GINGIVITIS ANDPERIODONTAL DISEASE

CHAPTER 20

Dentistry for the Child and Adolescent

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

It has been divided traditionally into the free and the attached gingiva.

The gingival tissues are normally light pink, although the color may be related to the

complexion of the person the thickness of the tissue the degree of keratinization. The gingival color of the young child

may be more reddish due to increased vascularity and thinner epithelium.

Probing depths around primary teeth is approximately 2 mm, with the facial and lingual probe sites shallower than the proximal sites.

Children have a wider periodontal ligament than the adult.

The 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 in the child.

The surface of the gingiva of a child appears less stippled or smoother than that of an adult.

In the healthy adult the marginal gingiva has a sharp, knifelike edge.

During the period of tooth eruption in the child, however, the gingivae are thicker and have rounded margins due to the migration and cervical constriction of the primary teeth.

Gingivitis

Gingivitis is an inflammation involving only the gingival tissues next to the tooth.

Microscopically, it is characterized by the presence of an inflammatory exudate and edema, some destruction of collagenous gingival fibers, and ulceration and proliferation of the epithelium facing the tooth.

Numerous studies indicate that marginal gingivitis is the most common form of periodontal disease and starts in early childhood.

Severe gingivitis is relatively uncommon in children,

although numerous surveys have shown that a large

portion of the pediatric population has a mild,reversible

type of gingivitis. The major etiologic factors associated with gingivitis

and more significant periodontal disease are uncalcified and calcified bacterial plaque.

However,gingivitis rarely progresses to periodontitis in the preschool and grade school child.

ERUPTION GINGIVITIS

A temporary type of gingivitis is often observed in young children when the primary teeth are erupting.

This gingivitis 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 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, and the continual impingement of food on the gingivae causes the inflammatory process.

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 . This inflammation is most commonly associated with

the eruption of the first and second permanent molars, partially covering the crown of the erupting first

permanent molar. The condition can be painful and can develop into a pericoronitis or a pericoronal abscess.

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.

GINGIVITIS ASSOCIATED WITH POORORAL HYGIENE

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.

Favorable occlusion and the chewing of coarse,detergent-type foods, such as raw carrots, celery,and apples, have a beneficial effect on oral cleanliness.

Gingivitis associated with poor oral hygiene is usually classified as early (slight), moderate, or advanced.

Early gingivitis is quickly reversible and can be treated with a good oral prophylactic treatment and instruction in good toothbrushing and flossing techniques to keep the teeth free of bacterial plaque .

Gingivitis is generally less severe in children than in adults with similar plaque levels.

ALLERGY AND GINGIVAL INFLAMMATION

significance of gingival reaction during short allergic seasons is difficult to assess.

patients with complex allergies who have symptoms for longer periods may be at higher risk for more significant adverse periodontal changes.

ACUTE GINGIVAL DISEASE HERPES SIMPLEX VIRUS INFECTION

RECURRENT APHTHOUS ULCER

recurrent aphthous stomatitis (RAS)—is a painful ulceration on the unattached mucous membrane that occurs in school-aged children and adults.

The peak age for RAU is between 10 and 19 years of age.

It has been reported to be the most common mucosal disorder in people of all ages and races in the world.

Lesions persist for 4 to 12 days and heal uneventfully, leaving scars only rarely and only in cases of unusually large lesions.

The cause of RAU is unknown. Local and systemic conditions and

genetic, immunologic, and infectious microbial factors have been identified as potential causes.

The condition may be caused by a delayed hypersensitivity to the L form of Streptococcus sanguis,which is a common constituent of the normal oral microbiota of humans.

Local factors include trauma, allergy to toothpaste constituents (sodium lauryl sulfate), and salivary gland dysfunction.

In a review of the clinical problem, Antoon and Miller suggested that minor trauma is a common precipitating factor accounting for as many as 75% of the episodes.

Nutritional deficiencies are found in 20% of persons with aphthous ulcers.

The clinically detectable deficiencies include deficiencies of iron, vitamin B12, and folic acid.

Stress may prove to be an important

precipitating factor.

treatment

The primary line of treatment uses topical gels, creams, and ointments as antiinflammatory agents.

Currently, a topical corticosteroid (e.g., 0.5% fluocinonide, 0.025triamcinolone,0.5% clobetasol) is applied to the area with amucosal adherent (e.g., isobutyl cyanoacrylate, Orabase).

The application of triamcinolone acetonide (Kenalog in Orabase) to the surface of the lesions before meals and before sleeping may also be helpful.

Topical rinses have also been helpful for relief of RAU.

The topical application of tetracyclines to the ulcers is often helpful in reducing the pain and in shortening the course of the disease.

Chlorhexidine mouthwash has also been known to alleviate the symptoms of RAU.

Swished dexamethasone elixir is useful to treat ulcerations in areas of the mouth that are difficult to access.

ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION)

The infectious disease commonly referred to as acute necrotizing ulcerative gingivitis (ANUG) is rare among preschool children in the United States

occurs occasionally in children 6 to 12 years old, and is common in young adults.

