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Acute periodontal condition means a condition that affect oral cavity such as gingiva and mucosa membrane which are associated with pain. 1) Abscess of periodontium (periapical,gingival,periodontal)

This is example of gingival abscess due to foreign body infection inside the periodontal sulcus this sometimes cause the injury of epithelium , area becomes good condition for bacteria accumulation and then swelling which is usually localize to marginal gingival and interdental papilla. Etiology: acute inflammatory response to foreign substances forced into gingiva sulcus/interdental papilla Clinical features: localize swelling of marginal gingival or interdental papilla,red smooth shiny surface bcs filled by fluid,may be painful,area is warmer than adjacent ts,appear pointed,purulent exudate may be present,no previous periodontal dz. Tx: eliminate foriegn body from tissue,drainaigepus through sulcus by probe or light scaling (make sure the area is clean, no foreign body or calculus there. Normally no complication. Then follow up after 24-48 hours. Periodontal abcess more advance because involve periodontal ligament and connective ts deeper than marginal gingiva and interdental papilla. It is a localize purulent infection within the ts adjacent to periodontal pocket that may lead to destruction of PDL and alveolar bone.There is lodgement of calculus or foreign body then

inflammation takes place, and no way for the fluid to escape, so they accumulate in periodontal ts to form abcess. Usually pre-existing chronic periodontitis present.

Abcess follow path of weakest structure for drainage. It extend to periodontal ts and periodontal attachment so its normally destroyed in these areas. Most of the cases can be treated and condition is reversible. Factors associated with abscess formation: --Occlusion of pocket orifice--We need to be careful during root planing and scaling, clean the abscess in periodontal pocket by flushing it because if calculus is dislodged from root surface but inside the pocket , epithelium has tendency to close the orifice of pocket during healing. So therell be occluding calculus forming abscess in sealed portion of the pocket. --It involve furcation area because difficult instrumentation / scaling at that area so pieces of calculus/foreign body give rise to periodontal abscess --Systemic antibiotic therapy (allow overgrowth of resistant bacteria)in long term antibiotic therapy for chronic dz. --Diabetes melitus: Pt is more tendency to periodontal abscess and generally more prone to periodontal dz and periodontitis. Clinical features: smooth, shiny swelling of gingiva (extend until keratinized gingiva),painful,tender to percussion, purulent exudate, increasing probing depth, mobile in severe case/percussion sensitive,tooth usually vital because tooth not been treated endodontically but if tooth non vital,it is due to perio lesion is periapical abscess.

Tx: --Anesthesia --Drainage ::via sulcus is prefered method ::surgical access for debridement by sharp scaler ::incision and drainage by scalpel ::extraction-sometime the extraction is solution ,but sometime we dont do extraction for treatment of periodontal abcess but if tooth is indicated for extraction are has advance periodontal destruction and periodontal abscess which is caused by long standing periodontal dz. --Limited occlusal adjustment :: occlusal trauma --Antimicrobials :: if condition is associate with systemic,fever,severe headache but not the first line of treatment --Culture and sensitivity :: done in immunocompromised pt ,but it is uncommon because time and money consuming to specify the bacteria causing bacteria invlove to give direct antibiotic to make sure infecxtion is eradicated. --Antibiotics :: Indicated when there is fever,malaise,lymphadenopathy,or inability to drainage. Penicillin and amoxicilin (w/o allergy) ,azithromycin,clindamycin (if allergic to penicillin). Alter therapy if indicated by culture/sensitivity. A periodontal evaluation following resolution of acute symptoms is essential. Pericoronal abscess most commonly known as pericoronitis which is localized purulent infection within ts surrounding the crown of partially erupted tooth. Most common adjacent to mandibular

3rd molar in young adults; usually caused by impaction of debris under soft ts flap. Normally localized or local spreading. Most commonly tooth affected is lower 3rd molar esp upper 3rd molar is fully erupting, and on mastication the occlusal force is causes the upper 3rd molar to biting on soft ts covering the lower 3rd molar.

