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Acute gingival infections- Dr Harshavardhan Patwal

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explained here is the some of the gingival infections ANUG , acute herpatic gingivostomatitis and Acute pericoronitis .. Dr Harshavardhan Patwal

Published in: Health & Medicine
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Acute gingival infections- Dr Harshavardhan Patwal

  1. 1. Dr Harshavardhan Patwal ACUTE GINGIVAL INFECTIONS
  2. 2. Contents Introduction Various Acute Gingival Diseases Abscess ANUG Acute Herpetic gingivostomatitis Acute Pericoronitis Other acute gingival infections
  3. 3. INTRODUCTION INFECTION -The lodgment and multiplication of a parasite in or on the tissue of a host constitute infection. It does not invariably results in disease. In fact, disease is but a rare consequences of infection, which is a common natural event. Gingival disease are a diverse family of complex & distinct pathological entities which are the result of variety of processes. The inflammatory response initiated in gingival disease appears to be prerequisite for destruction of connective tissue attachment apical to CEJ. (Page et al 1997)
  4. 4. The identification & treatment of gingival disease is important step in preventing more serious periodontal ailments. Acute lesions have a rapid onset & is accompanied by pain. Acute lesions are by definition, of sudden onset, limited duration & with well defined features in contrast with chronic lesions.
  5. 5. ABSCESS
  6. 6. Definition: An abscess is a cavity containing pus and surrounded by inflammed tissue, formed as a result of a localized infection. The formation of pus is termed suppuration.
  7. 7. Classification: Meng 1999 It has been classified into three diagnostic groups: Gingival abscess- Involves the marginal gingival and interdental tissues. Periodontal abscess- Is an infection located contiguous to the periodontal pocket and may result in destruction of the PDL & alveolar bone. Pericoronal abscess- Is associated with the crown of incompletely erupted tooth.
  8. 8. Gingival Abscess A localized purulent infection that involves the marginal gingiva or interdental papilla
  9. 9. Gingival Abscess Etiology Acute inflammatory response to foreign substances forced into the gingiva Clinical Features Localized swelling of marginal gingiva or papilla A red, smooth, shiny surface May be painful and appear pointed Purulent exudate may be present No previous periodontal disease
  10. 10. Treatment Treatment of gingival abscess is aimed at reversal of the acute phase and removal of the cause. 1. Topical or local anaesthesia by infiltration is administered. 2. When possible, SRP are completed to establish drainage and remove microbial deposits. 3. In acute cases, the fluctuant area is incised with a #15 scalpel blade and exudate may be expressed by gentle digital pressure.
  11. 11. 4. Any foreign material is removed. 5. The area is irrigated with warm saline water and covered with moist gauze under light pressure. 6. Once bleeding has stopped, patient is dismissed with instructions to rinse with warm saline water every 2 hrs. 7. After 24 hrs, the area is reassessed, and if resolution is sufficient, scaling not previously completed is undertaken. 8. If the lesion is large or poorly accessible, surgical access may be required.
  12. 12. Periodontal Abscess Definition: • A periodontal abscess is defined as a localized purulent infection affecting the tissues surrounding a periodontal pocket that can lead to the destruction of supporting structures (Meng 1999). • It is also known as a lateral abscess or parietal abscess. • It is the third most frequent dental emergency, representing 7–14% of all dental emergencies, and affecting 6–7‰ of all patients seen in a dental clinic. • It is typically found in patients with untreated periodontitis and in association with moderate to deep periodontal pockets. (Takei HH 2002)
  13. 13. Periodontal Abscess
  14. 14. Classification • Depending on the etiology • Periodontitis- related abscess • Non periodontitis- related abscess • Depending on the course of the lesion (Galego-Feal 1995). • Acute • Chronic • Depending on the number (Topoll et al. 1990). • Single • Multiple
  15. 15. Etiology • The existence of deep, tortuous pockets, with cul-de-sac, which eventually become isolated, may favour the formation of abscesses (Carranza 1990). • The marginal closure of a periodontal pocket, may lead to an extension of the infection into the surrounding periodontal tissues due to the pressure of the suppuration inside the closed pocket( DeWitt. 1985). • Fibrin secretions, leading to the local accumulation of pus may favour the closure of the gingival margin to the tooth surface (Galego-Feal 1995). • Changes in the composition of the microflora, bacterial virulence, or in host defenses (Kareha 1981) could also make the pocket lumen inefficient to drain the increased suppuration.
  16. 16. Clinical Features Smooth, shiny swelling of the gingiva Painful, tender to palpation Purulent exudate Increased probing depth Mobile and/or percussion sensitive Tooth usually vital
  17. 17. Treatment Administer Anesthesia Establish drainage Via sulcus is the preferred method Surgical access for debridement Incision and drainage Extraction
  18. 18. Antibiotic options AAP 2004 Antibiotic of choice: Amoxicillin, 500mg Loading dose- 1gm then 500mg tds for 3 days Reevaluation after 3 days to determine the need for continued or adjusted antibiotic therapy. Cephalexin or clindamycin can be used if the infection is not responding in 24 to 48 hours.
