Gingival Disease in children by >> najma alamami


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  • Their primary etiology is bacterial plaque, which can initiate destruction of the gingival tissues and periodontal attachment apparatus.1,2
    Chlorhexidine (CH) is a chlorophenyl biguanide with
    broad antimicrobial activity. It has been used commonly
    as an antiseptic skin and wound cleanser for presurgical
    preparation of the patient and as a handwash and surgical
    scrub for health care personnel. It has also been added
    as a preservative to ophthalmic products and has been
    used internally in very dilute concentrations in the peritoneal
    cavity and urinary bladder.
    In dentistry, CH has been studied for control of smooth
    surface caries, for use as a denture disinfectant, and as a
    plaque control agent. Its use in controlling dental plaque
    accumulations has received the most attention in dental
    research. Mouth rinses containing CH have been popular
    as therapeutic agents in several countries for some time,
    and in 1986 CH was approved for use in the United States.
    Two products under the trade names Peridex (Colgate-
    Palmolive Co., New York, NY) and PerioGard (Zila Pharmaceuticals,
    Phoenix, Ariz) have received FDA approval as
    prescription agents. This mouth rinse contains 0.12% CH
    gluconate as the active ingredient.
    Widespread use of CH mouth rinses over many years,
    especially in Europe, has had an excellent safety record.
    Few adverse side effects have been reported with CH
    mouth rinses, but their use has been linked to mouth
    dryness and burning sensations in some persons due to
    the alcohol base. An alcohol-free product is available.
    Generalized staining over long-term use and taste alterations
    have been reported. Poorly defi ned desquamative
    lesions have been observed in others after the mouth
    rinse was used. Allergic reactions to CH are rare. If the
    rinse is inadvertently swallowed, it has essentially little
    systemic effect due to poor absorption in the gastrointestinal
    Lِe and Schiِtt reported highly signifi cant inhibition
    of plaque formation and the prevention of gingivitis with
    use of an aqueous solution of 0.2% CH digluconate as a
    mouth rinse twice daily with swishing for 1 minute.31
    Yankell and associates have shown that dental stain from
    CH mouth rinse can be signifi cantly reduced with regular
    use of a tartar-control dentifrice.32
    It is important to recognize that the benefi cial use of
    CH as a therapeutic mouth rinse should be considered
    adjunctive to the practice of sound conventional plaque
    control measures as presented in Chapter 11 and elsewhere
    in this text. A study by Brecx and colleagues
    regarding the effi cacy of Listerine, Meridol, and
    chlorhexidine (CH) mouth rinses found CH to be the
    most effective to supplement habitual mechanical oral
    hygiene.33 They also found a combination of habitual
    self-performed and nonsupervised oral hygiene with Listerine
    or Meridol is more benefi cial for plaque control
    than the use of mechanical oral hygiene alone. Its adjunctive
    use would also seem most appropriate for therapy
    in cases in which attaining adequate plaque control
    is more diffi cult, such as during illness or convalescence
    after serious injuries.
    The rationale to include use of daily antimicrobial
    mouth rinse to the child and adolescent’s oral hygiene regimens when inadequate plaque control exists to control
    and prevent periodontal disease and deliver antimicrobial
    agents to mucosal sites harboring bacteria throughout
    the mouth thereby complementing plaque control is
    widely accepted.34,35
  • Thirty-four allergic children were examined
    during two successive spring seasons and the
    one intervening fall. Age- and sex-matched controls
    were also examined in the fall. Gingival infl ammation
    and the presence or absence of plaque were recorded,
    and a bleeding/plaque ratio was calculated for each subject.
    The results indicated an enhanced gingival infl ammatory
    reaction in the allergic children during the
    pollen seasons. Although the authors acknowledge that
    the signifi cance of gingival reaction during short allergic
    seasons is diffi cult to assess, they speculate that patients
    with complex allergies who have symptoms for longer
    periods may be at higher risk for more signifi cant adverse
    periodontal changes.
  • children 12 years of age and older.
    Other remedies for herpes simplex infection also include
    the amino acid lysine. The oral therapy is based on
    lysine’s antagonistic effect on another amino acid, arginine.
    Griffi th and associates conducted an initial study in
    which 250 patients were given daily lysine doses of
    1000 mg and were told to avoid eating arginine-rich foods,
    such as chocolate and nuts.16 The lysine therapy was continued
    until the patients had been lesion free for 6 months.
    L-Lysine monohydrochloride is available commercially in
    capsule form or tablets containing 100 or 312 mg of
    L-Lysine (General Nutrition Corp., Pittsburgh, Pa.). The
    patients reported that pain disappeared overnight in virtually
    every instance. New vesicles failed to appear, and a
    majority considered the resolution of the lesions to be
    more rapid than in the past. There was also a reduction in
    frequency of occurrences. Griffi th and colleagues concluded
    that improper food selection may make adequate
    lysine intake precarious for some persons.16 Ingestion of
    cereals, seeds, nuts, and chocolate would produce a high
    arginine/lysine ratio and favor the development of herpetic
    lesions. Similar results are obtained when arginine is
    added to the medium in the laboratory to induce herpes
    proliferation. The avoidance of these foods, coupled with
    the selection of foods with adequate lysine, such as dairy
    products and yeast, should discourage herpes infection
  • It has been reported to
    be the most common mucosal disorder in people of all
    ages and races in the world.
