Acute gingival infections PERIO ppt

I.A.AYISHA TALAT
BDS
FINAL YEAR SEM2

1. GOOD MORNING I.A.AYISHA TALAT

2. ACUTE GINGIVAL INFECTIONS 1. ANUG 2. Primary herpetic gingivostomatitis 3. Pericoronitis acute lesions is of sudden onset and short duration and is painful. They are manifested with severe pain along with systemic manifestations . Thus these lesions must be treted at earliest with a proper treatment protocol.

3. Acute Necrotizing Ulcerative Gingivitis Microbial disease of the gingiva in context of an impaired host response and is characterized by necrosis and sloughing of the gingival tissue. Vincents infections, acute ulceromembranous gingivitis, trench mouth, ulcerative gingivitis, Vincents stomatitis, plaut Vincent stomatitis, stomatitis ulcerosa, fedid stomatitis, fusospirillary gingivitis and putrid stomatitis.

4. HISTORY In 4th century BC Xenophon mentioned that Greek soldiers were affected with “sore mouth” and “foul smelling breath”. In 1778 John Hunter described the clinical features and differentiation of ANUG with scury and chronic destructive periodontal disease. Occured in epidemic form in the french army in 19th century. In 1886 Hersch german pathologist said that the features were associated with lymphadenopathy, fever, malaise, hypersalivation. In 1890 Plaut and Vincent describes the disease was originated to Fusiform bacilli and Spirochetes.

5. CLINICAL FEATURES Acute disease and can undergo diminution in severity without treatment leading to subacute stage. Involve single or group of teeth and can cause tissue destruction involving periodontal attachment apparatus in severe immunosuppression patients. When bone loss occurs the condition is called as necrotizing ulcerative periodontitis ( NUP )

6. ETIOLOGY ROLE OF BACTERIA : Plaut 1894 and Vincent 1896 introduced the concept NUG is caused by specific bacteria namely fusiform bacillus and Spirochete. Rosebury and co described a fusospiral complex consisting of T.macrodentium, intermediate Spirochetes, vibrios, fusiform bacilli, filamentous organisms to several Borrelia species. Loesche and co described a constant flora and a variable flora. Treatment with METRONIDAZOLE reduced Treponema species, prevotella intermedia and fusobacterium.

7. 2.ROLE OF HOST RESPONSE : Presence of organisms insufficient to cause disease. Insufficient host response. Seen in immunosuppressed patients. NUG patients displayed depression in leukocyte chemotaxis and phagocytosis Leads to immunodeficiency related to nutritional deficiencies, fatigue, health habits such as alcohol or drug abuse. Thus specific cause of NUG has not been established but complex bacterial organisms and requires underlying tissue changes to facilitate pathogenic activity of bacteria. 3.LOCAL PREDISPOSING FACTORS : Pre existing gingivitis, injury to gingiva (malocclusions) Smoking Pre existing chronic periodontitis, periodontal flaps

8. 4.SYSTEMIC FACTORS : Nutritional deficiencies dimishes immune response and alters the periodontal structures making it more susceptible. Debilitating diseases such as chronic disease (syphilis, cancer), GIT disorders, blood dyscrasias, AIDS. Stress ( Hypothalamus-pituitary-adrenal axis activation resulting in cortisol secretion and decrease in immune response. Increased level of cortisols and catecholamines leads to reduced gingival microbes and salivary flow which enhanced nutrition to P.intermedia. Decrease in neutrophils and lymphocytes functions lead to bacterial invasion and tissue damage.

9. ORAL SIGNS AND SYMPTOMS Punched out craterlike depression at the crest of the interdental papilla. Can extend into marginal and attached gingiva and oral mucosa. Surface of crater is covered by gray pseudomembranous slough demarcated from linear erythema. Removing slough exposes red hemorrhagic shiny surface which bleeds easily. Sensitive to touch, radiating gnawing pain intensified by eating spicy or got food and chewing.

10. Metallic foul taste and pasty saliva. Usually ambulatory Local lymphadenopathy, increase temperature, high fever, increase pulse rate, leukocytosis, loss of appetite, insomnia,constipation,headache,depression. Clinical course :

11. BACTERIA ~ANUG

12. TREATMENT: Alleviate acute symptoms by reducing microbial load and removalmof necrotic tissues. Treatment of chroic disease either underlying the acute involvement or elsewhere in the oral cavity. Alleviate generalized symptoms such as fever and malaise. Correction of the systemic conditions that contribute to initiation or progrssion.

13. Primary Herpetic Gingivostomatitis an infection of the oral cavity caused by HSV Type 1. Infants and children <6yrs of age. Males = Females Asymptomatic infections. PRIMARY INFECTION : Virus ascends through the sensory or autonomic nerves and persists in the ganglia that innervates the site as a latent HSV . SECONDARY INFECTION : Sunlight, trauma, fever, stress which are månifested as H.labialis, H.stomatitis, H.genitalis etc.

14. ORAL SIGNS AND SYMPTOMS: Diffuse erythematous shiny involvement of gingiva and adjacent oral mucosa. Edema and gingival bleeding. Dicrete spherical grey vesicles. Rupture of vesicles and formation of ulcers after 24hrs. Ulcer - small, painful,red, elevated, halo like margin with depressed yellowish grey white central portion. Widely spread or clustered Heals within 7- 10 days with no scarring. Soreness, difficulty in eating,drinking, irritability and refuse to take food in infants.

15. TREATMENT:

16. Pericoronitis Inflammation of the gingiva in relation to the crown of an incompletly erupted tooth. Most often in the mandibular third molar area. Acute, subacute, chronic.

17. CLINICAL FEATURES : Operculum - The space between crown of the tooth and the overlying gongival flap is an ideal area for the accumulation of food debris and bacterial growth. Gingival flap is often chronically inflamed infected and ulcerated and exacerbated by trauma, occlusion or foreign body trapped in the space. Acute pericoronitis is identified by inflammatory involvement of flap and adjacent structures as well as systemic complications.

18. Red, swollen, suppurating lesions that is tender with radiating pain to ear, throat, floor of mouth. Patient becomes uncomfortable due to pain, foul taste, inability to close jaws, swelling in cheek, lymphadenitis, trismus, fever, malaise, leukocytosis. Pericoronal abscess Peritonsillar abscess sequelae of acute Cellulitis pericoronitis Ludwigs angina Complications:

19. TREATMENT: