Clinical Exam

 Gingiva  Color change  Calculus Periodontal Disease  Edema  10% of children, 1/3 of  Bleeding on gentle probing teens  Gingival crevicular exudate  Common areas- lingual of in the Pediatric mandibular incisors and  GI (Gingival Index) used to assess gingival health buccal of maxillary molars  Bone loss Patient  Plaque Accumulation  Height of interproximal  Several plaque indices assess portion of tooth crest 1-2 mm below CEJ Yael Feldman DMD covered in plaque on BW in health

 Disclosant provides SBH Health System excellent oral hygiene instruction tool

Clinical Exam  Mucogingival problems  Determine width of attached gingiva- locate mucogingival  Attachment Loss junction and measure to free  Attachment Level- subtract the gingival margin distance from the CEJ to the free  Note sites with less than 1 mm gingival margin from the probing attached gingiva pocket depth (PPD) (distance from the free gingival margin to  Periodontal Screening and bottom of pocket) Recording (PSR)  Measure at 6 sites per tooth  System designed for easier  Loss or gain of 2mm or more is and faster screening of clinically meaningful periodontal health for adults  Transient deep pockets are  Uses probe with colored band normal in transitional dentition and from 3.5 to 5.5mm must be distinguished from true attachment loss by locating CEJ  If band is even partially submerged, a complete  More difficult to determine in younger patients because CEJ periodontal exam is indicated below free gingival margin  Can be used in children and adolescents, but erupting teeth give false positives

Clinical Features of Gingiva in the Radiographic Features of Primary Dentition Periodontium in the Primary

 Papillary Gingiva Dentition  Interdental saddle area instead of cols where spacing exists  Well keratinized  PDL  Marginal Gingiva  Sulcus depth greater  Wider and less dense  Free gingival margin thicker and rounder (due to cervical constriction of primary teeth)  Alveolar Bone  Flaccid and retractable- immature connective tissue, immature gingival fiber system, increased vascularization  Less calcified, more vascular, fewer but thicker  Attached gingiva trabeculae  Appears less dense and redder- thinner, less keratinized epithelium  Incidence of stippling- 35%  Larger marrow spaces, thinner lamina dura, flatter  Greater width interdental crests  Retrocuspid papilla-normal; 85% of children  Alveolar mucosa  Blood supply, lymphatic drainage more extensive  Redder  Width increases with age and eruption

1 Host response Gingival Diseases

 Cell mediated: T-cell predominate  Gingivitis does not always progress to response in children periodontitis, but periodontitis is always  Sensitized lymphocytes produce bone preceded by gingivitis resorbing lymphokines  Plaque and non-plaque induced

Non plaque induced gingival Gingival Diseases- Plaque Induced lesions  I-Gingivitis associated with plaque only  1)With or without other local contributing factors  I) Gingival lesions of specific bacterial origin  II-Gingival diseases modified by systemic factors  1)Associated with the endocrine system  II) Gingival lesions of viral origin  A) Puberty  III) Gingival lesions of fungal origin  B) Menstrual cycle  IV) Gingival lesions of genetic origin  C) Pregnancy  D) Diabetes  V) Gingival manifestations of systemic conditions  2) Associated with blood dyscrasia  1) Mucocutaneous disorders  A) Leukemia  2) Allergic reactions  B) Others  VI) Traumatic lesions  III-Gingival Diseases modified by medications  1) Drug influenced gingival enlargements  VII) Foreign body reactions  2)Drug influenced gingivitis  VIII) Not otherwise specified  3)Oral contraceptive associated gingivitis  4)Others  IV-Gingival diseases modified by malnutrition-  Ascorbic acid deficiency  Other