  19. 19. Penicillin allergy:- • Clindamycin Loading dose- 600mg then 300mg qid for 3 days. - Drug of choice in case of rapid local spread • Azithromycin ( or clarithromycin) Loading dose- 1gm then 500mg qid for 3 days • Metronidazole 200 - 400 mg tds 5-7 days
  20. 20. Pericoronal Abscess A localized purulent infection within the tissue surrounding the crown of a partially erupted tooth. Most common adjacent to mandibular third molars in young adults; usually caused by impaction of debris under the soft tissue flap
  21. 21. Pericoronal Abscess Clinical Features Operculum (soft tissue flap) Localized red, swollen tissue Area painful to touch Tissue trauma from opposing tooth common Purulent exudate, trismus, lymphadenopathy, fever, and malaise may be present
  22. 22. Pericoronal Abscess Treatment Options Debride/irrigate under pericoronal flap Tissue recontouring (removing tissue flap) Extraction of involved and/or opposing tooth Antimicrobials (local and/or systemic as needed) Culture and sensitivity Follow-up
  23. 23. ACUTE NECROTIZING ULCERATIVE GINGIVITIS
  24. 24. Necrotizing ulcerative gingivitis , necrotizing periodontitis, necrotizing stomatitis are the most severe inflammatory periodontal disorders caused by plaque bacteria. They are rapidly destructive & debilitating & represents various stages of same disease process (Horing & Cohen 1995). They are also referred to as ulceromembraneous gingivitis, necrotizing gingivostomatitis, vincent’s gingivostomatitis,& trench mouth( Pickard 1973, Johnson & Engle 1986, Horing & Cohen 1995). It is characterized by death & sloughing of gingival tissue & presents with characteristics signs & symptoms.
  25. 25. EPIDEMIOLOGY & PREVALENCE NUG often occurs in groups in an epidemic form. During world war I & II “ epidemics “ broke out among the allied troops. Epidemic like outbreaks have also occurred among civilian populations. In developing countries, the prevalence of NPD is higher than in the industrialized countries, & the disease frequently affects the children. In India, 54- 64 % of NPD cases occurred in children below 10 yrs of age.( Migliani& Sharma 1965; Pindborg et al 1996). NUG occurs at all ages, with the highest incidence reported between ages 20 & 30 yrs & ages 15 -20 yrs.
  26. 26. The disease seems to occur slightly more among HIV infected individuals. Studies among groups of HIV infected individuals have revealed prevalence of NPD between 0 & 27.7%. (Reichart et al 2003). NP was found in 1% of 200 HIV seropositive individuals (Riley et al 1992) & the prevalence may not in fact, differ from much of the general population ( Drinkard et al 1991 );This is particularly true after introduction of antiretroviral therapy.
  27. 27. ETIOLOGY It includes,  Role of microorganism  Role of host response  Predisposing factors includes 1. Local predisposing factor 2. Systemic predisposing factor
  28. 28. ROLE OF BACTERIA Plaut & Vincent introduced the concept that NUG is caused by specific bacteria ; fusiform bacillus & spirochetal organism. Loesche et al described a predominant constant flora & a variable flora associated with NUG. The constant flora is composed of prevotella intermedia, treponema sp, selenomonas sp, & fusobacterium sp. The variable flora consists of heterogeneous array of bacterial types. The bacteriologic findings have been supported by immunologic data from Chung et al. - reported increased antibody titers for spirochetes & P.intermedia in NUG patients compared with titers in those with chronic gingivitis & healthy controls.
  29. 29. Borrelia, gram positive cocci, b-hemolytic streptococci & Candida albicans have been isolated from the lesions of HIV associated NUP.(Reichart & Schiodt 1989). It has also been proposed that human cytomegalovirus may play a role in the pathogenesis of NPD. (Sabiston 1986).
  30. 30. Pathogenic potential of microorganism An important aspects in the pathogenesis of periodontitis is the capacity of the microorganism to invade the host tissues. Among the bacteria isolated from necrotizing lesions, spirochetes & fusobacterium can in fact invade the epithelium. (Heylings 1967). The spirochetes can also invade the vital connective tissue (Lisgarten 1965). The pathogenic potential is further substantiated by the fact that both fusobacterium & spirochetes can liberate endotoxins (Kristoffersen et al).
  31. 31. Gram negative bacteria liberate endotoxins in close contact with connective tissue. Endotoxins may produce tissue destruction both by direct toxic effects & indirectly by activating & modifying tissue responses of the host.(Wilton & Lehner 1980) Through a direct effect, endotoxins may lead to damage of cells & vessels. Necrosis is a prominent feature so-called Schwartzman reaction which is caused by endotoxins. Indirectly endotoxins contribute to tissue damage in several ways; They can function as antigens & elicit immune reactions. They can activate compliment directly through the alternative pathway & thereby liberate chemotoxins.
  32. 32. They can also activate macrophages, T & B lymphocytes & influence the host immune reactions by interfering with cytokines produced by these cells. Studies have shown that endotoxins can stimulate catabolic processes with degradation of both connective tissue & bone induced by the released cytokines. The extent to which such reactions contribute to the host defense or tissue damage is not yet known.
  33. 33. Fusobacterium & Spirochetes are found in moderate numbers of other oral diseases, as well as in apparently healthy mouths suggests that predisposing factors are essential to the development of ANUG. The disease has never been produced experimentally in either human beings or animals simply by oral inoculation of materials from lesion in patients with disease. (Schwartz & Grossman). King also attempted to produce disease in his own mouth by inoculation of infected material but he was unsuccessful even after traumatizing gingiva & the organism promptly disappeared. But he did show characteristic signs of ANUG however after he became ill with several colds, a short time later.
  34. 34. ROLE OF HOST RESPONSE Regardless of whether specific bacteria are implicated in the etiology of NUG, the presence of these organism is insufficient to cause the disease. The role of an impaired host response in NUG has long been recognized. It is particularly evident for HIV-infected patients that the disease is associated with diminished host resistance; among other predisposing factors, the basic mechanism may include altered host immunity. Changes in leukocyte function & the immune system have been observed.(Johnson & Engle et al)
  35. 35. NUG is not found in well nourished individuals with a fully functional immune system. All the predisposing factor for NUG is associated with immunosuppresion. Cohen et al described a depression in host defense mechanism particularly in PMN. Total leukocyte count have been found to be similar for patients & controls. Patients with NG shows marked depression in polymorphonuclear leukocyte chemotaxis & phagocytosis as compared with control individuals. Reduced proliferation of peripheral blood lymphocytes has also been found in those patients. It was also suggested that elevated levels of blood steroids may account for the reduced chemotactic & phagocytic responses.
