in women • Pocket formation increased constantly with age: peak at ages 52–55 years • Abnormal tooth mobility – Rarely encountered before 25 years of age – Increased sharply from 25% at ages 35–39 to 49% at ages 40–48 – steady rise to 79% at age 60
  127. 127. Incidence • Localized or generalized suppuration – occurred spontaneously or under digital pressure – 40% of subjects at age 40 – approximately 50% in the older age groups • 60% of the teeth had been lost by the age 60 • 26% of patients were completely edentulous
  128. 128. CLINICAL FEATURES • Earlier pathologic finding: tiny ulceration of the crevicular epithelium • Unless the irritants are removed, more plaque and calculus are deposited with the passage of time, and the marginal gingivitis becomes more severe. • It proliferates as a result of the inflammation: tendency for the epithelial attachment to extend or ‘migrate’ apically on the tooth.
  129. 129. CLINICAL FEATURES: Early • Gingival crevice gradually becomes deeper and is classified as an early periodontal pocket • PDL pockets measuring more than 3–4 mm: destruction of periodontal ligament and alveolar bone resorption. • Clinically, the presence of calculus may be detected at this stage. • Mild visible swelling and hyperemia of the gingivae: tendency to bleed readily • An unpleasant, foul type of halitosis is also present
  130. 130. CLINICAL FEATURES: Severe • Tooth mobility • Dull sound and TOP positive • Suppurative material and other debris - slight pressure on the gingiva. • embrasures may be open because the interdental papillae are deficient • festooning is not apparent • gingivae appear ‘boggy’ because of hyperemia and edema; • no stippling is detected, • smooth, shiny, and perhaps redder or bluer than normal • Patient may have no subjective symptoms
  131. 131. CLINICAL FEATURES: LATE • C/o bad taste • bleeding gums • hypersensitivity of the necks of the teeth due to exposure of cementum as the soft tissues recede • Gingival recession – gingival tissues recede toward the apex, exposing the cementum – cementum is softer than enamel: often worn away by a toothbrush and an abrasive dentifrice
  132. 132. CLINICAL FEATURES: LATE
  133. 133. CLINICAL FEATURES: LATE • Gingival recession – occur more rapidly: rapid alveolar bone loss – often begins as a thin break in the free gingiva adjacent to the center of a tooth – called as Stillman’s cleft
  134. 134. Histologic Features • Early m/s signs: osteoclasts on the surface of the bone crest • Sooner forms little bays of bone resorption: Howship’s lacunae • Alveolar bone changes occurs prior to PDL changes • Later if irritation persist, epithelial attachment proliferates apically down onto the cementum
  135. 135. Histologic Features • Alveolar crest of bone is resorbed further apically • Principal PDL fibers become disorganized and detached from the tooth • PDL pocket exists between the free gingiva and the tooth: more than 2 mm apically. • Leukocytic cellular exudate from the inflamed soft tissue of the pocket wall progresses the disease
  136. 136. Histologic Features • The vicious cycle of irritant collection, inflammation and detachment continues, along with periodontal bone resorption in an apical direction
  137. 137. Classification: Periodontal Pockets • Gingival Pocket: gingival enlargement – Also known as Pseudo Pocket – gingival tissues increase in bulk, causing an increase in the depth of the pocket around the teeth • Periodontal Pocket: base of the pocket has invaded further into the periodontium. It may be – Infrabony Pocket: bone on its lateral wall. It may be either 1 wall defect, 2 wall defect or 3 wall defect – Suprabony Pocket: horizontal loss of the crest of the alveolar bone
  138. 138. Radiographic Features • Earliest change – Loss of continuity of Lamina Durra – Widening of PDL space – blunting of the alveolar crest due to the beginning of bone resorption • Horizontal Bone loss: straight line along the edge of alveolar bone • Vertical Bone loss: tendency for cupping out of the interdental alveolar bone
  139. 139. Radiographic Features
  140. 140. Treatment • Periodontal loss is irreversible, but it can be stopped as it is or can be reconstructed by periodontal surgery. • By careful complete periodontal treatment, the teeth can be saved – if the bone loss has not been too extreme – if irritants are removed by scaling and curettage – if pockets are eliminated by gingival recession – surgical removal of the gingiva (gingivectomy), – if osseous deformities are eliminated – tooth-supporting tissues are recontoured to a normal physiologic architecture, – if occlusal forces are balanced – systemic factors are corrected.