I-Gingivitis Gingivitis

 Definition: inflammation of gingival tissues  Etiology- bacterial plaque  Without bone loss or attachment loss  Early species- gram positive cocci and small rods  Reversible with improved oral hygiene (streptococci and actinomyces)  Home care  Later replacements- filamentous forms, spirochetes  Periodic professional reinforcement  Reactivity gradually increases with age  Clinical signs:  Erythema  May be related to steroid hormones  Bleeding on probing  Local factors that contribute to gingivitis in children:  Edema  Crowded teeth  Early primary dentition- gingivitis uncommon  Orthodontic appliances  Peaks during puberty (60% of teenagers-bleeding on  Mouth breathing probing)  Eruption  After puberty declines slightly and constant into adulthood  Calculus (10% of children, 1/3 of teens)

2 Gingivitis in Children Gingivitis-Treatment

 Occurs to varying  Scaling and root planing degrees, increases with age, eruption, puberty  Topical antibacterial agents  Rounded gingival  If gingivitis remains following removal of margins accentuate inflammatory changes plaque and local factors, evaluate for  Reversible with improved systemic factors oral hygiene  Does not occur to same degree as adults with comparable plaque

Objectives of Scaling and Root Chronic Inflammatory Gingival Planing Enlargement

 Long standing gingivitis in young patients  Removal of dental calculus and plaque  Clinical features  Reduce bacteria below a threshold level  Ballooning of interdental papilla and/or marginal gingiva  Gingiva is red or bluish/red, soft and friable with smooth shiny capable of initiating clinical inflammation surface and bleeds easily  May be generalized or localized  Success is determined by evaluation of  Caused by prolonged exposure to plaque tissues following treatment and during  Common local contributory factors-  Mouth breathing maintenance phase  Orthodontic appliances  Often resolves when plaque control is instituted

Plaque Induced Gingival II-Gingival Diseases Modified by Systemic Factors Enlargement A) Associated with the Endocrine System  Clinical features  Enlargement of interdental papilla and or marginal gingiva  Ranges from pale and fibrotic to red and friable  1) Puberty- dramatic rise in steroid  Generalized or localized hormone levels (esp. estrogen and  Caused by prolonged exposure to plaque progesterone) has transient effect on  Common local contributing factors  Mouthbreathing inflammatory status of the gingiva  Orthodontic appliances   Treatment 2) Menstrual cycle- inflammatory changes  Thorough oral hygiene routines, use of powered toothbrush occur at ovulatory surge  Gingivectomy or gingivoplasty may be required  3) Pregnancy-during 2nd or 3rd trimester

3 4) Insulin Dependant Diabetes Mellitus III-Drug Induced Gingival Diseases (Type 1) 1)Drug Influenced Gingival Enlargements

 Phenytoin (Dilantin,  Insulin Dependant Diabetes Mellitus Associated Gingivitis anti-epilectic)  Greater response to local factors  Cyclosporin  Consistent in children with poorly controlled type 1 (immunosuppressant) diabetes  Level of diabetic control is most important aspect  Calcium channel  Plaque control can limit severity blockers (Nifedipine,  Higher rates of periodontal disease in IDDM Nitrendipine,  Increased risk and earlier onset of periodontitis diltiazem) in both IDDM and NIDDM

III-Drug Induced Gingival Diseases Drug Influenced Gingival Enlargements 1)Drug Influenced Gingival Enlargements Treatment  Regresses and may disappear  Inter and intra patient variation after cessation of drug therapy  Higher prevalence in children  Replace with alternate drug if  Onset within 3 months of starting drug possible  Change in gingival contour leads to modification of size  Professional prophylaxis and rigorous home care  Predilection for anterior gingiva  Daily use of chlorhexidine may  Enlargement first observed at interdental papilla be beneficial  May progress to cover crowns  Surgery -gingivectomy or flap  Pronounced inflammation in relation to amount of plaque with internal bevel or  Reduction in plaque can limit severity gingivoplasty  Overgrowth is fibroepithelial  Will recur  Painless overgrowth, fibrous, firm, pale pink, little tendency to bleed  Surgery indicated- appearance unacceptable to patient, interferes with function, pocket depth cannot be maintained in healthy state