    It has been reported to
    be the most common mucosal disorder in people of all
    ages and races in the world.
  • antiinfl ammatory and antiallergic medication
    in the form of a topical paste.
    The paste is applied to the ulcer four times
    daily, after meals and at bedtime, until the ulcer heals.
    Zilactin (Zila Pharmaceuticals, Phoenix, Ariz), a topical
    paste with hydroxypropyl cellulose fi lm, has also been
    used to adhere to the mucosa and cover the ulcer while
    providing pain relief for an extended period of time. Occlusive
    topical 2-otylcyanoacrylate adheres for 6 hours.
    Aloe vera freeze-dried gel extract adheres and forms an
    occlusive protective patch. In severe cases, oral prednisone
    has been prescribed.
  • A therapeutic
    trial of antibiotics reduces the acute symptoms in ANUG but not in the viral infection. Acute herpetic gingivostomatitis
    is most frequently seen in preschool children,
    and its onset is rapid. As stated earlier, ANUG rarely
    occurs in the preschool-aged group and develops over a
    longer period, usually in a mouth in which irritants and
    poor oral hygiene are present. On the other hand, acute
    oral infections initially diagnosed as ANUG have frequently
    been found later to be an oral manifestation of
    one of the xanthomatoses. The early stages of conditions
    such as Hand-Schüller-Christian disease and Letterer-
    Siwe disease are associated with many of the symptoms
    of ANUG.
  • Although the tissue usually appears pale and
    fi rm, the surgical procedure is accompanied by excessive
    hemorrhage. Therefore quadrant surgery is usually recommended.
    Brown and colleagues have reported a case
    in which apically positioned fl ap surgery and CO2 laser
    evaporation were used to reduce the gingival tissue.41
  • Some authors report a positive relationship between the
    level of phenytoin in serum and saliva and the severity of
    PIGO in some cases.44-46 Other investigators have reported
    that no such correlation exists.47,48 It is generally agreed
    that a relationship exists between dosage and PIGO when
    the level of phenytoin per unit body weight or actual serum
    level is considered. Sasaki and Maita reported a signifi
    cant correlation between the degree of gingival overgrowth
    and a high level of basic fi broblast growth factor
    in serum.49 No such correlations were observed for patient
    age, daily or total phenytoin dose, duration of therapy, or
    serum phenytoin level.
  • No cure exists and treatment is often symptomatic in nature. Antihistamines, topical
    corticosteroids, ascorbic acid (vitamin C) supplements,
    topical antibiotics, and alkaline mouthwashes have
    been used with limited success and are considered to be
    Steinberg and Steinberg describe current recommended
  • less severe type of gingivitis resulting from vitamin
    C deficiency is probably much more common than
    most dentists realize.
  • Gingival Disease in children by >> najma alamami

    1. 1. Presented by : Najma M.I.Alamami Supervised by : Prof. Dr. Nadia AzizTopics in pediaTric denTisTry 08 607
    2. 2. ouTlines:  Introduction .  criteria of healthy gingival tissue  Classification of gingival diseases.  Eruption Gingivitis  Dental Plaque Induced Gingivitis  Allergy And Gingival Inflammation  Acute Gingival Disease 1) Herpes Simplex Virus Infection. 2) Recurrent Aphthous Ulcer (Canker Sore). 3) Acute Necrotizing Ulcerative Gingivitis (Vincent Infection) 4) Acute Candidiasis (Thrush, Candidosis, Moniliasis). 5) Acute Bacterial Infections.
    3. 3. ouTlines:  Chronic Nonspecific Gingivitis.  Gingival Diseases Modified By Systemic Factors 1) Gingival Diseases Associated With The Endocrine System 2) Gingival Lesions of Genetic Origin. 3) Drugs Induced Gingival Overgrowth. 4) Ascorbic Acid Deficiency Gingivitis (Scorbutic Gingivitis)
    4. 4. Introduction The gingiva is the part of the oral mucous membrane that covers the alveolar processes and the cervical portions of the teeth.
    5. 5. Cont…..<<< The free gingiva is the tissue coronal to the bottom of the gingival sulcus. The attached gingiva extends apically from the free gingival groove to the mucogingival junction.