  36. 36. LOCAL PREDISPOSING FACTORS It includes poor oral hygiene, preexisting gingivitis , injury to gingiva, & smoking It may also occur in disease free mouth, it most often occurs superimposed on preexisting chronic gingival disease & periodontal pockets. Areas of gingiva traumatized by opposing teeth in malocclusion – may predispose to NUG. Pindborg et al – 98% of his patients with NUG were smokers & that the frequency of disease increases with an increase exposure to smoke.
  37. 37. Systemic predisposing factors It includes nutritional deficiency (malnutrition), debilitating diseases, fatigue caused by chronic sleep deficiency, psychological stress, immunodeficiency, other health habits like alcohol & drug abuse.
  38. 38. MALNUTRITION Malnutrition results in lowered tissue resistance - most common public health problem affecting children who are most often affected by NPD. (Enwonwu 1985, 1994). In response to periodontal pathogens phagocytes elaborate destructive oxidants, proteinases & other factors. Periodontal damage may often occur as a result of the balance between these two factors, antioxidants & host derived anti proteinases.
  39. 39. Malnutrition is characterized by marked tissue depletion of the key antioxidant nutrients, & impaired acute phase reactions to the infections. This is due to impairment in the production & cellular action of cytokines. Malnutrition – defective mucosal integrity, hormonal imbalance. Malnutrition usually involves concomitant deficiencies of several essential macro & micronutrients, & therefore has the potential to adversely influence the prognosis of periodontal infections. (Enwonwu 1994). It also accentuates the severity of the pathologic changes when fusospirocheal complex is injected to the animals. (Smith DT et al)
  40. 40. Debilitating disease Debilitating systemic disease may predispose the patient to the development of NUG. It includes chronic disease ( eg. Syphilis, cancer), severe gastrointestinal disorders such as ulcerative colitis, blood dyscracias (anemia , leukemia) & acquired immunodeficiency syndrome. Nutritional deficiency resulting from debilitating disease may be an additional pre disposing factor. Ulceronecrotic lesions appear in the gingival margins of hamsters exposed to total body irradiation.(Mayo J et al)
  41. 41. PSYCOSOMATIC FACTORS Psychological factors appear to be important in the etiology of NUG. The disease often occur with association with stressful situation (Induction in to armed forces, examination periods, emotional disorders, patients feeling inadequate at handling life situations). Cohen – Cole et al – psychiatric disturbance and the impact of negative life events may lead to activation of hypothalamic- pituitary adrenal axis resulting in elevation of cortisol levels. This may reduce gingival microcirculation & salivary flow & enhance nutrition to prevotella intermedia, but also depresses neutrophil & lymphocyte functions which facilitate bacterial invasion & damage.(Johnson et al)
  42. 42. Significant correlation between the disease incidence & two personality traits – dominance & abasement – suggests the presence of an ANUG prone personality.(Formicola AJ et al). The mechanisms whereby psychological factors create or predispose to gingival damage have not been established, but alterations in digital & gingival capillary response suggestive of increased autonomic nervous activity have been demonstrated in patients with ANUG.
  43. 43. Smoking The relationship between tobacco usage & NPD appears to be complex. Smokers in general poorer oral hygiene than the non smokers. Smoking could lead to increased disease activity by influencing host response & tissue reactions. As examples, smokers have depressed numbers of T- helper lymphocytes, & tobacco smoke can also impair chemotaxis and phagocytosis of oral & peripheral phagocytes.( Lannan et al 1992, Selby et al 1992) Nicotine- induced secretion of epinephrine resulting in gingival vasoconstriction – possible mechanism by which smoking may influence tissue susceptibility.( Bergstrom & Preber 1986)
  44. 44. HIV infection HIV infection attacks the T- helper cells of the body, causing drastic change in the T-helper (CD4+)/T-suppressor(CD8+) ratio with severe impairment of the host resistance to infection. Depleted T- helper lymphocyte counts correlate closely with the occurrence of NG as demonstrated in the study of 390 US HIV seropositive soldiers (Thompson et al 1992). A complete absence of T cells in gingival tissue of HIV infected patients with periodontitis. (Steidley et al 1992). The lack of local immune effectors & regulatory cells in the HIV seropositive individuals could explain the characteristic & rapidly progressive nature of periodontitis in these patients.
  45. 45. Moreover, a protective effect has been encountered with antiviral treatment of the HIV infection against NPD (Tappuni & Flemming et al 2001) as well as against HIV-associated gingivitis & periodontitis. (Masouredis et al 1992).
  46. 46. Clinical features - Oral signs NG – an inflammatory destructive gingival condition, characterized by punched out crater like depressions at the crest of the interdental papillae, subsequently extending to the marginal gingiva and rarely to the attached gingiva & oral mucosa. The surface of the craters is covered by a gray pseudomembranous slough, demarcated from the remainder of the gingival mucosa by a pronounced linear erythema. In some cases the lesions are denuded of the surface pseudomembrane, exposing the gingival margin which is red, shiny, & hemorrhagic. The characteristic lesion may progressively destroy the gingiva & underlying periodontal tissues.
  47. 47. Initial punched out lesion
  48. 48. Spontaneous gingival hemorrhage or pronounced bleeding after the slight stimulation are characteristic clinical signs. A characteristic & pronounced foetor ex ore is often associated with this disease & also there is increased salivation.
  49. 49. Oral symptoms The lesion is extremely sensitive to touch, & the patient may often complains of a constant radiating, gnawing pain that is often intensified by eating spicy or hot foods & chewing. There is metallic foul taste & an excessive amount of pasty saliva.