IV-Gingival Diseases Modified by Malnutrition Vitamin C Deficiency Gingivitis

 Rare in US or developing  Edematous, spongy gingiva, clinical countries appearance of non-specific gingivitis  Precise role of nutrition in initiation/progression of  Spontaneous bleeding disease yet to be determined  Impaired wound healing  Individuals on restricted  Dental management diets may be at risk for Treatment of the underlying deficiency ascorbutic gingivitis (avitaminosis C) Plaque control  May be a concern in anorexic/bulimic patients

4 Non- plaque Induced Gingival Lesions Non-Plaque Induced Gingival Lesions V-Gingival Manifestations of Systemic Conditions  I-Gingival lesions of specific bacterial origin  Nieserria gonorrhea  Treponema pallidum 1)Mucocutaneous disorders 2)Allergic reactions   Streptococcal species  Lichen planus Dental restorative materials  II-Gingival lesions of viral origin  Pemphigoid  Mercury  Primary herpetic gingivostomatitis  Pemphigus vulgaris  Nickel   Erythema multiforme Recurrent oral herpes  Acrylic  Lupus erythematous  Varicella zoster  Oral care products  Drug induced  III-Gingival lesions of fungal origin  Dentrifice  Other  Mouthwash  Candida species  Linear gingival erythema (manifestation of candidiasis in HIV  Tartar control agents positive individuals)  Chewing gum additives  Histoplasmosis  Cinnamon  IV-Gingival lesions of genetic origin  Food and food additives  Hereditary gingival fibromatosis

Non-Plaque Induced Gingival Herpes Simplex Virus Type I Lesions

 VI-Traumatic lesions (factitious, iatrogenic,  Includes gingivitis  Febrile, pain, lymphadenopathy accidental, self mutilation)  Diagnosis- clinical appearance of soft tissues Chemical injury  Viral culture provides definitive diagnosis however not routinely performed Physical injury  Treatment- palliative therapy Thermal injury  Self limiiting and resolves 7-10 days  Systemic acyclovir for immunocompromised patients with herpetic gingivitis

Periodontitis- Further Classification of Periodontitis Characterized by:

 I-Chronic Periodontitis (localized, generalized) (more common in adults)  Degree of attachment loss  II-Aggressive Periodontitis (localized, generalized) (may be more common in children and adolescents  Slight  III-Periodontitis as manifestation of systemic diseases  1) Hematologic disorders  Moderate  2) Genetic disorders  3) Not otherwise specified  Severe  IV-Necrotizing periodontal diseases (NUG, NUP)  Extent  V-Abscesses of the periodontium (gingival, periodontal, pericoronal)  VI-Periodontitis associated with endodontic lesions  Localized  VII-Developmental or acquired deformities and conditions  1) Localized tooth related factors  Generalized  2) Mucogingival deformities/ conditions around teeth  Post treatment status  3) Mucogingival deformities/ conditions on edentulous ridges  4) Occlusal trauma  Recurrent  Refractory

5 Periodontitis- Therapeutic Periodontitis Approaches

 Anti infective treatment  Loss of gingival Designed to halt progression of attachment attachment loss by removing etiologic factors  Loss of bony support  Regenerative therapy  Chronic gingivitis (adults)  Responds to local Includes anti infective treatment and is therapy intended to restore structures destroyed by  Age 5-11 1% disease  Age 12-17 20%  Periodontal maintenance essential to both approaches

Periodontitis-Objectives of Periodontitis- Treatment Therapy

 Halt disease progression  Scaling and Root Planing  Resolve inflammation  Pharmacological Therapy  Reducing etiologic factors below the Systemic drug administration threshold capable of producing breakdown Local Delivery  Allow repair of the affected region  Surgical Therapy  Regenerative Surgical Therapy