    6. 6. criteria of healthy gingival tissue
    7. 7. criteria of healthy gingival tissue criteria adult child color light pink more reddish due to increased vascularity and thinner epithelium. The surface of the gingiva (stippling ) stippled less stippled or smoother the marginal gingiva sharp, knifelike edge During the period of tooth eruption in the child, the gingivae are thicker and have rounded margins due to the migration and cervical constriction of the primary teeth. depths around tooth Normally 3mm to be approximately 2 mm, with the facial and lingual probe sites shallower than the proximal sites Periodontal ligament normal width wider periodontal ligament than the adult
    8. 8. Note:  width of the attached gingiva is narrower in the mandible than in the maxilla, and both widths increase with the transition from the primary to permanent dentition The alveolar bone surrounding the primary dentition demonstrates fewer trabeculae, less calcification, and larger marrow spaces
    9. 9. Gingivitis Definition : is inflammation of the gingiva that does not result in clinical attachment loss .
    10. 10. Classification of gingival diseases. Eruption Gingivitis Dental Plaque Induced GingivitisAllergy And Gingival Inflammation Acute Gingival Disease 1)Herpes Simplex Virus Infection. 2)Recurrent Aphthous Ulcer 3)ANUG 4)Acute Candidiasis 5)Acute Bacterial Infections Chronic Nonspecific Gingivitis. Gingival Diseases Modified By Systemic Factors 1)Gingival Diseases Associated With The Endocrine System 2) Gingival Lesions of Genetic Origin. 3)Drugs Induced Gingival Overgrowth. 4)Ascorbic Acid Deficiency Gingivitis (Scorbutic Gingivitis)
    11. 11. Microscopically: 1) inflammatory exudate . 2) Edema . 3) some destruction of collagenous. 4) and ulceration and proliferation of the epithelium facing the tooth and attaching the gingiva to it.
    12. 12. Etiologic Factors  Bacterial plaque, which is composed of soft bacterial deposits that adhere firmly to the teeth, consisting of dense masses of microorganisms embedded in an intermicrobial matrix (biofilm).  In sufficient concentration it can disturb the host-parasite relationship and cause gingival and periodontal disease. Calcified(calculus)Uncalcified:
    13. 13. Etiologic Factors
    14. 14. 1(ERUPTION GINGIVITIS  A transitory type of gingivitis is often observed in young children when the primary teeth are erupting.  often localized and associated with difficult eruption, subsides after the teeth emerge into the oral cavity.
    15. 15. 1(ERUPTION GINGIVITIS  The greatest increase in the incidence of gingivitis in children is often seen in the 6- to 7-year age group when the permanent teeth begin to erupt.  This inflammation is most commonly associated with the eruption of the first and second permanent molars, and the condition can be painful and can develop into a pericoronitis or a pericoronal abscess.
    16. 16. Cause:  This increase in gingivitis apparently occurs because the gingival margin receives no protection from the coronal contour of the tooth during the early stage of active eruption, where Food debris, materia alba, and bacterial plaque often collect around and beneath the free tissue, partially cover the crown of the erupting tooth, and cause the development of an inflammatory process.
    17. 17. treatment  Mild eruption gingivitis requires no treatment other than improved oral hygiene.  Painful pericoronitis may be helped when the area is irrigated with a counterirritant, such as Peroxyl.  Pericoronitis accompanied by swelling and lymph node involvement should be treated with antibiotic therapy.
    18. 18. 1(ERUPTION GINGIVITIS definition A transitory type of gingivitis is often observed in young children when the primary teeth are erupting. group 1) seen in the 6- to 7-year 2) associated with the eruption of the first and second permanent molars cause during the early stage of active eruption, where Food debris, materia alba, and bacterial plaque often collect around and beneath the free tissue treatment Mild eruption gingivitis requires no treatment other than improved oral hygiene.  Painful pericoronitis may be helped when the area is irrigated with a counterirritant, such as Peroxyl.  Pericoronitis accompanied by swelling and lymph node involvement should be treated with antibiotic therapy.
    19. 19. 1(ERUPTION GINGIVITIS pericoronitis
    20. 20. 2(DENTAL PLAQUE INDUCED GINGIVITIS  The degree of dental cleanliness and the condition of the gingival tissues in children are related.  Adequate mouth hygiene and cleanliness of the teeth are related to frequency of brushing and the thoroughness with which bacterial plaque is removed from the teeth.
    21. 21. 2(DENTAL PLAQUE INDUCED GINGIVITIS  Gingivitis is generally less severe in children than in adults with similar plaque levels.  Gingivitis associated with poor oral hygiene is usually classified as: 1)early (slight). 2)Moderate. 3)advanced.  the importanceof a good standard of oral cleanliness in reducing gingivitis and, ideally, preventing the progression of the disease in later life.
    22. 22. treatment
    23. 23. Gingival health was greatly improved after a thorough plaque removalregimen was initiated at home.a Localized gingival infl ammation and recession associated with minimal plaque accumulation on mandibular right central incisor
    24. 24. 3(ALLERGY AND GINGIVAL INFLAMMATION  Matsson and Moller studied the degree of seasonal variation of gingival infl ammation in children with allergies to birch pollen.  Gingival inflammation and the presence or absence of plaque.  gingival infl ammatory reaction in the allergic children during the pollen seasons.  gingival reaction during short allergic seasons is difficult to assess.