  50. 50. Extra oral & systemic signs & symptoms In mild & moderate stages of disease Local lymphadenopathy & slight elevation in temperature. In severe cases High fever, increased pulse rate, leucocytois, loss of appetite & general lassitude. Systemic reactions are more severe in children. Insomnia, constipation, gastro-intestinal disorders, headache, & mental depression sometimes accompany the condition. In very rare cases, severe squeal such as gangrenous stomatitis & noma have been described.
  51. 51. Stages in the progress of NUG BY PINDBORG et al
  52. 52. Stages of oral necrotizing disease – by Horning & Cohen Stage 1- necrosis of the top of the interdental papilla. Stage 2- necrosis of entire papilla Stage 3- necrosis extending to the gingival margin. Stage 4- necrosis extending to the attached gingiva. Stage 5– necrosis extending to labial & buccal mucosa. Stage 6- necrosis exposing alveolar bone. Stage 7– necrosis perforating skin of cheek.
  53. 53. The lesion are seldom associated with deep pocket formation, - extensive gingival necrosis coincides with rapid loss of crestal alveolar bone. The gingival necrosis develops rapidly & within a few days the involved papillae is often separated into one facial & one lingual portion with an interposed necrotic depression. The central necrosis produces considerable tissue destruction & regular crater is formed. At this stage of disease, the disease process usually involves the periodontal ligament & alveolar bone.(NECROTIZING PERIODONTITIS)
  54. 54. Further progression of disease leads to involvement of underlying bone resulting in sequestrum formation (necrosis of small or large parts of alveolar bone). Also the necrotic process progress beyond the mucogingival junction , the condition is referred to as Necrotizing Stomatitis.
  55. 55. Necrotizing Ulcerative Periodontitis
  56. 56. Necrotizing stomatitis NOMA- Cancrum oris
  57. 57. HISTOPATOLOGICAL FEATURE Histopathologically, NG lesions is characterized by ulceration with necrosis of epithelium & superficial layers of the connective tissue & an non specific inflammatory reaction. The histological findings demonstrate the formation of regular layers with certain characteristics (Lisgarten 1965) but there may be variations in regularity. The surface epithelium is destroyed & replaced by a meshwork of fibrin, necrotic epithelium, PMNs & various types of microorganism. This appears clinically as the surface pseudomembrane. Below this necrotic pseudomembrane, the epithelium is edematous, & the individual cells exhibit varying degrees of hydropic degeneration.
  58. 58. The underlying connective tissue is extremely hyperemic with numerous engorged capillaries & dense infiltration of PMNs. This acutely inflamed zone appears clinically as the linear erythema. Numerous plasma cells may appear in the periphery of the infiltrate. This is interpreted as an area of established chronic gingivitis on which acute lesion is superimposed.
  59. 59. RELATION OF BACTERIA TO THE CHARACTERISTIC LESION The light microscope & the electron microscope have been used to study the relationship of bacteria to the characteristic lesion of ANUG. LISGARTEN described the following four zones which blend with each other & may not all be present in every case; Zone1 – bacterial zone Zone 2 – neutrophil rich zone Zone 3 – necrotic zone Zone 4 – zone of spirochetal infiltration
  60. 60. Electron micrograph demonstrating phagocytosing (N)neutrophil close to the surface of a sequestrum, numerous spirochetes and rods.
  61. 61. DIAGNOSIS The diagnosis of NG, NP, NS is based on clinical findings as described above. The histopathology of the necrotizing disease is not pathognomonic of NG & biopsy is not certainly indicated. Bacterial studies are useful in the differential diagnosis of NUG & specific infections of oral cavity.
  62. 62. Diagnostic essentials for NUG Lesions are painful. Lesions are gingival ulcers, punched out crater like of interdental papilla & may involve marginal gingiva. Non essential clinical features of NUG the absence which does not preclude the diagnosis of NUG Pseudomembrane of sloughed necrotic debris & bacteria covering the ulcerated area. Foetor ex ore. Fever, malaise & lymphadenopathy
  63. 63. Differential diagnosis Herpetic gingivostomatitis Desquamative gingivitis Streptococcal gingivostomatitis Apthous stomatitis Candidiasis Agranulocytosis Gonococcal gingivostomatitis Tuberculous gingival lesion
  64. 64. Important characteristics for differential diagnosis between NPD & PHG NPD PHG Etiology Bacteria Herpes simplex virus Age 15-30 Frequently children Site Interdental papilla. Rarely outside the gingiva Gingiva and entire oral mucosa Symptoms •Ulcerations and necrotic tissue and a yellowish –white plaque •Fetor ex ore •Moderate Fever may occur •Multiple vesicles which disrupt, leaving small round fibrin covered ulcerations •Fetor ex ore •Fever Duration 1-2 days if treated 1-2weeks Contagious - + Immunity - Partial Healing Destruction of periodontal tissue remains No permanent destruction
  65. 65. TREATMENT The treatment of necrotizing periodontal disease is divided into two phases, 1)acute phase treatment 2)maintenance phase treatment ACUTE PHASE TREATMENT The aim is to eliminate the disease activity as manifest by ongoing tissue necrosis developing laterally & apically. It is also to avoid pain & general discomfort which may severely compromise food intake.
  66. 66. FIRST VISIT General examination of the patient The oral cavity is examined for the characteristic feature of NUG, its distribution,& possible involvement of oropharyngeal region. Oral hygiene is evaluated with special attention to the presence of pericoronal flaps, periodontal pockets & local factors. Treatment during initial visits includes, It is mainly confined to the acutely involved areas After application of topical anesthetics, the pseudomembrane & non attached surface debris is removed using a moistened cotton pellet.
