Presentation on theme: "SESSION PLAN COURSE # AND TITLE: PEDS 538, Pediatric Dentistry"— Presentation transcript:
1 SESSION PLANCOURSE # AND TITLE: PEDS 538, Pediatric DentistrySESSION # AND TOPIC: # 10 Periodontal Disease and Assessment in Children. Other Oral Problems, and Oral Manifestation of DiseaseDURATION: Equivalent to 1 hourFACULTY: Dr. Glenn MinahGENERAL GOALS: Become familiar with various soft tissue abnormalities and diseases found in childrenSPECIFIC OBJECTIVES: The student should be able to:1. Discuss the etiology, clinical appearance and treatment of pericoronitis, pre-pubertal periodontitis, localized juvenile periodontitis, NUG and gingival hyperplasia.
2 SESSION PLANSPECIFIC OBJECTIVES: The student should be able to:2. Discuss the etiology, clinical appearance and implications regarding dental treatment for herpetic gingivostomatitis, recurrent herpes simplex, varicella-zoster, herpangina, impetigo, hand, foot and mouth disease, candidosis, scarlet fever and certain systemic diseases.METHODOLOGY: Web LectureASSIGNMENT: McDonald RE, Avery DR. Dentistry for the Child and Adolescent. Mosby, St. Louis, 7th ed Chapter 20, p.440EVALUATION: Written exam. Questions will come form the text portion of this presentation.TEXT
4 Periodontal Diseases and Disorders TEXTChild versus adult periodontium: In the child: 1) The interdental papillae are larger. 2) The gingival margins are less sharp and the tissue is thinner, less tight and may appear more erythematous. 3) Pseudopockets are often present due to partially erupting teeth. (Sulcular depth in healthy crevices may be slightly deeper than in adults, i.e., ~1.0mm.) 4) Plaque levels often do not correlate with gingivitis. It is not uncommon to observe abundant plaque with little or no gingivitis.Chronic gingivitis: Chronic gingivitis is more of a problem in teens than in children with early mixed or primary dentitions. In teens, careful periodontal examination is necessary since early onset periodontal diseases can be easily overlooked. Plaque control should be a prevention priority since many teens develop periodontitis at an early age.Periodontal Diseases and Disorders1.2.
5 PERIODONTAL DISORDERS Adult versus child:adultchildadultAdults show longer interdental papillae.childadultchildThe adult in health vs a child has shallower crevice depths and tighter denser gingivaeAdult gingivae shows inflammatory changes with plaque build-up, but the child’s frequently does not.
7 Tissue response to plaque: CHRONIC GINGIVITISTissue response to plaque:CHILDADULT
8 TEXTPeriodontal Disease and DisordersPericoronitis: Pericoronitis is a localized infection characterized by gingival inflammation and often systemic sequelae which accompany a partially erupted tooth (usually permanent and most commonly 3rd molars). If fever and local lymph node swelling are evident, systemic antibiotics are indicated. Patients should also rinse 2 to 3 times daily with astringent mouthrinses (warm saline or commercial mouthrinse).Eruption gingivitis: This occurs around erupting teeth due to non-physiologic position of emerging crowns and adjacent gingivae. When teeth are fully erupted, cervical contours will shield tissue from food impaction or other masticatory trauma. Treatment is seldom necessary.3.4.
9 PERIODONTAL DISORDERS Treatment:Pericoronitis:If systemic signs of inflammation are present antibiotics are indicated.Saline or commercial mouthwashing is beneficial.This often accompanies 3rd molar eruption.PERIDEX0.1%SALT
11 TEXTPeriodontal Disease and DisordersNecrotizing ulcerative gingivitis (NUG): This disease occurs ordinarily in young adults, but the population may include teenagers. Symptoms and clinical findings are 1) oral pain upon eating or brushing teeth, 2) interdental ulceration in area of mandibular incisors (usually) with pseudo-membrane covering affected tissue, 3) characteristic fetid breath and 4) low fever. The etiology of NUG is not clearly understood, but involves stress and anaerobic bacteria among which Treponema species (spirochetes) are the predominant microorganisms in the lesions and will invade superficial connective tissue. A viral etiology has also been proposed. The disease is self-limiting and persists for 10 to14 days. Debridement of affected areas and antibiotics may enhance resolution.5.