    25. 25. 4(Acute Gingival Disease A. Herpes Simplex Virus Infection. B. Recurrent Aphthous Ulcer (Canker Sore). C. Acute Necrotizing Ulcerative Gingivitis (Vincent Infection) D. Acute Candidiasis (Thrush, Candidosis, Moniliasis). E. Acute Bacterial Infections.
    26. 26. A) HERPES SIMPLEX VIRUS INFECTION Herpes virus causes one of the most widespread viral infections. The primary infection usually occurs in a child younger than 6 years of age who has had no contact with the type 1 herpes simplex virus (HSV-1) and who therefore has no neutralizing antibodies.  It is believed that 99% of all primary infections are of the subclinical type. The infection may also occur in susceptible adults who have not had a primary infection
    27. 27. Cont…..<<<  the primary infection may be manifested by acute symptoms (acute herpetic gingivostomatitis). which runs a course of 10 to 14 days.  The active symptoms of the acute disease can occur in children with clean mouths and healthy oral tissues.  May be characterized by only one or two mild sores on the oral mucous membranes, which may be of little concern to the child or may go unnoticed by the parents.
    28. 28. Cont…..<<< The symptoms of the disease develop suddenly and include :  fiery red gingival tissues.  Malaise.  irritability.  headache.  and pain associated with the intake of food and liquids of acid content.
    29. 29. characteristic oral finding in the acute primary disease 1) Is the presence of yellow or white liquid-fi lled vesicles. 2) In a few days the vesicles rupture and form painful ulcers 1 to 3 mm in diameter . 3) covered with a whitish gray membrane and have a circumscribed area of inflammation. 4) The ulcers may be observed on any area of the mucous membrane, including buccal mucosa,tongue, lips, hard and soft palate, and the tonsillar areas. 5) Large ulcerated lesions may occasionally be observed on the palate or gingival tissues or in the region of the mucobuccal fold. 6) This distribution makes the differential diagnosis more diffi cult.
    30. 30. Cont……<<<  Primary herpetic infection has been observed on the dorsal surface of the thumb of a pediatric patient The child was a thumb sucker, and the acute primary infection was present in the mouth.  The dorsal surface of the thumb, which rested on the lower incisor teeth, apparently became irritated, and an inoculation of the virus took place.  The oral condition and the lesions on the thumb subsided in 2 weeks. Primary herpetic infection involving the dorsal surface of the thumb of a 3-year-old child. An acute primary infection was present in the mouth.
    31. 31. Several large, painful ulcers are evident on the tongue of a preschool child with acute herpetic gingivostomatitis. Note: An additional diagnostic criterion is a fourfold rise of serum antibodies to HSV-1. The lesion culture also shows positive results for HSV-1.
    32. 32. Treatment of acute herpetic gingivostomatitis in children the treatments described may be useful, they are only palliative.. A. specifi c antiviral medication as well as provision for the relief of the acute symptoms . B. The application of a mild topical anesthetic, such as dyclonine hydrochloride (0.5%) (Dyclone), before mealtime temporarily relieves the pain . C. allows the child to take in soft food.. D. Because fruit juices are usually irritating to the ulcerated area, ingestion of a vitamin supplement during the course of the disease is indicated. E. Bed rest . F. isolation from other children .
    33. 33. vitamins antiviral topical anesthetic
    34. 34. Examples of drugs used:  The antiviral medications currently available are acyclovir, famciclovir, and valacyclovir. These medications inhibit viral replication in cells infected with the virus. shouldbe administered in five daily doses to equal 1000 mg per day for 10 days.  mainstay of definitive therapy is regular doses of specifi c systemic antiviral medication combined with systemic analgesics (acetaminophen or ibuprofen) during the course of the disease.  Another topical anesthetic, lidocaine (Xylocaine Viscous), can be prescribed for the child who can hold 1 teaspoon of the anesthetic in the mouth for 2 to 3 minutes and then expectorate the solution  Schaaf recommends as an alternative to the anesthetic a mixture of equal parts of diphenhydramine (Benadryl) elixir and Kaopectate. The diphenhydramine has mild analgesic and antiinfl ammatory properties,whereas the kaolin-pectin compound coats the lesions.
    35. 35. Ulcerative stage of primary herpetic gingivostomatitis:(a) palatal gingiva; (b) lower lip mucosa.
    36. 36. recurrent herpes labialis (RHL(.  After the initial primary attack during early childhood, the herpes simplex virus becomes inactive and resides in sensory nerve ganglia.  The virus often reappears later as the familiar cold sore or fever blister, usually on the outside of the lips .  approximately 5% of recurrences are intraoral.