  67. 67. After the area is cleansed with warm water supragingival calculus is removed using ultrasonic scalers. Subgingival scaling & curettage is contraindicated at this time. Procedures such as extractions or periodontal surgery are postponed until the patient has been symptom free for 4 weeks, to minimize the likelihood of exacerbating the acute symptoms. Patients with moderate or severe NUG & local lymphadenopathy or systemic signs or symptoms are placed on an antibiotic regimen of amoxicillin, 500mg orally every 6 hrs for 10 days. Other antibiotics such as erythromycin (500mg every 6 hrs) or metronidazole (500mg twice daily for 7 days) are used.
  68. 68. Metronidazole three times daily has been found effective against spirochetes & appears to be the first choice treatment of NPD. (Loesche et al). The adjunctive use of metronidazole in HIV associated NPD is reported to be extremely effective in reducing acute pain & promoting rapid healing.(Scully et al). Topical application of antibiotics is not indicated in the treatment of NPD because intralesional bacteria are frequent &topical application does not results in sufficient intralesional concentration of antibiotics.
  69. 69. Hydrogen peroxide & other oxygen releasing agents also have a long standing tradition in the treatment of NPD. Hydrogen peroxide (3%) is used for debridement in necrotic areas & as a mouth rinse (equal portions 3% H2O2 & warm water). Favorable effects of hydrogen peroxide may be due to mechanical cleaning,& the influence on anaerobic bacterial flora of the liberated oxygen. (Macphee & Cowley 1981). Further adjunctive local therapy of NPD showed a more rapid clinical restitution with less periodontal destruction than in a group without oxygen therapy. (Gaggl et al 2006)
  70. 70. Twice daily rinsing with a 0.2% chlorhexidine solution is a very effective adjunct to reduce plaque formation, when particularly tooth brushing is not performed. It also assists self performed oral hygiene during the first weeks of treatment. Appropriate treatment alleviates symptoms with in few days.(5 days) Second visit Systematic subgingival scaling should be continued with increasing intensity as the symptoms subside. Correction of restoration margins & polishing of restorations & root surfaces should be completed after healing of ulcers. When ulcerated areas are healed local treatment is supplemented with oral hygiene & patient motivation.
  71. 71. Supportive systemic treatment In addition to systemic antibiotics, supportive treatment consists of copious fluid consumption & administration of analgesics for relief of pain. Bed rest is necessary for the patients with systemic complication such as high fever, malaise, anorexia & general debility.
  72. 72. Nutritional supplements The rationale for the nutritional supplements in the treatment of ANUG is based on the following; 1) lesions resembling those of the ANUG have been produced experimentally in animals with nutritional deficiencies. 2) isolated clinical studies report fewer recurrences when local treatment of ANUG is supplemented with vitamin B & vitamin C. (Linghorne WJ et al) And hence nutritional supplements may be indicated along with local treatment to ward off deficiencies of these vitamins.
  73. 73. MAINTENANCE PHASE TREATMENT On further visits, When the acute phase treatment has been completed, necrosis & acute symptoms in NPD have disappeared. The formerly necrotic areas are healed & the gingival craters are reduced in size, although some defects usually persists. Bacterial plaque accumulates & therefore may predispose to recurrences of NPD or to further destruction because of a persisting chronic inflammatory process or both. These sites therefore requires surgical correction.
  74. 74. Shallow craters can be removed by simple gingivectomy, while the elimination of deep defects may require flap surgery. Treatment of NG is not completed until all gingival defects have been eliminated & optimal conditions for future plaque control have been established. Elimination of predisposing factors is also very important to prevent recurrences.
  75. 75. Gingival changes with healing The characteristic lesion of NUG undergoes the following changes in the course of healing in response to treatment, Removal of pseudomembrane exposes the underlying red haemorrhagic crater like depression in the gingiva. In the next stage, the bulk & redness of the crater margins are reduced. Followed by the early signs of restoration of normal gingival contour & colour. In the final stage the normal gingival consistency, surface texture, & contour may be restored. Portion of the root exposed by the acute disease may be covered by healthy gingiva.
  76. 76. Persistent or recurrent cases Adequate local therapy with optimal home care will resolve most cases of NUG. If it persists despite therapy or recurs , the patient should be revaluated with the focus on the following factors, Reassessment of differential diagnosis to rule out the disease that resembles NUG. Underlying systemic disease that cause immunosuppresion. Inadequate local therapy. Inadequate compliance
  77. 77. PRIMARY HERPETIC GINGIVOSTOMATITIS
  78. 78. INTRODUCTION Herpetic gingivostomatitis is acute infection that can involve the gingiva, other oral tissues, the lips, & occasionally the face circumorally. Primary infection with herpes virus leads to acute herpetic gingivostomatitis. The primary attack is believed to confer immunity. It is caused by herpes simplex virus type-1 (HSV-1). It occurs most often in the children younger than 6 years of age, but it is also seen in adolescents & adults. It occurs with equal frequency in male & female patients. In most patients, the primary infection is asymptomatic.
  79. 79. HERPES SIMPLEX VIRUS Herpes simplex Virus is a DNA virus & is a member of the human herpes virus family (HHV) family known as herpetoviridae. TYPES  Type 1 – HSV 1 or HHV 2  Type 2 – HSV 2 or HHV 2 Other members of HHV family includes  Varicella zoster virus ( HHV 3)  Epstein barr virus ( HHV 4)  Cytomegalo virus ( HHV 5)  Others – HHV 6, HHV 7, HHV 8
  80. 80. Humans are the only natural reservoirs and all the HHVs have the ability to reside for life within the infected host. After the initial infection variable periods of latency & reactivation with viral shedding are seen. The two types of HSV are structurally similar structurally but different antigenically. HSV -1 is spread predominantly through infected saliva or active perioral lesions. HSV-1 - responsible for oral, facial, and ocular lesions.
