gingival disease in children by >> najma alamami

Presented by : Najma M.I.Alamami

Supervised by : Prof. Dr. Nadia AzizTopics in pediatric Dentistry 08 607

Outlines: Introduction . criteria of healthy gingival tissue Classification of gingival diseases. Eruption Gingivitis Dental Plaque Induced Gingivitis Allergy And Gingival Inflammation Acute Gingival Disease1) 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.

Outlines: Chronic Nonspecific Gingivitis. Gingival Diseases Modified By Systemic Factors1) Gingival Diseases Associated With The Endocrine System2) Gingival Lesions of Genetic Origin.3) Drugs Induced Gingival Overgrowth.4) Ascorbic Acid Deficiency Gingivitis (Scorbutic Gingivitis)

Introduction

The gingiva is the part of the oral mucous membrane that covers the alveolar processes and the cervical portions of the teeth.

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.

criteria of healthy gingival tissue

criteria of healthy gingival tissuecriteriaadultchild

color light pinkmore reddish due to increased vascularity and thinner epithelium.

The surface of the gingiva (stippling )

stippledless 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 toothNormally 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

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

GingivitisDefinition : is inflammation of the gingiva that does not result in

clinical attachment loss .

Classification of gingival diseases.

Eruption Gingivitis

Dental Plaque Induced GingivitisAllergy And Gingival

Inflammation

Acute Gingival Disease1)Herpes Simplex Virus Infection.2)Recurrent Aphthous Ulcer 3)ANUG4)Acute Candidiasis 5)Acute Bacterial Infections

Chronic Nonspecific Gingivitis.

Gingival Diseases Modified By Systemic Factors1)Gingival Diseases Associated With The Endocrine System2) Gingival Lesions of Genetic Origin.3)Drugs Induced Gingival Overgrowth.4)Ascorbic Acid Deficiency Gingivitis (Scorbutic Gingivitis)

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.

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:

Etiologic Factors

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.

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.

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.

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.

1)ERUPTION GINGIVITISdefinitionA transitory type of gingivitis is often observed in young children when

the primary teeth are erupting.

group1) seen in the 6- to 7-year2) associated with the eruption of the first and second permanent molars

causeduring the early stage of active eruption, where Food debris, materia alba, and bacterial plaque often collect around and beneath the free tissue

treatmentMild 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.

pericoronitis

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.

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.

treatment

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

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.

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.

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

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.

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.

characteristic oral finding in the acute primary disease1) 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.

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 dorsalsurface of the thumb of a 3-year-old child. An acute primary infection was present in the mouth.

Several large, painful ulcers are evident on

thetongue 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.

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 .

vitamins

antiviral topical anesthetic

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.

Ulcerative stage of primaryherpetic gingivostomatitis:(a) palatal

gingiva; (b) lower lip mucosa.

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.

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 .

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.

Herpetic 'cold sore' at thevermilion border.

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.

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)

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.

Classified to :Minor

herpetifom

less common and has been referred to as periadenitis mucosa necrotica recurrens and Sutton disease.

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.

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

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.

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.

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.

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.

recurrent aphthous ulcer .

herpetifom

C) ACUTE NECROTIZING ULCERATIVEGINGIVITIS (VINCENT INFECTION)

rare among preschool children . occurs occasionally in children 6 to 12 years old,

and is common in young adults.

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

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.

Causitive agent :Two microorganisms, Borrelia vincentii And fusiform

bacilli, referred to as spirochetal organisms, are generally believed to be responsible for the disease.

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.

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 5-year-old Ethiopian boywith necrotizing ulcerative gingivitis.

distinguishing ANUGfrom acute herpetic gingivostomatitis

criteriaacute herpetic gingivostomatitis

shapRound ulcers with red areolaeon the lips and cheeks

involvement of the interproximal papillae and the presence of a pseudo-membranous necrotic covering of the marginal tissue

Therapeutic(antibiotics) 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

onsetonset is rapiddevelops over a longer period, usually in a mouth in which irritants and poor oral hygiene are present

distinguishing ANUGfrom acute herpetic gingivostomatitis

acute herpetic gingivostomatitisANUG

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 .

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.

Treatmentcont: >>>..…

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.

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.

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

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

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.

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.

Malocclusionfaulty restorations

overhanging marginsmouthbreathing

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.

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)

A) GINGIVAL DISEASES ASSOCIATEDWITH 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 .

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.

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.

Chronic marginal gingivitis

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.

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

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.

histologically

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.

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 blockers4) valproic acid.5) and phenobarbital.

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.

, 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.

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

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.

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.

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

moderate PIGO

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.

severe PIGO

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..

Preoperative picture showing gingival enlargement

Intra-operative view

Positive pressure appliance Six months post-operative view

Drug (phenytoin)-induced gingival enlargement in a 12-year-old boy.

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.

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.

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.

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.

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

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