13 NUG Pain upon eating or brushing Interdental ulceration Fetid breath Slight temperaturespirochetes invade connective tissue.Treatment:PEN or MET reducestime-course ofinfection. Both killspirochetes.Darkfield microscopy indicates that spirochetes dominate the flora
14 TEXTPeriodontal Disease and DisordersHormonal gingivitis: This appears during the second trimester of pregnancy and during puberty. In both cases gingival inflammation is caused indirectly by excessive sex hormones in the circulation. These act as ecological determinants for certain oral anaerobic bacteria (e.g., Prevotella intermedia) which become more numerous in plaque and induce gingival inflammation which can sometimes be acute. Plaque control and Peridex mouthrinses (0.1% chlorhexidine) 2x/day are recommended.6.
16 TEXTPeriodontal Disease and DisordersPhenytoin-induced gingivitis (Dilantin hyperplasia): This condition often accompanies phenytoin administration which is used to control epileptic seizures, appearing in 40 to 50% of drug recipients. It may also develop with administration of calcium channel blockers and cyclosporins. Clinically it appears as gingival overgrowths with low levels of inflammation, but the tissue is not hyperplastic, histologically. Severity may be related to dose of dilantin, but genetic predisposition is also suspected. Gingival surgery is recommended in extreme case (where mastication of tissue occurs) and extraction of teeth will eliminate the overgrowth at the extraction site. Plaque control will help reduce tissue growth and cessation of the medication will cause reversal of the condition. Other treatments are topical administration of folic acid, topical vancomycin and positive pressure appliances.7.
17 PHENYTOIN-INDUCED GINGIVITIS Dilantin Hyperplasia:Tissue is not hyperplastic and responds to presence or absence of plaque and to dose of Dilantin.Genetic predisposition is suspected.Treatments include a) gingival surgery, b) folic acid, c) topical vancomycin or d) positive pressure appliances.Calcium channel blockers and cyclosporins also may cause the condition.
18 Periodontal Disease and Disorders TEXTLocalized juvenile periodontitis (LJP): LJP is a form of aggressive periodontitis which affects up to 1% of 12 to 16 year olds. It is characterized by rapid periodontal pocketing at incisor and molar sites, low tissue inflammation and plaque levels and low caries rates. The etiology is related to high plaque levels of Actinobacillus actinomycetemcomitans (Aa) and immune defects (impaired chemotaxis) and occurs often in family members of the patient (thought to be genetically related). Treatments consist of periodontal scaling, systemic tetracycline and local irrigation with either Peridex (0.1% chlorhexidine), a baking soda-salt-hydrogen peroxide solution or chloramine T. (Careful periodontal probing should be conducted routinely in teens, as LJP may be easily overlooked.)Pre-pubertal periodontitis (PPP): This is aggressive periodontitis which differs from LJP in that it affects the primary dentition (patients younger than 12), Aa is not as prevalent and pocketing may be localized or generalized. Genetic immune defects are usually present and familial patterns of occurrence are observed. Treatment is similar to LJP. PPP also is part of Papillion-Lefevre syndrome (PL) wherein planar hyper-keratosis of palms along with PPP are distinctive symptoms. PL is caused by an autosomal recessive genetic abnormality.8.9.
19 AGGRESSIVE PERIODONTITIS PPPLJPRPPAP, ChronicAge<1212-1616-35>35PlaqueLowLow/highhighCariesnormalTeeth affectedAllIncisors and molarsallHost defectsYes?noPathogensAaPg spirochetes AaGeneticM/F ratio1:13:1Localized (L)Generalized (G) bone lossL, GL
20 LOCALIZED JUVENILE PERIODONTITIS, LJP (Old terminology) Vertical bone loss around molars and incisors.LEUKOTOXINAaAa secretes leukotoxin which kills leukocytesHigh levels of Aa in pocketsTreatment:PMN chemotaxis is impaired (genetic defect)Antibiotics – TET, METscaling
26 TEXTPeriodontal Disease and DisordersGingival recession: This occurs in regions of mandibular or maxillary incisors. Causes are 1) a narrow band of attached gingiva, 2) high frenum attachment, 3) malocclusion, 4) deep bite and, rarely in children, 5) periodontitis. Treatment consists of appropriate surgery, scaling and/or orthodontics.High frenum attachments: In addition to gingival recession, these may cause diastemas or speech impediments.10.11.