Scaling and Root Planing Systemic Drug Administration

 Beneficial  Systemic antibiotics indicated for:  Reduce clinical inflammation  Multiple sites unresponsive to mechanical debridement  Acute infections  Microbial shift to less pathogenic subgingival flora  Medically compromised patients  Decreased probing depth  Presence of tissue invasive organisms  Gain of clinical attachment  Ongoing disease progression  Less disease progression  Identify pathogenic organisms  Some sites do not respond to therapy  Antibiotic sensitivity testing  Root anatomy- concavities  NSAIDs  Furcations  Sub-antimicrobial dose doxycycline  Deep probing depths  Risks and benefits  Reevaluation several weeks later  Since patients with chronic periodontitis respond to conventional  Must be combined with personal plaque control therapy it is unnecessary to routinely administer systemic  Contributing systemic factors must be addressed medications such as antibiotics, NSAIDs or sub-antimicrobial dosing with doxycycline

6 Local Delivery Surgical Therapy

 Controlled delivery of chemotherapeutic  Provides better access for removal of agents within periodontal pockets can alter etiologic factors pathogenic flora and improve clinical signs  Reduce deep probing depths of periodontitis  Regenerate or reconstruct lost periodontal  Benefits tissues Delivered at the site of disease activity at a bactericidal concentration Facilitates prolonged drug delivery

I-Chronic Periodontitis Regenerative Surgical Therapy Formerly-Adult Onset Periodontitis

 Features  Use of adjunctive surgical technique devices and  Loss of attachment and bone  Can be arrested materials  Prevalence  ½ of adult population affected  Chemical agents that modify the root surface while  20% of 14-17 year olds have attachment loss of at least 2mm in one or more sites  Often begins in adolescence promoting new attachment- variable results  Increases with age  Can be localized(<30% of dentition) or generalized >30% of dentition)  Bone grafting  Pathogenesis  Bacterial plaque dependant  Polymicrobial infection  Guided tissue regeneration (GTR) with or without bone  Most common-Porphyromonas gingivalis  Neutrophil primary host defense mechanism replacement grafts  Host inflammatory response contributes to disease  Treatment  Biologically engineeered tissue inductive proteins (eg  OHI  Scaling/root planing growth factors, extracellular matrix proteins and bone  Correction of local contributory factors (overhang restorations, calculus)  Lasers (evidence insufficient to suggest any specific laser approach superior to traditional mechanical morphogenic proteins) therapy)  Prevention  NO smoking  Maintain good OH  Smoking, Diabetes- RISK FACTORS  Also increases with age and male gender

Chronic Periodontitis II-Aggressive Periodontitis  Primary features  Otherwise healthy patient  Can be localized(<30% of dentition) or generalized  Secondary features  Rapid loss of attachment  Amounts of microbial (>30% of dentition) and bone deposits inconsistent with  Most prevalent in adults  Familial aggregation severity of periodontal  ?Genetic Predisposition tissue destruction  Can occur in children and adolescents  Independent of age of  Elevated Aa (Actinobacillus actinomycetemcomitans)  Low to moderate rate of progression that may include onset  Localized and generalized and P. gingivalis (some periods of rapid destruction forms populations)  Phagocyte abnormalities  Severity  Hyperresponsive  Mild: 1-2mm of clinical attachment loss macrophage phenotype  Moderate: 3-4 mm of clinical attachment loss  Progression of attachment/bone loss may  Severe: >= 5 mm clinical attachment loss be self arresting

7 Localized Aggressive Periodontitis Localized Aggressive Periodontitis (LAgP)- Primary Dentition (LAgP)- Primary Dentition