The example of lower 3rd molar of partially erupting. The impaction of food debris and bacteria around the developing crown causes the swelling. Clinical features: Very painful when touch, it spread to pharyngeal space causing limited mouth opening, severe pain on mastication, fever, headache, around the operculum, red swollen ts, ts trauma from opposing tooth common,lymphadenopathy,,malaise. Tx: Debride/irrigate under pericoronal flap, ts recontouring (remove ts flap), extraction of involve opposing tooth, antimicrobials (local and systemic as needed),culture and sensitivity,follow up In case of severe, pt need antibiotic immediately to decrease syptoms and minimize the bacteria. Debride the area by hydrogen peroxide or chlorhexidine. After infection is reduce we do operculactomy. In severe cases/ recurrent cases we need antibiotics but this is not the main practice clinically. Then follow up the pt, and in most cases this is enough to control the disease. But if teeth is likely to erupt later, which is incline mesioangular against the root of 2nd molar, teeth will not erupted by itself. This need to be consider long term tx. Imagine the pericoronitis is associated with mesioangular semi horizontally impacted lower 3rd molar is against the root of 2nd Molar while the distal part of tooth is covered by soft ts then the infection come engage to surrounding ts around the tooth. While the upper 3rd molar is erupting and each time the patient biting, he impinge on soft ts of lower 3rd molar and this is very painful. The easiest way to alleviate the pain temporarily is to remove the upper 3rd molar as lower 3rd molar is no longer to preserve. After the infection subside, ower 3rd molar is removed.

2)Necrotizing periodontal dz, sometimes u find in the book says acute necrotizing ulcerative
periodontitis or acute necrotizing ulcerative gingivitis but now they are collectively called necrotizing

periodontal condition which are included NUG,NUP,necrotizing ulcerative stomatitis and noma. For the time being just concentrate on NUG and NUP. NUG is very painful, bad odour, necrotizing of interdental papillae and clinically called punched out. U can grasp the papillae by sharp instrument then it will punch away. The remaining ts are irregular, abnormal in shape and ulcerative. So beside the infection, there are groups of microbacteria and this is characterized by gingival necrosis, there are lost of interdental papillae, bleeding and associated with pain.

Historical terminology :Previously this disease also is called Vincent dz and trench mouth (which refer to soldier in battlefield because there were high prevalence among them and the causes are low immunity,stress and malnutrion). Characteristic features : the infection is limited only to gingival ts, estimated prevalence is 0.6% in general population, young adults average 23 y/o,more common in caucasians. The types of bacteria associated are spirochetes (treponema sp), prevotella intermedia (more prevalence in pregnancy female because these bact use steroids as growth factor) and fusiform bacteria. Clinical features : gingival necrosis esp tips of papillae, gingival bleeding, pain, fetid breath, pseudomembranous formation caused by necrosis and serum of blood in this area. Predisposing factors: emotional stress, poor oral hygiene, cigarette smoking, poor nutrition,immunosuppression (HIV,AIDS) take note to underlying causes to avoid recurrent Necrotizing ulcerative periodontitis more severe,involve periodontal ts and bone destruction. Bone destruction is very rapid and we cant see pocket because the infection destroy everything since it not select the area at gingival and not leaving sometimes for the formation of pocket.

Clinical feat: clinical appearance of NUG, severe deep aching pain, very rapid rate of bone destruction, deep pocket formation not evidence tx: a)Make sure to debride the area very well - Most cases treated by local debridement and sc/rp - Anaesthetic is needed -Consider avoiding ultrasonic instrumentation due to risk of HIV transimission b)OHI instruction c)Oral rinses - chlorhexidine gluconate 0.12%;1/2 oz 2x daily - hydrogen peroxide/water - povidone iodine d) Pain control (depend on severity such as NSAID) e) Antibiotics -systemic/severe involvement -metronidazole -avoid broad spectrum in AIDS pt f) Modify predisposing factors g) Proper follow up -frequent until resolution of symptoms -comprehensive periodontal evaluation following acute phase Most of cases when the patient come during first visit, we cant touch the ts by curette or scaler, so debridement is by frequent, atleast when pain subside allowing effective OH using pieces of gauze soaked in hydrogen peroxide and cleaning at the facet of papillae. OHI and pain killer are given a week after when the patient comes for proper debridement and most of the time patient is gave anaesthesia.