    37. 37. Recurrent herpes labialis. A, Early vesicular lesions. B, Mature vesicular lesion. C, Appearance of herpes labialis after rupture of vesicles and crusting of the lesion. A B C
    38. 38. The recurrence of the disease has often been related to: 1) emotional stress . 2) lowered tissue resistance resulting from various types of trauma. 3) Excessiveexposure to sunlight. Use of sun screen can prevent sun-induced recurrences. 4) Lesions on the lip may also appear after dental treatment and may be related to irritation from rubber dam material or even routine daily procedures.
    39. 39. Herpetic 'cold sore' at the vermilion border.
    40. 40. recurrent herpes labialis (RHL(. treatment  systemic antiviral medications daily dosages are the same as those for the primary infection, but the course of treatment is usually 5 days instead of 10.  Food and Drug Administration (FDA) in children 12 years and older is valacyclovir 2 g, initially and 2 g 12 hours later.  topical antiviral agent, penciclovir Cream may be applied to perioral lesions but should not be applied to intraoral lesions Every 2 hours while awake for 4 days, and it is approved for use in children 12 years of age and older.  Topical 5% acyclovir cream may be prescribed for use five times daily for 4 days in children 12 years of age and older are frequently exposed to HSV-1.
    41. 41. B)RECURRENT APHTHOUS ULCER (CANKER SORE( Definition : is a painful ulceration on the unattached mucous membrane that occurs in school-aged children and adults. also referred to as recurrent aphthous stomatitis (RAS)
    42. 42. B)RECURRENT APHTHOUS ULCER (CANKER SORE( The peak age is between 10 and 19 years of age. characterized by :  recurrent ulcerations on the moist mucous membranes of the mouth, in which both discrete and confluent lesions form rapidly in certain sites and feature .  round to oval crateriform base, raised reddened margins, and pain.
    43. 43. B)RECURRENT APHTHOUS ULCER (CANKER SORE( Classified to : Minor Major herpetifom less common and has been referred to as periadenitis mucosa necrotica recurrens and Sutton disease.
    44. 44. Etological factors The cause of RAU is unknown.But It is possible that the lesions are caused by :  Local and systemic conditions &gastrointestinal disorders.  genetic predisposition.  immunologic and infectious microbial factors.  delayed hypersensitivity to the L form of Streptococcus sanguis,  autoimmune reaction of the oral epithelium.  Local factors include trauma, allergy to toothpaste constituents (sodium lauryl sulfate), and salivary gland dysfunction.
    45. 45. Etological factors  Nutritional defi ciencies are found in 20% of persons with aphthous ulcers.  The clinically detectable deficiencies include deficiencies of iron, vitamin B12, and folic acid.  Stress  Ship and colleagues also suggested herpes simplex virus, humanherpesvirus type 6, cytomegalovirus, Epstein-Barr virus,and varicella-zoster virus as possible causes of RAS
    46. 46. RAS has been associated with other systemic diseases:  PFAPA (periodic fever, aphthous stomatitis, pharyngitis, adenitis), Behçet disease,  Crohn disease,  ulcerative colitis,  celiac disease,  neutropenia,  immunodefi ciency syndromes,  Reiter syndrome,  systemic lupus erythematosus,  MAGIC (mouth and genital ulcers with infl amed cartilage)syndrome.
    47. 47. Treatment of RAU  Lesions persist for 4 to 12 days and heal uneventfully, leaving scars only rarely and only in cases of unusually large lesions .  Current treatment is focused on: 1) promoting ulcer healing, 2) reducing ulcer duration and patient pain, 3) maintaining the patient’s nutritional intake, 4)and preventing or reducing the frequency of recurrence of the disease.
    48. 48. A variety of treatments have been recommended for RAU, but a completely successful therapy has not been found.  topical gels, creams, and ointments as antiinfl ammatory agents.  analgesic medicines and/or systemic immuno- modulating and immunosuppression agents .ex : topical corticosteroid (e.g., 0.5% fl uocinonide, 0.025% triamcinolone, 0.5% clobetasol) is applied to the area with a mucosal adherent (e.g., isobutyl cyanoacrylate, Orabase) before meals and before sleeping may also be helpful or four times daily.
    49. 49. Cont….. <<<  The topical application of tetracycline to the ulcers is often helpful in reducing the pain and in shortening the course of the disease.  A mouthwash containing suspension of one of the tetracyclines has been helpful to some, but the mouthwash should not be swallowed.  Chlorhexidine mouthwash has also been known to alleviate the symptoms of RAU.
    50. 50. recurrent aphthous ulcer. Minor Major herpetifom
    51. 51. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION(  rare among preschool children .  occurs occasionally in children 6 to 12 years old, and is common in young adults.
    52. 52. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION( ANUG can be easily diagnosed because of the involvement of the interproximal papillae and the presence of a pseudomembranous necrotic covering of the marginal tissue
    53. 53. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION( The clinical manifestations of the disease include:  inflamed, painful, bleeding gingival tissue,  poor appetite,  temperature as high as 40°C (104°F),  general malaise,  and a fetid odor.
    54. 54. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION( Causitive agent : Two microorganisms, Borrelia vincentii And fusiform bacilli, referred to as spirochetal organisms, are generally believed to be responsible for the disease.