27 GINGIVAL RECESSIONFrom fingernail traumaFrom a deep overbite
31 TEXTViral InfectionsAcute herpetic gingivo-stomatitis (primary herpes infection): Primary herpes is a viral infection of the oral mucosa caused by Type I herpes simplex virus (HSV-1). It affects young children (usually under 5 years) who have not developed resistance to the virus. Clinically, patients present with multiple painful ulcers, 1 to 2mm in diameter surrounded by erythematous tissue on all mucosal surfaces of the oral cavity. Pain upon eating, especially salty or acidic foods, is common and tooth-brushing is painful if ulcers appear on gingivae. Low fever and malaise also are present and patients often become under-nourished or dehydrated from insufficient food or liquids. The infection which sheds viruses from ulcers, is highly contagious and can spread to other mucous membranes such as eye tissue. The condition is self-limiting and will subside within 10 to 14 days. Palliative treatment includes topical viscous xylocaine or benadryl elixir plus kaopectate (to relieve for pain, especially upon eating) and Pedelite, a balanced nutrient drink to compensate for insufficient diets. Acylovir (Zovirax; 400mg q3h for 10 days) may be administered in extreme cases to inhibit the virus. (Note: steroids should not be used as the inflammatory reaction constitutes the first line of defense against the virus.) Differential diagnosis must rule out candidaisis (thrush) which is not painful and produces a white membranous patches on mucosal surfaces.1.
32 Primary herpes infection: VIRAL INFECTIONSPrimary herpes infection:Symptoms:Painful generalized ulcers on oral mucosa. Sometimes it appears extra-orally.Low fever and malaise. Patients often are under-nourished due to pain upon eating.Self-limiting. Will last 10 to 14 days.Occurs frequently in young children
34 VIRAL INFECTIONS cytolytic Primary herpes infection: Transformation to lytic form. Virus destroys cell and is shed.Cause: Herpes simples virus, type 1 (HSV-1)mucosacytolyticLatent form. Viral genes combine with host DNAnucleus
35 TEXTViral InfectionsRecurrent herpes labialis (cold sore): This is a HSV-1 infection which occurs in individuals who previously experienced a primary herpes infection. The virus remains dormant in sensory nerve ganglia after the first infection, but can erupt following episodes of emotional stress, excessive exposure to sunlight, trauma, dental procedures or intake of certain foods to form single ulcerated lesions on the vermilion border of the lips and mouth (usually). The common occurrence during “cold seasons” when resistance is often compromised accounts for the name (cold sore). In addition, foods containing high levels of arginine such as cereals, nuts and chocolate can activate the virus. The limited manifestation, versus primary herpes, is due to immunity developed after the first exposure to the virus. The condition is self-limiting, lasting 10 to 14 days. Remedies which may enhance resolution of the ulcer are alloe or acyclovir which inhibit HSV-1. Foods high in lysine such dairy products and yeast may alleviate the condition by counteracting the effect of arginine.2.
36 VIRAL INFECTIONSRecurrent herpes labialis:After a primary infection HSV-1 travels up a sensory nerve and remains dormant in a ganglion (trigeminal).It can revert to the lytic form upon certain stimulation and usually erupts at the vermillion border of the lips.
37 TEXTViral InfectionsHerpangina: This is caused by the cocksackie A virus and is evidenced by multiple painful ulcers on oral mucosa similar to primary herpes infections. The susceptible age is similar to that of primary herpes, being before age 5, but it is less common and affects mainly the distal portion of the mouth or throat. Treatment and progress of the condition is similar to that of primary herpes. Hand, foot and mouth disease: The causative agent is cocksackie A virus and clinical appearance is herpetic-like multiple ulcers on the hard palate, tongue and buccal mucosa. The susceptible ages are 1 to 10 years and the condition is less common than primary herpes. In addition, characteristic ulcerative lesions appear on soles of feet and plams. Treatment and course of the disease are similar to primary herpes. Herpes zoster infection (varicella zoster virus, Type 3 Herpes Simplex virus): This is commonly known as chicken pox when it affects school age children and first appears as papular lesions on the skin which form encrusted ulcers. If the virus infects adults, shingles, a painful dermal condition, will develop. In chicken pox oral lesions appear on oral mucosa secondarily to skin lesions and resemble herpetic ulcers, but are not painful (usually). The disease confers immunity and is self-limiting within 14 days.3.4.5.