3)Gingival disease of viral origin herpes virus which is acute manifestation of viral infection of
oral mucosa, characterized by redness and multiple vesicle that easily rupture to form painful ulcers affecting the gingiva. Primary Herpetic Gingivostomatitis

One of the common virus inside oral cavity is Herpers Simplex Virus (HSV). Normally in nature we have HSV Type I and HSV Type II. The most commonly type of virus associated with oral infection is HSV Type I which is mainly in young children and sometimes babies. 90% of primary oral infections are asymptomatic. Clinical feat: painful severe gingivitis with ulcerations,edema,and stomatitis,vesicles rupture,coalance and form ulcers, fever and lymphadenopathy are classic features, lesion usually resolve in 7-14 days. Normally it is associated with severe symptom such as painful and loss of apetite. Child normally is in a poor condition. Parents are very worried and come to our clinic with confusion what to do. We need to know that the patient or the child need to be provided with good nutrition and fluid basically because the child unable to masticate as normal. We try to provide them with soft food full of nutrient, protein and one of the good things is jelly. It is high in protein and lots of flavour surely children will like it and easily swallowed. Tx: a) Bed rest b) Fluid-forced c) Nutrition d) Antipyretics e) Pain relief -viscous lidocaine -benadryl elixir -50% benadryl elixir/50%maalox f) Antiviral medications (immunocompromised pt)

Normally it is self-limiting. Unluckily this infection leave behind a lethal virus that will be reactivated later in a secondary herpetic gingivostomatitis that occur during adulthood. For the treatment, we use panadol acetaminophen instead of aspirin. We avoid using aspirin because of high risk of Reyes Syndrome which is sometimes fatal. We also can use topical anesthesia gel. For recurrent oral herpes, sometimes we call it fever blister or cold sores. Its normally type I HSV because type II basically associated with ulceration of female genital area. There are intraoral hepers and herpes labialis. Herpes labialis normally on vermillion border while intra oral normally in gingival tissue. Its less severe but sometimes it is painful. Recurrent infection in 20-40% of those with primary infections.

Clinical feat: prodormal syndrome, lesion start as vesicle, rupture than leave ulcers, a cluster of small painful ulcers on attached gingiva or lips, can cause pot-operative pain following dental tx. Virus reactivation: a) Fever b) Systemic infection c) Ultraviolet radiation d) Stress e) Immune system changes f) Trauma g) Unidentified causes Tx: a) Palliative b) Antiviral medications - consider for tx of immunocompromised pt, but not for periodic recurrence in healthy pt.

4) RAS
- canker sore - Etiology unknown - Prevalence 10-20% of general population - Usually begin in childhood - Outbreaks sporadic, decreasing w age Clinical feat: affect mobile mucosa, most common oral ulcers conditions, minor, major,herpitorm

Clinical feat: most common, small shallow ulcerations w slightly raised erythematous border, central area covered by yellow-white pseudomembrane, heals w/o scarring in 10-40 days

Clinical feat: larger than 0.5cm in diameter, may persist for months, frequently heals with scarring

Herpetiform aphtae Clinical feat: small, discrete crops of multiple ulcerations, lesion similiar to herpitic stomatitis but no vesicles, heals within 7-10 days w/o scarring Predisposing factors: trauma, stress, food hypersensitivity, previous viral infections, nutritional deficiency Tx: a) Palliative b) Pain relief topical anaesthetic rinses c) Adequate fluid and nutrition d) Corticosteroids e) Oral rinses (chlorhexidine has been anecdotally reported to shorten the course of aphtous stomatitis) f) Topical band aids g) Chemical or laser ablation of lesion

5)Allergic reaction
Intra oral ocurrance uncommon, higher concentrations of allergen required for allergic reaction to ocur in oral mucosa than in skin and other surface Examples: a) Dental restorative materials (mercury, nickle,zinc,chromium,acrylics) b) Toothpaste and mouthwashes (flavour additives-cinnamon) / preservatives c) Food (peanuts, red pepper) Clinical feat : varies, resemble oral lichen planus or leukoplakia, ulcerated lesion, fiery red edematous gingivitis Tx: a)Comprehensive history and interview b)Lesion resolve after elemination of offending agent

Forgive us for any mistakes and good luck, Nadya and bushra