    55. 55. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION( Treatment : The disease responds dramatically within 24 to 48 hours to : 1) subgingival curettage, 2) débridement, 3) use of mildoxidizing solutions. 4) If the gingival tissues are acutely and extensively infl amed when the patient is first seen, antibiotic therapy is indicated. 5) Improved oral hygiene, 6) the use of mild oxidizing mouth rinses after each meal, and twicedaily rinsing with chlorhexidine will aid in overcoming theinfection.
    56. 56. A) rare example of necrotizing ulcerative gingivitis in an 8-year-old boy. B) Local treatment and improved oral hygiene produced a dramatic recovery from the infection. A B
    57. 57. A 5-year-old Ethiopian boy with necrotizing ulcerative gingivitis.
    58. 58. distinguishing ANUG from acute herpetic gingivostomatitis criteria acute herpetic gingivostomatitis ANUG shap Round ulcers with red areolae on the lips and cheeks involvement of the interproximal papillae and the presence of a pseudo- membranous necrotic covering of the marginal tissue Therapeutic(antibi otics) prophylaxis and débridement not response in the viral infection. a favorable response in cases of ANUG&reduces the acute symptoms in ANUG. Age group most frequently seen in preschool children Rarely occurs in the preschool-aged group onset onset is rapid develops over a longer period, usually in a mouth in which irritants and poor oral hygiene are present
    59. 59. distinguishing ANUG from acute herpetic gingivostomatitis acute herpetic gingivostomatitis ANUG
    60. 60. D) ACUTE CANDIDIASIS (THRUSH, CANDIDOSIS, MONILIASIS(  The lesions of the oral disease appear as raised, furry, white patches, which can be removed easily to produce a bleeding underlying surface  Neonatal candidiasis, contracted during passage through the vagina and eruptingclinically during the fi rst 2 weeks of life, is a common occurrence. This infection is also common in immunosuppressed Patients.  sometimes develop thrush after local antibiotictherapy .
    62. 62. D) ACUTE CANDIDIASIS (THRUSH, CANDIDOSIS, MONILIASIS( Treatment : Antifungal antibiotics control thrush.  For infants and very young children, a suspension of 1 mL (100,000 U) of nystatin (Mycostatin) may be dropped into the mouth for local action four times a day. The drug is nonirritating and nontoxic.  Clotrimazole suspension (10 mg/mL), 1 to 2 mL applied to affected areas four times daily, is an effective antifungal medication.  Systemic fluconazole suspension (10 mg/mL) is safe to use in infants at a total dosage of 6 mg/kg or less per day.
    63. 63. Treatment cont…..<<< :  For children old enough to manage solid medication allowed to dissolve in the mouth, clotrimazole troches or nystatin pastilles are recommended, because the therapeutic agent remains in the saliva longer than with the liquid medication. For children old enough to swallow, systemic fluconazole (100-mg tablets) in a 14- day course may be prescribed for patients whose infection has not responded to topical antifungal agents.
    64. 64. E) ACUTE BACTERIAL INFECTIONS  The prevalence of acute bacterial infection in the oral cavity is unknown.  acute streptococcal gingivitis with painful, vivid red gingivae that bled easily was reported .  The papillae had enlarged, and gingival abscesses had developed.  Cultures showed a predominance of hemolytic streptococci.
    65. 65. E) ACUTE BACTERIAL INFECTIONS treatment :  Broad-spectrum antibiotics are recommended if the infection is believed to be bacterial in origin.  Improved oral hygiene is important in treating the infection.  chlorhexidine mouth rinses are also appropriate.  The placement of dental restorations to restore adequate function and contour after the reduction of acute symptoms is equally important
    66. 66. 5(CHRONIC NONSPECIFIC GINGIVITIS  A type of gingivitis commonly seen during the preteenage and teenage years .  May be localized to the anterior region, or it may be more generalized.  Although the condition is rarely painful, it may persist for long periods without much improvement
    67. 67. 5(CHRONIC NONSPECIFIC GINGIVITIS Characterized by :  the fiery red gingival lesion is not accompanied by enlarged interdental labial papillae or closely associated with local irritants.  The gingivitis showed little improvement after a prophylactic treatment.  The age of the patients involved and the prevalence of the disease in girls suggested a hormonal imbalance as a possible factor.  Histologic examination of tissue sections and the use of special stains ruled out a bacterial infection.
    69. 69. Ethological factors:  multitude of local and systemic factors.  dietary inadequacies  Inadequate oral hygiene.  Malocclusion, and crowded teeth, which make oral hygiene and plaque removal more difficult,  Carious lesions with irritating sharp margins .  faulty restorations with overhanging margins.  mouthbreathing is often responsible for the development of the chronic hyperplastic form of gingivitis, particularly in the maxillary arch.