  81. 81. Clinically evident infections with HSV -1 exhibit two patterns. The initial exposure to an individual without antibodies to the virus is called the primary infection. Occurs at an young age & often is asymptomatic. The virus is then taken up by the sensory nerves & transported to the associated sensory or less frequently, the autonomic ganglia. With oral HSV 1 infection the trigeminal ganglion is colonized and the virus remains at this site in a latent state. The viruses uses the axons of the sensory neurons to travel back & froth to the peripheral skin or mucosa.
  82. 82. SECONDARY , RECURRENT OR RECRUDESENT HSV 1 INFECTION occurs with reactivation of the virus although many patients may show only asymptomatic viral shedding in the saliva. Symptomatic recurrences are fairly common & affect the epithelium fairly supplied by the sensory ganglion. Spread to an uninfected host can occur easily during periods of asymptomatic viral shedding or from symptomatic active lesions. Numerous conditions such as old age, ultraviolet light, emotional stress, pregnancy, allergy, trauma, respiratory illness, systemic disease or malignancy are associated with reactivation of virus.
  83. 83. Recurrent Oral Herpes
  84. 84. HSV does not survive in the external environment & almost all the primary infections occur from contact with an infected person who is releasing the virus. The usual incubation period is 3 to 9 days. HSV -1 is acquired from contact with contaminated saliva or active perioral lesions, poor hygiene promote exposure.
  85. 85. CLINICAL FEATURES
  86. 86. Most cases of acute herpetic gingivostomatitis arise between the ages of 6 months & 5 years. The onset is abrupt & accompanied by anterior cervical lymphadenopathy, fever, anorexia, irritability, and sore mouth lesions. Initially the affected mucosa develops numerous pinhead vesicles, which rapidly collapse to form numerous small red lesions. These initial lesions enlarge slightly & develop central areas of ulceration which are covered by yellow fibrin. Both the movable & attached oral mucosa can be affected,& the number of lesions is highly variable. In all the cases the gingiva is enlarged, painful, & extremely erythematous.
  87. 87. In addition the affected gingiva often exhibits distinctive punched out erosions along the mid facial free gingival margins. An important diagnostic criteria in this disease is the appearance of a generalized acute marginal gingivitis. The entire gingiva is edematous & inflamed. Several small gingival ulcers are also present. There is inflammation in the posterior pharynx & the submandibular & cervical lymph nodes are enlarged & tender. Satellite vesicles of the perioral skin are fairly common. Mild cases usually resolve within 5 to 7 days; severe cases may extend to 2 weeks.
  88. 88. Primary HSV in other wise healthy children is a self limiting disease. The fever ordinarily disappears within 3 or 4 days & the lesion begin healing in a week to 10 days, although to continue to be present in the saliva for up to a 10 month after the onset of disease.
  89. 89. Secondary herpes labialis A patient who has suffered an attack of HGS carries humoral & possibly cellular antibodies throughout life. After infection has taken place some virus survives in a latent stage in the nerve ganglion & may on provocation produce a recurrence. (secondary herpes labialis, fever blister, cold sore) The fever blister is a single vesicle or a group of vesicles on the vermilion border of the lip before an eruption occurs there is often a prodromal period of burning & tingling in the area. The blisters break after a few days & form a crust. The lesion heals after about 2 weeks.
  90. 90. Recurrent herpes labialis & recurrent intraoral herpes
  91. 91. Recurrences can also affect the oral mucosa. In the immunocompetent patient, involvement is almost always limited to keratinized mucosa, which is bound to bone (attached gingiva and hard palate). The lesion begins as 1 to 3 mm vesicles, which rapidly collapse to form a cluster of erythematous macules. The damaged epithelium is lost & a central area of ulceration develops. Healing takes place within 7 to 10 days.
  92. 92. TRANSFER OF INFECTIONS Transfer of the herpes virus may be by direct contact or by contact with contaminated materials or surfaces. The dental professional is at risk & an infection occasionally affects on the hand or finger ( HERPETIC WHITLOW). From such sites the virus may be transferred to the patients. Each infected individual serves as a permanent carrier who is intermittently infectious.
  93. 93. HISTOPATHOLOGICAL FEATURE The virus exerts its main effects on the epithelial cells. infected epithelial cells exhibits acantholysis , nuclear clearing,& nuclear enlargement – ballooning degeneration. The acantholytic epithelial cells are termed as TZANCK CELLS. There is presence of intranuclear inclusion bodies – lipschutz bodies. Nucleolar fragmentation occurs with the condensation of chromatin around the periphery of the nucleus. -peri inclusion halo.
  94. 94. Intracellular edema leads to the development of intraepithelial vesicles. The vesicle ruptures & the mucosal lesion demonstrate a surface fibrinopurulent membrane. There is secondary infiltration by inflammatory cells in subadjacent connective tissue.
  95. 95. DIAGNOSIS Patients are easily diagnosed - who present with atypical clinical picture of generalized symptoms followed by an eruption of oral vesicles, round shallow symmetrical oral ulcers & acute marginal gingivitis & who do not have a history of recurrent herpes. Materials may be obtained from the lesions & submitted to the laboratory for confirmatory tests, including virus culture and immunologic tests using monoclonal antibodies or DNA hybridization techniques.
  96. 96. Most commonly used diagnostic procedures - cytological smear & tissue biopsy Serological tests for HSV antibodies are positive 4 to 8 days after initial exposure. These antibody titers are useful in documenting past exposure & are used primarily in epidemiologic studies.