 Formerly Localized prepubertal periodontitis (LPP)  Suggested etiologic factors  Features  Leukocyte chemotactic defect  Attachment loss and bone loss around primary teeth  Cementum defect  Affects only some deciduous teeth  Most commonly affects primary molars  Usually (but not always) associated with Aa  Mild to moderate inflammation (not prominent feature)  Has not been studied as much as LAP in permanent dentition  May have less plaque and inflammation than seen in chronic  Causative bacteria has not been identified periodontitis  Heavier than average plaque deposits  Dental Management  Most commonly in African Americans  Little data  Children otherwise systemically healthy  Scaling and root planing, extraction of primary teeth  Commonly diagnosed during late primary or early transitional dentition  Antibiotic therapy: amoxicillin +/- metronidazole for 7-10 days or  Prevalence less than 1% azithromycin for 3-5 days  May progress to LAgP in the permanent dentition  Not tetracycline

Localized Aggressive Periodontitis Localized Aggressive Periodontitis (LAgP)-Permanent Dentition (LAgP)-Permanent Dentition

 Formerly Localized Juvenile Periodontitis (LJP)  Radiographic signs (Distinctive):  Prevalence is 1%  .2% Whites  Vertical bone loss around molars  2.6% in African Americans  Horizontal bone loss around incisors  Increase in Latinos  Rapid rate of progression-3x that of chronic periodontitis  Features:  Circumpubertal onset typically (not age dependant) (10-15 years of age)  Etiology  Robust serum antibody response to infecting agents (Aa)  Genetic basis? Familial aggregation  Localized to permanent first molar/incisor (loss of attachment and bone) and no more than 2 other teeth  Aa (most but not all cases)  Minimal inflammation  No single species in all cases  Conflicting data on plaque and calculus   Patient otherwise systemically healthy Depressed neutrophil chemotaxis in 70%  Frequently preceded by bone loss in primary dentition (LPP) (50%)  Possible defect in phagocytosis  Probably same disease as LAgP in primary dentition  Over-reactive monocyte response  May have less plaque and inflammation than seen in chronic periodontitis-often first detected at 10-15 years olf  Genetic defects in gene coding IgG2

Localized Aggressive Periodontitis Generalized Aggressive (LAgP)-Permanent Dentition Periodontitis (GAgP)

 Diagnosis  Clinical: attachment loss on at least two permanent first molars and incisors with and no more than 2 teeth other than those molars or  Previously Generalized Juvenile Periodontitis incisors  Prevalence 0.15% or less in US  Laboratory: cultures and/or DNA probes  Treatment:  Greater prevalence in males, African Americans  Scaling, curettage, root planing  No association with age?  Antibiotic therapy (metronidazole most effective, may be used in combination with amoxicillin, tetracycline) (local antibiotic therapy not  Considered a disease of adolescents and young adults effective) (12-30), onset often circumpubertal  Microbiologic monitoring needed to ascertain eradication of Aa  Surgery  In the US prevalence in adolescents(14-17) is 0.13 percent  Regenerative techniques: root conditioning composite graft, ePTFE  Features membranes  Poor serum antibody response to infecting agents  Pronounced episodic nature of attachment/bone loss

8 Generalized Aggressive Generalized Aggressive Periodontitis (GAgP) Periodontitis (GAgP)

 Rapid, severe periodontal destruction around most teeth  Etiology:  Clinical diagnosis:4 or more mm of attachment loss  Neutrophil chemotactic disorder around 8 or more teeth, at least 3 teeth other than  Aa, P. gingivalis, E. corrodens molars and incisors  Microbiological profile similar to chronic disease  More gingival inflammation than LAgP  Subgingival bacterial cultures: non motile facultatively anaerobic  Inflammation can be severe gram - rods  More local irritants (plaque, calculus) than LAgP  Treatment  Probably progression of LAgP  Scaling, surgery, curettage, root planing, antibiotics  Smoking is a risk factor  Does not always respond to conventional mechanical and  Radiographic signs: rapidly progressing bone loss antibiotic therapy around multiple teeth including molars/incisors  Culture and sensitivity helpful in refractive cases