  141. 141. PROGNOSIS • Usually a shrinkage or recession of the gingival tissues remains permanently even though inflammation is diminished • Reattachment: re-establishment of fibrous connection of the tooth to the alveolar bone and gingiva by periodontal fibers in an area of cementum which is adjacent to a pathologic pocket • A typical epithelial attachment is described as reforming • The cellular elements that would make reattachment possible are all present in the periodontium • resorption of the bone and rebuilding of new bone with reattachment of new PDL fibers go on constantly
  142. 142. AGGRESSIVE PERIODONTITIS • Rapidly progressing type of periodontitis that occurs in patients who do not have large accumulations of plaque and calculus • This may be either localized or generalized • Earlier it was called Juvenile periodontitis and Rapidly progressive periodontitis
  143. 143. AGGRESSIVE PERIODONTITIS Presence of a large amount of plaque, calculus and gingival infection
  144. 144. AGGRESSIVE PERIODONTITIS Loss of bone support involving more than three teeth other than first molars and incisors
  145. 145. Etiology • Familial tendency suggesting a genetic predisposition • Defect in the immune response rather than plaque and calculus deposition. • Disease is specific • Microbiology – Actinobacillus actinomycetemcomitans – Porphyromonas gingivalis – P. gingivalis – Bacteriodes forsythus – Other species related are Capnocytophaga sputigena, Mycoplasma subspecies and Spirochetes
  146. 146. Histological Features • functional defects of polymorphonuclear leukocyte, monocytes, or both • but without any systemic manifestations • Because of this, their defensive ability against some of the periodontal pathogens is defective • The bactericidal activity against Actinobacillus actinomycetemcomitans is particularly faulty in localized form.
  147. 147. Clinical Features: Localized form • Usually occurs around puberty • Strong familial tendency • Localized to the first molars and incisors • Attachment loss in at least two permanent teeth, one of which is the first molar • Striking feature: absence of clinical inflammation with minimal local factors despite the presence of a deep periodontal pocket • Rate of alveolar bone loss is considerably higher than in chronic periodontitis • Associated primarily with A.actinomycetemcomitans.
  148. 148. Clinical Features: Generalized form • Usually affects patients under 30 years of age • Involves at least three teeth other than the first molar and incisor • Exhibits poor serum antibody response to infecting agents • Many cases represent the localized form which becomes generalized with time • organism associated with the generalized form is more complex and closely resembles chronic periodontitis
  149. 149. Diagnosis • Definitive diagnosis – family history, – clinical, – radiographical, – microbiological, – histological examination with leukocyte function tests
  150. 150. Papillon-Lefèvre syndrome • Autosomal recessive disorder: oral and skin lesion • Oral manifestations – aggressive periodontitis – severe destruction of the alveolar bone involving both the deciduous and permanent dentitions • Skin lesions: keratotic lesions of palmar and plantar surfaces • Rapid bone loss, mobility and pathological migration occurs • Loss of the entire dentition at a much younger age
  151. 151. Papillon-Lefèvre syndrome
  152. 152. Papillon-Lefèvre syndrome
  153. 153. Radiographic Features • Localized form – vertical loss of alveolar bone is seen around the first molar and incisor – arc-shaped alveolar bone loss extends from the distal surface of the second premolar to the mesial surface of the second molar – widening of the PDL space – ‘vertical’ pocket formation, differs from the ‘horizontal’ type of bone loss seen in chronic periodontitis appears to be ‘horizontal.’ • Generalized form – bone loss may range from the involvement of one or two teeth to a maximum number of teeth