    70. 70. 5(CHRONIC NONSPECIFIC GINGIVITIS Malocclusionfaulty restorations overhanging margins mouthbreathing
    71. 71. 5(CHRONIC NONSPECIFIC GINGIVITIS Treatment : An improved dietary intake of vitamins and the use of multiple-vitamin supplements will improve the gingival condition in many children. Improved oral hygiene.
    72. 72. 6(Gingival Diseases Modified By Systemic Factors A. Gingival Diseases Associated With The Endocrine System B. Gingival Lesions of Genetic Origin. C. Drugs Induced Gingival Overgrowth. D. Ascorbic Acid Deficiency Gingivitis (Scorbutic Gingivitis)
    73. 73. A) GINGIVAL DISEASES ASSOCIATED WITH THE ENDOCRINE SYSTEM  Puberty gingivitis is a distinctive type of gingivitis that occasionally develops in children in the prepubertal and pubertal period.  The gingival enlargement was marginal in distribution and, in the presence of local irritants, was characterized by prominent bulbous inter proximal papillae far greater than gingival enlargements  associated with local factors.  anterior segment and may be present in only one arch.  The lingual gingival tissue generally remains unaffected .
    75. 75. A) GINGIVAL DISEASES ASSOCIATED WITH THE ENDOCRINE SYSTEM Treatment  improved oral hygiene,  removal of all local irritants,  restoration of carious teeth,  dietary changes necessary to ensure an adequate nutritional status.  oral administration of 500 mg of ascorbic acid. However, the improvement did not occur until the vitamin had been taken for approximately 4 weeks.
    76. 76. A) GINGIVAL DISEASES ASSOCIATED WITH THE ENDOCRINE SYSTEM  Severe cases of hyperplastic gingivitis that do not respond to local or systemic therapy should be treated by gingivoplasty.. Recurrence of any hyperplastic tissue will be minimal if adequate oral hygiene is maintained.
    77. 77. Chronic marginal gingivitis
    78. 78. B) GINGIVAL LESIONS OF GENETIC ORIGIN  Hereditary gingival fibromatosis (HGF) .  This rare type of gingivitis has been referred to as elephantiasis gingivae or hereditary hyperplasia of the gums  is characterized :by a slow, progressive, benign enlargement of the gingivae.  has an autosomal dominant mode of inheritance.
    79. 79. B) GINGIVAL LESIONS OF GENETIC ORIGIN  The gingival tissues appear normal at birth but begin to enlarge with the eruption of the primary Teeth.  the gingival tissues usually continue to enlarge with eruption of the permanent teeth until the tissues essentially cover the clinical crowns of the teeth .  The dense fibrous tissue often causes displacement of the teeth and malocclusion.  The condition is not painful until the tissue enlarges to the extent that it partially covers the occlusal surface of the molars and becomes traumatized during mastication
    81. 81. B) GINGIVAL LESIONS OF GENETIC ORIGIN histologically  as a moderate hyperplasia of the epithelium,with hyperkeratosis and elongation of the rete pegs.  The increase in tissue mass is primarily the result of an increase and thickening of the collagenous bundles inthe connective tissue stroma.  The tissue shows a high degree of differentiation, and a few young fi broblasts are present.
    82. 82. B) GINGIVAL LESIONS OF GENETIC ORIGIN histologically
    83. 83. B) GINGIVAL LESIONS OF GENETIC ORIGIN Treatment :  Surgical removal of the hyperplastic tissue achieves a more favorable oral and facial appearance.  Hyperplasia can recur within a few months after the surgical procedure and can return to the original condition within a few years.  importance of excellent plaque control should be stressed to the patient because this delays the recurrence of the gingival overgrowth.
    84. 84. C)Drugs -INDUCED GINGIVAL OVERGROWTH Many drugs that have been reported to induce gingival overgrowth in some patients include: 1) Phenytoin (Dilantin, or diphenylhydantoin) anticonvulsant. 2) cyclosporin. 3) calcium channel blockers 4) valproic acid. 5) and phenobarbital.
    85. 85. PHENYTOIN-INDUCED GINGIVAL OVERGROWTH  Phenytoin (Dilantin, or diphenylhydantoin), a major anticonvulsant agent used in the treatment of epilepsy.  side effects of varying degrees of gingival hyperplasia first described by Kimball in 1939.  phenytoin-induced gingival overgrowth. an increase in the number of fibroblasts in patients receiving Dilantin.
    87. 87. PHENYTOIN-INDUCED GINGIVAL OVERGROWTH , begins to appear as : Early as 2 to 3 weeks after initiation of phenytoin therapy and peaks at 18 to 24 months. The initial clinical appearance is :  painless enlargement of the interproximal gingiva.  The buccal and anterior segments are more often affected than the lingual and posterior segments.  The affected areas are isolated at first but can become more generalized later.