38 VIRAL INFECTIONSVaricella (chicken pox) – zoster (shingles). Human Herpes Virus-3; HHV-3:Coxsackie A virus:HerpanginachickenpoxshinglesHand foot and mouth disease
39 TEXTBacterial InfectionsImpetigo: This is typified by dermal lesions on face or extremities and often affects groins and axillae. Lesions, which may be either bullous (blisters which rupture) or non-bullous (smaller and encrusted) are highly contagious. The causative agent of bullous lesions is Staphylococcus aureus and of non-bullous lesions is Group A, hemolytic streptococcus. Topical or systemic antibiotics are the customary treatment.Scarlet fever: Scarlet fever is an infection by group A streptococci (Streptococcus pyogenes) and is characterized by a bright red papular rash on the trunk. In the oral cavity “strawberry tongue” is common which is a red tongue covered by a removable coating and presence of distinctive swollen papilla. Treatment consists of systemic antibiotic regimens and complications include rheumatic fever, arthritis and glomerulonephritis.1.2.
40 BACTERIAL INFECTIONSImpetigo:The ruptured blister, encrusted lesions are caused by beta hemolytic Group A streptococci.The bullous lesions are caused by Staphylococcus aureusimpetigo
41 TEXTFungal InfectionsCandidosis (thrush) is the most common oral fungal infection and frequently affects young children. It appears as white patchy lesions on the oral mucosa. When the white patches are removed a bright red tissue surface is seen which is usually non-painful. Sometimes a distinctive yeasty oral odor is present. Occurrence frequently follows broad spectrum antibiotics, but it may also be transmitted from vaginal yeast infections. Diagnosis may be confirmed by identification of Candida albicans in mucosal specimens and treatment consists of topical anti-fungal ointment such as Nystatin.
43 Cell wall with no peptidoglycan TREATMENTCell wall with no peptidoglycanYeast cellCell membranePOLYENESnystatinAmphotercin BThese adsorb tocell membranesand disruptergosterolsergosterolAZOLESmiconazolefluconazoleketoconazoleThese inhibitsynthesis ofergosterols
45 Recurrent Aphthous Ulcer (canker sore) TEXTRecurrent Aphthous Ulcer (canker sore)This appears as single (usually) painful erythematous ulcers on oral mucous membranes which are slightly larger than herpetic lesions. The condition is self-limiting within 14 days, but contains no virus. The etiology has not been definitively established, but may involve autoimmune reactions to antigens from Streptococcus sanguis. Several palliative non-prescription remedies are available including kenalog in orabase (a steroid anti-inflammatory agent; Note: steroids may be used since viral etiology is not suspected.)
46 RECURRENT APHTHOUS ULCER (CANKER SORE) The condition is self-limiting and is treated by palliative measures.A definitive cause is not known.
47 Systemic Disorders with Oral Manifestations TEXTSystemic Disorders with Oral ManifestationsDiabetes mellitus (Type 1, insulin dependent): Oral manifestations are 1) high salivary glucose concentrations (>120mg/100ml; normal >80mg/100ml), which may cause increased dental caries rates, 2) LJP-like periodontitis, 3) intra-oral abscesses, 4) hypo-salivation and 5) yeast infections. Acute lymphocytic leukemia (ALL): This is one of the most common malignancies affecting children (occurrence = 4 in 100,000). Oral manifestations include 1) exudation from gingivae, 2) hematomas, 3) lymphadenopathy, 4) oral ulceration and 5) pharyngitis. Acquired immunodeficiency syndrome (AIDS): Oral manifestations are 1) thrush (this may appear before AIDS is apparent), 2) parotid swelling, 3) acute marginal gingivitis (appears commonly on the facial) and 4) herpetic ulceration on mucosal surfaces. HIV and AIDS in children stem largely from maternal transmission during birth and secondarily from blood transfusions. Children often develop Pneumocystis carnii pneumonia and exhibit high counts of CD4 lymphocytes.1.2.3.
48 SYSTEMIC DISORDERS WITH ORAL MANIFESTATIONS Diabetes:High salivary glucose = cariesLJP-like periodontitisIntraoral abscessesHyposalivationYeast infectionsAcute lymphocytic leukemia:Exudations from gingivaeHematomasLymphadenopathyOral ulcerationPharyngitis
49 SYSTEMIC DISORDERS WITH ORAL MANIFESTATIONS AIDS:Parotid swellingthrushgingivitisperiodontitisHerpetic ulceration
50 SYSTEMIC DISORDERS WITH ORAL MANIFESTATIONS AIDS:AIDS periodontitisAIDS gingivitisParotitis