  97. 97. DIFFERENTIAL DIAGNOSIS It includes Necrotizing ulcerative gingivitis Erythema multiformae Stevens – Johnson syndrome Bullous lichen planus Desquamative gingivitis Lesions of recurrent aphthous stomatitis
  98. 98. TREATMENT Treatment of primary HSV infection is usually palliative. Milder cases can be managed by supportive care only, since primary HSV in otherwise healthy individuals is a self limiting disease. It is important to instruct patient to avoid contact with active lesions to prevent the spread to other sites and people. Systemic use of systemic antiviral drugs is indicated in severe cases of primary HSV , recurrent disease & in immunocompromised patients.
  99. 99. ANTIVIRAL THERAPY Amir et al demonstrated that antiviral therapy with 15mg/kg of an acyclovir suspension given five times daily for 7 days substantially changes the course of disease without significant side effects. Acyclovir has shown to decrease symptoms of primary HSV infection in children, including days of fever & viral shedding. Newer antiherpes drugs are available, including valacyclovir & famciclovir. The newer drugs have increased bioavailability allowing effective treatment with fewer daily doses. Recommended doses Acyclovir – 200mg 5 times daily for 10 days. Valacyclovir – 100mg 2 times daily for 10 days.
  100. 100. Studies comparing topical antiviral medications for treating recurrent herpes labialis have been published. Topical pencyclovir reduces the duration & pain of RHL by 1 to 2 days. Acyclovir as well as N –Docosanol cream also available for topical use. Topical acyclovir has been reported to decrease duration of RHL lesions by 12 hrs & found to be more effective than N-docosanol in treating RHL. Immunosuppressed patients with HSV infection respond well to acyclovir administered orally or intravenously. Foscarnet, another antiviral drug has been effective therapy for these patients.
  101. 101. PERICORONITIS
  102. 102. INTRODUCTION A healthy ,fully erupted tooth is surrounded by a gingival tissue that typically extends not more than 2 to 3mm coronally. For a variety of anatomical reasons- partial eruption, malposition, the immediate proximity of the ramus – the crowns of the third molars & occasionally other teeth may covered with gingiva & sometimes mucosa. The potential space between the crown & the soft tissue is of considerable depth & volume. A diverse & extensive microflora colonizes these pockets & gingival inflammation is almost always present.
  103. 103. These sites may acutely infected & may produce symptoms then they are defined as Pericoronitis. It was first described by GUNNELL in1844. It is defined as “ an inflammatory condition of the gingiva & other supporting tissues that surround the crown of an incompletely or completely erupted tooth, especially distal tooth in the arch.( kay 1966) It is an inflammation of gingiva & contiguous tissues about crown of an incompletely erupted tooth. (Orban)
  104. 104. Common sites of involvement In decreasing order of frequency Mandibular third molars Mandibular second molars Mandibular first molars Maxillary third molars.
  105. 105. RISK FACTORS LOCAL FACTORS includes Impacted third molars, more with vertical & distoagular impactions (taehan, chikkwa, uesa) Third molars favoring deep distal or distobuccal pocket formation. Opposing teeth impinging on operculum. Poor oral hygiene SYSTEMIC FACTORS includes Upper respiratory tract infections Tonsillitis Emotional stress Smoking General debilitating disease Chronic fatigue
  106. 106. AETIOPATHOGENESIS MULTIFACTORIAL .it includes Incomplete eruption due to anatomical limitation. Food impaction & poor oral hygiene. Oral microbiota
  107. 107. The occlusal surface of an involved tooth may be partly covered by a flap of tissue, the operculum, which exists during the eruption of the tooth & may persist afterward. The operculum is ideal area for accumulation of food debris and bacterial growth, since the performance of adequate oral hygiene in this area is difficult. It is more vulnerable for irritation & is often directly traumatized when it is caught between the crown that it covers & the antagonist tooth during closure. These factors predisposes to acute infection of the pericoronal tissue.
  108. 108. RISK PREDICTORS OF PREICORONITIS  Based on the criteria; - Vertical or distal tipping of third molars - Follicular space more than 3mm, the incidence of getting pericoronitis is 44 times more. (ANDREASON)
  109. 109. MICROBIOLOGICAL ETIOLOGY Organism implicated includes Streptococcus viridans Spirochetes & fusobacteria Staphylococcus Prevotella sp. Bacteriodes capnocytophaga
  110. 110. CLINICAL FEATURES Based on the duration , pericoronitis may be Acute Sub- acute Chronic Also there is an acute exacerbation in chronically inflamed pericoronal tissue.
  111. 111. Acute pericoronitis  It is identified by varying degrees of inflammatory involvement of the pericoronal flap & adjacent structures as well as by systemic complications. The inflammatory fluid & cellular exudate increases the bulk of the flap, which may interferes with complete closure of the jaw & traumatized by contact with the opposing jaw. There is red, swollen, suppurating lesion that is tender, with severe throbbing intermittent pain, exaggerated by chewing & interfering with sleep. Pain radiates to ear, throat & floor of mouth. Foul taste, halitosis, & inability to close the mouth.
  112. 112. Swelling of the cheek in the angle of the jaw & lymphadenitis are common. Systemic complications includes, fever, malaise, leucocytois , increased pulse & respiratory rate. Submandibular lymph nodes may be enlarged & tender on palpation.
  113. 113. Sub acute stage Continuous dull ache, radiates infrequently Stiffness of jaws, intraoral swelling, unpleasant taste. Causes less systemic upset Trismus might be present Chronic stage Dull pain or mild discomfort lasting for only a day or so, interspersed with remissions lasting for several months. Unpleasant taste
  114. 114. DIAGNOSIS Can be made by Careful history taking Clinical examination Radiographic examination.
  115. 115. TREATMENT  Treatment of pericoronitis focuses on infection control.  It depends on initial assessment of two issues. 1. The severity of infection & the extent to which it has disseminated from the primary site. 2. The relative importance of the affected tooth & whether the pericoronal tissue can be returned to & maintained in healthy state.