III-Periodontitis as a Manifestation Leukemia of Systemic Disease

 1) Hematological Disorders  Most common from of childhood cancer  ALL (acute lymphoblastic leukemia)  Acquired neutropenia  Most common  Leukemia  Best prognosis  Others  AML (acute myeloid leukemia)  2) Genetic Disorders  20% of childhood leukemia  Poorer long term survival rate  Familial/cyclic neutropenia  AML (not ALL) may present with gingival enlargement (infiltrates of leukemic cells), Lesions-  Down Syndrome blue/red and may invade bone  Leukocyte adhesion deficiency syndromes  Gingiva hyperplastic, edematous, bluish red  Fever, malaise, bone or joint pain, gingival or other bleeding  Papillon-Lefevre syndrome  Petechiae and mucosal ulcerations in any form of leukemia  Chediak Higashi syndrome  Initial diagnosis by CBC  Langerhans cell Histiocytosis  Infantile genetic agranulocytosis  Hypophosphatasia  Glycogen Storage Disease  Cohen syndrome  Ehlers Danlos syndrome (Type IV and VIII)

Neutropenia Neutropenia

 Decreased circulating PMNs  Periodontal symptoms  Several forms  Severe gingivitis with ulcerations  Cyclic neutropenia  Attachment loss and alveolar bone loss  Chronic benign neutropenia of childhood  Early loss of primary teeth  Chronic idiopathic neutropenia  Severe periodontal disease in the permanent dentition  Familial benign neutropenia  History of other recurrent soft tissue infections  Can be cyclic, transient or persistent  Otitis media, respiratory and skin infections  Cyclic/ Familial Neutropenia  Diagnosed by white blood cell differential count  Reduction of PMNs every 19-21 days typically (14-30 days more  Depressed neutrophils inclusive)  Dental management  Neutropenia 5-10 days duration  Rigorous local measures to control plaque  Severe ulcerative gingivitis  Antibiotic therapy  Alveolar bone loss  Extraction of affected teeth  Periodontal treatment as indicated  Systemically administered granulocyte colony stimulating factor (G- CSF) to treat underlying cause

9 Leukocyte Adhesion Deficiency Down Syndrome (LAD)

 Prevalence 60-100%, all under age 30, increases with age  Primary dentition involved in 36%  Rare, autosomal recessive genetic disease  Mandibular incisors often affected  Higher prevalence in trisomy 21 than general MR population  Etiology:  Higher rates of ANUG in institutionalized  Leukocyte surface glycoprotein defect  Susceptibility to periodontitis appears to be due to innate immune system abnormalities  Dental management  Poor leukocyte adherence  Oral hygiene routines  Poor migration to infection sites  Periodontal treatment as indicated based on periodontal diagnosis  Probable pathogenesis  Impaired phagocytic function  Capillary fragility  Chemotactic/phagocytic defects of PMNs (“lazy leukocyte syndrome”)  Patients susceptible to bacterial infections  Low numbers of mature T cells  Including periodontitis (in primary and young  Abnormal thymus  Early colonization by pathogenic bacteria permanent dentition)  Frequent respiratory, ear, skin and other soft tissue bacterial infections

LAD Papillon-Lefevre syndrome

 Formerly Generalized Prepubertal Periodontitis  Dental symptoms manifest in early primary dentition  Involves all primary teeth, if untreated will involve permanent teeth  Highly acute inflammation, clefting, recession

 Rapid destruction of bone  Autosomal recessive  Severe generalized periodontitis refractory to treatment  1 of 19 different forms of palmoplantar keratoderma  Stem cell transplantation can be curative  Rare  Erythematous hyperkeratosis of palms and soles (variable)  Treatment  Nail dystrophy  Oral hygiene measures  Ectopic calcification of dura periodontitis  Antibiotic therapy  Rapid loss of bone and attachment  Extractions of affected teeth  Inflammation can be severe  Due to chronic problems with illness, adequate compliance difficult  Premature loss of primary and permanent teeth  Aa infection, also Bacteroides and Fusobacterium  Treatment-  Antibiotic therapy  Extraction of affected teeth  Local measures to control plaque