    88. 88. PHENYTOIN-INDUCED GINGIVAL OVERGROWTH  Unless secondary infection or infl ammation is present, the gingiva appears pink and firm and does not bleed easily on probing.  As the interdental lobulations grow, clefting becomes apparent at the midline of the tooth.  With time the lobulations coalesce at the midline, forming pseudopockets and covering more of the crown of the tooth.  The epithelial attachment level usually remains constant.  In some cases, the entire occlusal surface of the teeth becomes covered.  These lesions may remain purely fibrotic in nature or may be combined with a noticeable infl ammatory component
    90. 90. PHENYTOIN-INDUCED GINGIVAL OVERGROWTH Complication : 1) problems of esthetics. 2) diffi culty in mastication. 3) speech impairment. 4) delayed tooth eruption. 5)tissue trauma, and secondary infl ammation leading to periodontal disease.
    91. 91. PHENYTOIN-INDUCED GINGIVAL OVERGROWTH dental treatment based on clinical oral signs and symptoms. 1) mild PIGO (less than one third of the clinical crown is covered) oral hygiene and more frequent dental care. a series of four consecutive weekly office visits for prophylaxis and topical stannous fluoride application is recommended.
    92. 92. Cont……<<< 2) moderate PIGO ( one third to two thirds of the clinical crown is covered)  oral home care.  use of an irrigating device may be needed.  Use of an antiplaque mouth rinse (0.12% chlorhexidine gluconate) in the device further helps control bacterial growth.  Phenytoin levels should be checked (normal therapeutic  range is 10 to 15 mg/mL).  If there has been no change, consultation with the patient’s physician concerning the possibility of using a different anticonvulsant drug may be helpful.  surgical removal of the overgrowth may be recommended
    93. 93. moderate PIGO
    94. 94. Cont……<<< 3) severe PIGO (i.e., more than two thirds of the tooth is covered) who do not respond to the previously mentioned therapeutic regimens. surgical removal is necessary. scaling and root planing before surgery and meticulous oral hygiene after surgery . no PIGO recurrence for as long as 9 months postoperatively. If surgery is required a second time and the patient has a history of rapid recurrence, a pressure appliance should be considered as an adjunct to home oral care.
    95. 95. severe PIGO
    96. 96. pressure appliance  Immediately after the surgical removal of hyperplastic tissue, an impression was taken and a positive pressure splint was constructed.  Periodontal dressings were removed at the end of 1 week, and the positivepressure appliance was inserted.  The natural rubber, mouth-protector type of appliance and the type with a cast chromium-cobalt framework lined with soft plastic were equally effective.  The appliance is generally used only at night but may be worn night and day if such a schedule is required 8 weeks of therapy..
    97. 97. Preoperative picture showing gingival enlargement Intra-operative view Positive pressure applianceSix months post-operative view
    98. 98. Drug (phenytoin)-induced gingival enlargement in a 12-year-old boy.
    99. 99. D) ASCORBIC ACID DEFICIENCY GINGIVITIS (SCORBUTIC GINGIVITIS(  Scorbutic gingivitis is associated with vitamin C deficiency and differs from the type of gingivitis related to poor oral hygiene.  The involvement is usually limited to the marginal tissues and papillae.  The child with scorbutic gingivitis may complain of severe pain, and spontaneous hemorrhage is evident.
    101. 101. D) ASCORBIC ACID DEFICIENCY GINGIVITIS (SCORBUTIC GINGIVITIS(  Severe clinical scorbutic gingivitis is rare in children.  it may occur in children allergic to fruit juices.  Inflammation and enlargement of the marginal gingival tissue and papillae in the absence of local predisposing factors are possible evidence of scorbutic gingivitis. Treatment : daily administration of 250 to 500 mg of ascorbic acid. Older children and adults may require 1 g of vitamin C for 2 weeks to speed recovery.
    102. 102. Mild gingivitis caused by a vitamin C defi ciency. The marginal tissue and papillae were painfully enlarged. A dietary history revealed that the child’s diet was grossly defi cient in fruits and vegetables. B, Improvement in diet and greater emphasis on oral hygiene resulted in great improvement in the oral health.
    103. 103. conclusion  Gingivitis is a reversible disease. Therapy is aimed primarily at reduction of etiologic factors to reduce or eliminate inflammation, thereby allowing gingival tissues to heal.  Appropriate supportive periodontal maintenance that includes personal and professional care is important in preventing re-initiation of inflammation.  Complete dental care, improved oral hygiene, and supplementation with vitamin C and other water-soluble vitamins will greatly improve the gingival condition.  As with all disorders affecting periodontal tissues, maintaining excellent oral hygiene is the primary key to successful therapy.
    104. 104. REFERENCES  Dentistry For The Child & Adolescent, MCDONALD, 9TH EDITION.  The American Academy Of Pediatric Dentistry (Aapd) Guidelines 2013.  Pinkham JR. Patient Guidance. In: Pinkham JR, Casamassimo PS, Fields HW Jr, Mctigue DJ, Nowak AJ, Eds. Pediatric Dentistry - Infancy Through Adolescence. 5th Ed. St Louis, Mo. Elsevier-saunders Co;pp.113-139, 2012