  116. 116. Well localized mild to moderate pericoronitis affecting a tooth that is to be retained is managed conservatively. Consists of debridement & drainage of the pocket by gentle curettage & external pressure. During & after curettage the pocket should be irrigated with sterile saline solution. Irrigation can also be done with antimicrobial solution such as 10%providone iodine. In case of fluctuant abscess drainage should be accomplished by incision. The patient should be instructed to rinse the area with warm water or saline solution at frequent intervals until symptoms subside. Post treatment monitoring is necessary to ensure the resolution of the acute phase.
  117. 117. When signs & symptoms have regressed the need for corrective surgery should be considered. Resection of some or all pericoronal tissue (operculectomy) depending on tooth position in the jaw & soft tissue relationships, reduces the chances of recurrent infection. Operculectomy – surgical removal of operculum. It can be done using hand instruments, or electrosurgery or LASER.
  118. 118. Operculectomy – using hand instruments
  119. 119. Operculectomy using electrosurgical scalpel or radiosurgical loop.
  120. 120. If an opposing third molar is hyper erupted or will require removal in the near future & is in contact with the inflamed tissue over the third molar, it can be removed to help decrease pain & hasten recovery from pericoronitis. If the affected tooth is non functional or considered unsalvageable because of malposition or other reasons extraction is usually appropriate. If pericoronitis is localized with no evidence of abscess, extraction may be proceeded or delayed until the acute inflammation is subsided.
  121. 121. If pus is present , the drainage should be accomplished & resolution of acute phase before elective extraction. If immediate extraction is necessary, perioperative and systemic antimicrobial therapy is used. Most severe pericoronitis with evidence of regional dissemination should be treated as described previously. In addition, antimicrobial chemotherapy should be started immediately. Close monitoring of the outcomes is necessary. Extraction should be postponed until the infection shows definite signs of localization or has completely resolved.
  122. 122. ANTIMICROBIALS- IN TREATMENT OF PERICORONITIS Commonly used antibiotics includes, Amoxicillin 250-500mg Metronidazole 200-400mg Alternative drugs includes, Ampicillin 250-500mg Erythromycin 250-500mg Tetracycline 250-500mg Doxycyline 200mg once daily for the first day followed by 100mg twice daily
  123. 123. SEQULAE The involvement may be localized in the form of a pericoronal abscess. It may spread posteriorly into oropharngeal area & medially to the base of the tongue, making it difficult for the patient to swallow. Depending on the severity & extent of the infection there is involvement of submaxillary, posterior cervical, & the retropharyngeal lymph nodes. Untreated pericoronitis may develop into ANUG. Since pericoronal flaps are one of the primary incubation zones.
  124. 124. COMPLICATIONS LOCALIZED Cyst formation (craig) Sinus & fistula formation Root resorption of second molar (kielley & kay) LOCAL Migratory abscess of buccal sulcus Buccal space infection Peritonsillar abscess Retropharyngeal & submandibular space infection.
  125. 125. SERIOUS LIFE- THREATENING COMPLICATION Ludwig’s angina Acute meningitis Cavernous sinus thrombosis These complications are infrequent but potent squeal of acute pericoronitis.
  126. 126. Other acute infections of bacterial origin- in gingiva It includes, Infection with Neisseria gonorrhea (Scully et al 1995) Treponema pallidum ( Ramirez –Amador et al 1996) Streptococci, mycobacterium chelonae (Pedersson et al 1989) or other micro organism.
  127. 127. CLINICAL FEATURES STREPTOCOCCAL GINGIVOSTOMATITIS It is a rare condition characterized by a diffuse erythema of the posterior areas of the oral mucosa, sometimes including the gingiva. Necrosis of the gingival margin is not seen & also there is no notably fetid odor.
  128. 128. GONOCOCCAL STOMATITIS The oral mucosa is covered with a grayish membrane that sloughs off in areas to expose an underlying bleeding area. It is most common in newborns & is caused by transmission of infection from the maternal passages & in adults it results from direct contact.
  129. 129. Biopsy supplemented by microbiologic examination reveals the background of the lesions. Once diagnosed, it is then treated with appropriate antimicrobials & by conventional means.
  130. 130. REFERENCES  CARRANZA’S CLINICAL PERIODONTOLOGTY  CLINICALPERIODONTOLOGY & IMPLANT DENTISTRY –JAN LINDHE  PERIODONTAL & GINGIVAL HEALTH & DISEASE  DECISION MAKING IN PERIODONTOLOGY - WALTER B. HALL  PERIODONTICS – GRANT  PERIODONTICS- ROSE & MALLEY  ORAL & MAXILLOFACIAL PATHOLOGY – ALLEN  TEXT BOOK OF ORAL PATHOLOGY - SHAFER  BURKET’S ORAL MEDICINE  ORAL & MAXILLOFACIAL INFECTIONS – TOPAZIAN.  ORAL & MAXILLOFACIAL SURGERY – HARRY ARCHER
  131. 131.  OUTLINE OF PERIODONTICS – MANSON & ELLEY  PERIODONTOLOGY 2OOO – 2002 VOL 30.  THE DENTAL CLINICS OF NORTH AMERICA – 2005 – 49, 15-29.  THE PERIODONTAL ABSCESS: A REVIEW HERRERA D, ROLDA´N S, SANZ M: JOURNAL OF CLINICAL PERIODONTOLOGY2000  PERIODONTAL ABSCESS: HUAN XIN MENG : ANNALS OF PERIODONTOLOGY 1999  DIAGNOSIS OF ACUTE PERIODONTAL LESIONS ESMONDE F CORBETT 2004 PERIODONTOLGY 2000
  132. 132. Thank YOU

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