Langerhans Cell Histiocytosis Chediak Higashi Syndrome Formerly Histiocytosis X Non Lipid Reticuloendothelioses  Autosomal recessive  Group of disorders with variable  Oral manifestations in 10% of symptoms resulting from abnormal patients  Rare proliferation and dissemination of  Necrotic gingivitis histiocytic cells of the Langerhans  Neutrophils with giant system  Furcation bone loss cytoplasmic granules  Disorder of mononuclear  Radiolucent lesions of mandible and cranium  Recurrent infections phagocytes  Multiple hard and soft tissue  Bone lesions produce “floating  Severe gingivitis and lesions containing histiocytes and teeth” periodontitis eosinophils  Gingival enlargement   Ulceration  Oculocutaneous albinism Diagnosis by biopsy  Mobility of teeth with alveolar  Photophobia expansion  Nystagmus  Treatment-radiation, surgery, systemic chemotherapy  Peripheral neuropathy

10 Histiocytosis Langerhans Cell Histiocytosis

 Rare disorder of childhood  Letterer-Siwe (acute disseminated)- most severe, affects infants, prominent skin and  Presentation as infiltration of bones, skin, visceral involvement liver and other organs by histiocytes  Hand-Schuller-Christian (chronic disseminated)-  10-20% of cases initial infiltrates are in children>3 years, mostly bony sites, skull oral cavity- usually the mandible lesions, diabetes insipidus, exopthalmos  Eosinophilic Granuloma (acute localized)- older children, most benign form

Hypophosphatasia – Rathbun Hypophosphatasia Syndrome

 Autosomal recessive  Genetic disorder  5 groups: perinatal (lethal), infantile (severe), childhood (milder), adult  Premature loss of primary teeth (especially single rooted teeth) (tarda) and odontohypophosphatasia  Loss of teeth due to cementum defect  Phenotypes range from premature  Weakened attachment of tooth to bone loss of primary teeth to severe bone abnormalities leading to neonatal  Clinical features in permanent dentition similar to LAP death  Dental prognosis for permanent teeth is good  Early loss of primary teeth may be first clinical sign in mild forms  Typical presentation  Earlier presentation of symptoms the  Primary incisors exfoliate before age 4 more severe the disease  Teeth exfoliate with intact roots, usually before root formation complete  Low serum tissue-non specific alkaline  Teeth lost in order of eruption phosphatase   High urinary phosphoethanolamine Other primary teeth are affected to varying degrees  Permanent dentition may be normal in odontohypophatasia  Enlarged pulp chambers, acementogenesis, dentinal dysplasia

IV-Necrotizing Periodontal Hypophosphatasia Diseases (NUG, NUP)(NPD)

 Rapid Onset  Systemic treatment  Painful gingivitis with interproximal and marginal necrosis and ulceration  NUG may progress to NUP in immunocompromised individuals Enzyme replacement therapy, Asfotase  Febrile Alpha, approved for perinatal, infantile and  Incidence  Late teens and early 20s in North America and Europe juvenile onset hypophasphatasia  Young children in undeveloped countries  Varying but low frequency in North America and Europe (<1%)   2-5% in developing areas of Africa, Asia and South America Dental management  Predisposing factors  Malnutrition Supportive therapy to address concerns and  Viral infection(including HIV) prevent long term consequences or early  Stress  Lack of sleep tooth loss  Spirochetes and Prevotella intermedia  Treatment  Local debridement (ultrasonic scaling excellent)  Antibiotic therapy may be indicated (Penicillin, Metronidazole)  NSAIDs for pain