  154. 154. Management • Antibiotics should be administered in combination with mechanical removal of plaque and inflamed periodontal tissues. • Periodontal surgery should be performed with prophylactic antibiotic cover • Postoperative usage of chlorhexidine mouthrinse • Periodic follow-up is necessary since there is possibility of reinfection
  155. 155. Necrotizing Ulcerative Periodontitis (NUP) • Occurs in younger patients than those with chronic periodontitis • Accompanied by fever, malaise, and lymphadenopathy • NUP associated with an infection of MCOs – Treponema and Selenomonas species – Fusobacterium nucleatum – Prevotella intermedia – Porphyromonas gingivalis
  156. 156. Necrotizing Ulcerative Periodontitis (NUP)
  157. 157. Necrotizing Ulcerative Periodontitis (NUP) • may be observed in HIV-positive patients • CD4+ cell count is below 200 cells/mm in more than 90% of the HIV-infected patients with NUP • In HIV-positive patients – ulceration and necrosis of gingiva with pain – spontaneous bleeding – exposed underlying bone then undergoes rapid destruction.
  158. 158. Management and Prognosis • If underlying immunosuppression and malnutrition is corrected: responds to oral hygiene and antibiotics • Roughly 72.9% of the HIV-infected patients have the cumulative probability of death in 24 months from the time of the diagnosis
  159. 159. Lateral Periodontal Abscess • Also known as Lateral abscess • Related directly to a preexisting periodontal pocket • Precipitating factors – subgingival flora, – host resistance, – or both. • When such a pocket reaches sufficient depth, around 5–8 mm, the soft tissues around the neck of the tooth approximate the tooth so tightly that the orifice of the pocket is occluded
  160. 160. Lateral Periodontal Abscess • Bacteria multiply in the depth of the pocket : acute abscess with exudation of pus into this area. • Foreign body, particularly food debris, may also lead to abscess formation • This may result in enough swelling to destroy the cortical plate of bone, • If it still exists, allow the abscess to balloon the overlying tissues, forming a ‘gum boil’, or parulis
  161. 161. Lateral Periodontal Abscess
  162. 162. Clinical Features • usually occurs in adults and is rare in children • most common cause of periodontal abscess is foreign bodies • acute periodontal abscess will cause the afflicted tooth to be tender to percussion. • Pain, foul taste, mobility of the involved tooth, • tenderness over the corresponding gingiva, • lymphadenopathy
  163. 163. Clinical Features
  164. 164. Histologic Features • resembles an abscess elsewhere • consists of a central cavity filled with pus walled off on one side by the root of the tooth and on the other by connective tissue • Most of cases the epithelial lining of the crevice would have been destroyed by the inflammatory process.
  165. 165. Treatment • Treatment is similar to that of an abscess elsewhere • direct incision, perpendicular to the long axis of the involved tooth, releases pus. • Careful insertion of a dull probe into the pocket along the tooth will usually induce drainage • Subsequently acute symptoms will subside • Abscess will recur, unless the cause is removed and the depth of the pocket is reduced • Cases in which normal tissue contours cannot be developed and maintained, extraction of the tooth is advised after the acute symptoms have subsided.
  166. 166. Refrences • Shafers, Oral Pathology 6th edition • Regezi: Oral Pathology: Clinical Pathologic Correlations, 5th ed • Essential of Oral Pathology and medicine 7th ed : Cawsons & odell • Color atlas of Oral Pathology: Nevile • Pathology of the Head and Neck: Antonio Cardesa, Pieter J. Slootweg • Essential of Oral Pathology : Swapan Kumar Purkait
  167. 167. THANKS…… Like, share and comment on https://www.facebook.com/notesdental http://www.slideshare.net/DeepakKumarGupta2 www.facebook.com/notesdental

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