11 V-Abscesses of the Periodontium NUG/NUP (Gingival, Periodontal, Pericoronal)

 NUG  NUP  Gingival abscess  Specific bacterial accumulations  Manifests as rapid necrosis and  Localized, painful lesion of marginal gingiva or  Lowered host resistance destruction of gingiva and periodontal attachment apparatus interdental papilla  Personal plaque control and professional debridement  Gingival bleeding and pain and  Sudden onset represents an extension of NUG  Systemic antibiotics if  Bacterial infection following gingival trauma , typically lymphadenopathy or fever with oral  HIV + and – symptoms  Management caused by embedded foreign object  Chemotherapeutic rinses during initial  Debridement  Popcorn hull treatment stages  Irrigation with antiseptics(eg povidone iodine), antimicrobial mouth rinses (eg chlorhexidine)  Fingernail fragment and systemic antibiotics  Treatment-

 Debridement and establish drainage  Chlorhexidine irrigation

Pericornitis Mucogingival Defects

 Inflammation of gingiva covering partially  Pocket depth exceeds width of attached erupted tooth keratinized gingiva  Most common around erupting 3rd molars  Lower incisor most common location  Food trap, environment conducive to bacterial growth  May result from labial positioning of tooth  Pericoronal flap becomes inflamed and swollen through band of attached gingiva  Enlarged flap traumatized by occlusion, very painful  Dental Management- debridement, antibiotic therapy for systemic involvement, chlorhexidine irrigation

 Maxillary and mandibular labial frena-  Treatment indicated to Defects of Attached Gingiva Frena prevent  Stripping of the labial tissue  Mandibular incisors can erupt labial to alveolar ridge leading to a narrow  Common finding in children  Loss of alveolar bone band of attached gingiva  Prominent maxillary frenum  Loss of tooth  Small loss of attachment -> mucogingival defect and recession and midline diastema   Loss of attachment and recession with a labially malpositioned tooth may be Restrictive lingual frenum  Immediate treatment  Tongue tie or called stripping usually unnecessary  Other factors that cause recession Ankyloglossia  Treatment delayed until  Smokeless tobacco  If limits normal tongue permanent incisors and  Habit related to self induced injury mobility treatment may be cuspids are erupted (allows  Nail biting indicated natural closure)  Tooth brushing  Will also make speech  Orthodontic movement  If ortho planned- surgical easier treatment should be  Treatment for severe recession:  Gingival graft (commonly from palate) postponed until diastema  If defect not severe should postpone until after ortho closed  Ortho movement of labially malpositioned tooth  If appearance unacceptable after closure then frenectomy indicated  Laser

12 Localized Juvenile Spongiotic Frenectomy Gingival Hyperplasia (LJSGH)

 Recent  Benign condition  Affects the gingiva of children and young adults  Clinically distinctive  Presents as a localized area of erythema on the attached gingiva, with a subtly papillary surface architecture  Generally biopsied  Prominent intercellular edema (spongiosis) and neutrophil infiltrate  Lack of resolution with conservative oral hygiene therapeutic measures  Esthetic concerns  Histopathology  Subtle papillary epithelial hyperplasia  Acute inflammation  Numerous engorged capillary vascular spaces in the lamina propria  Clinical correlation is necessary to make the diagnosis

LJSGH LJSGH

 Lack of a good clinical response to conventional therapy  Excisional biopsies were performed to establish the diagnosis  Plaque control reinforced  Additional antiseptic local treatment was administered  Persistence of some bright reddish gingival masses in sone of the patients these lesions were treated by surgical excision  Overall clinical outcome was good and stable after one year

References

 American Academy of Pediatric Dentistry The Handbook, 5th edition  McDonald, Avery, Dean, Dentistry for the Child and Adolescent, Eighth Edition,2004  Pinkham, Casamassimo, Fields, McTigue, Nowak, Pediatric Dentistry, Infancy Through Adolescence, Fourth Edition, 2005  Comprehensive Review of Pediatric Dentistry, Course Manual 2010  AAPD Policies and Guidelines 2017-2018

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