Treponema vincentii and gram-negative fusiform bacilli

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, fever as high as 40° C (104° F),general malaise, and a fetid odor.

The disease responds dramatically within 24 to 48 hours to subgingival curettage, debridement, and the use of mild oxidizing solutions.

If the gingival tissues are acutely and extensively inflamed when the patient is first seen, antibiotic therapy is indicated.

Improved oral hygiene, the use of mild oxidizing mouthrinses after each meal, and twice-daily rinsing with chlorhexidine will aid in overcoming the infection.

ACUTE BACTERIAL INFECTIONS

The prevalence of acute bacterial infection in the oral cavity is unknown.

acute streptococcal gingivitis : painful, vivid red gingiva that bleeds easily.

The papillae are enlarged, and gingival abscesses developes.

Cultures show a predominance of hemolytic streptococci.

Broadspectrum antibiotics are recommended if the infection is believed to be bacterial in origin.

Improved oral hygiene is important in treating the infection.

As with any acute microbial oral infection, chlorhexidine mouthrinses are also appropriate.

The placement of dental restorations to restore adequate function and contour after the reduction of acute symptoms is equally important.

CHRONIC NONSPECIFICGINGIVITIS

A type of gingivitis commonly seen during the preteenage and teenage years is often referred to as chronic nonspecific gingivitis.

The chronic gingival inflammation 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.

prevalence of the disease in girls suggests a hormonal imbalance as a possible factor. Inadequate oral hygiene, which allows food

impaction and the accumulation of materia alba and bacterial plaque, is undoubtedly the major cause of this chronic type of gingivitis.

the chronic gingivitis group had a larger percentage of AB blood types and a smaller percentage of 0 blood type than the control group.

The cause of gingivitis is complex and is considered to be based on a multitude of local and systemic factors.

Because dietary inadequacies are often found in the preteenage and teenage groups, an improved dietary intake of vitamins and the use of multiple-vitamin supplements will improve the gingival condition in many children.

Malocclusion, which prevents adequate function, and crowded teeth, which make oral hygiene and plaque removal more difficult, are also important predisposing factors in gingivitis.

Carious lesions with irritating sharp margins, as well as faulty restorations with overhanging margins(both of which cause food accumulation) also favor the development of the chronic type of gingivitis.

The irritation to the gingival tissue produced by mouth breathing is often responsible for the development of the chronic hyperplastic form of gingivitis, particularly in the maxillary arch.

GINGIVAL DISEASES MODIFIEDBY SYSTEMIC FACTORS

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 enlargement of the gingival tissues in puberty gingivitis is confined to the anterior segment and may be present in only one arch.

The lingual gingival tissue generally remains unaffected

treatment

Treatment of puberty gingivitis should be directed toward improved oral hygiene, removal of all local irritants, restoration of carious teeth, and dietary changes necessary to ensure an adequate nutritional status.

Severe cases of hyperplastic gingivitis that do not respond to local or systemic therapy should be treated by gingivoplasty.

GINGIVAL LESIONS OF GENETIC ORIGIN

Hereditary gingival fibromatosis (HGF): autosomal dominant mode of inheritance.

elephantiasis gingivae or hereditary hyperplasia of the gums

The gingival tissues appear normal at birth but begin to enlarge with the eruption of the primary teeth.

Although mild cases are observed, 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.

The increase in tissue mass is primarily the result of an increase and thickening of the collagenous bundles in the connective tissue stroma.

The tissue shows a high degree of differentiation, and a few young fibroblasts are present.

treatment

Surgical removal of the hyperplastic tissue achieves a more favorable oral and facial appearance.

However, hyperplasia can recur within a few months after the surgical procedure and can return to the original condition within a few years.

Although the tissue usually appears pale and firm, the surgical procedure is accompanied by excessive hemorrhage. Therefore quadrant surgery is usually recommended.

The importance of excellent plaque control should be stressed to the patient because this delays the recurrence of the gingival overgrowth.

PHENYTOIN-INDUCED GINGIVAL OVERGROWTH

The influence of serum and salivary levels of phenytoin on the development of PIGO has also been investigated.

I t 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.

No such correlations were observed for patient age, daily or total phenytoin dose, duration of therapy, or serum phenytoin level.

Most investigators agree on the existence of a close relationship between oral hygiene and PIGO.

PIGO can be decreased or prevented by scrupulous oral hygiene and dental prophylaxis.

PIGO, when it does develop, 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 .

The affected areas are isolated at first but can become more generalized later.

Unless secondary infection or inflammation 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.

treatment

Patients with mild PIGO : less than one third of the clinical crown

is covered Daily meticulous oral hygiene and more

frequent dental care.

For patients with moderate PIGO (i.e., one third to two thirds of the clinical crown is covered) meticulous oral home care and the judicious use of an irrigating device may be needed.

Use of an antiplaque mouthrinse (0.12% chlorhexidine gluconate) in the device will further help control bacterial growth.

Initially, a series of four consecutive weekly office visits for prophylaxis and topical stannous fluorid application is recommended.

The fifth week is used to evaluate the gingivae and note any change in size.

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.

If no improvement occurs, surgical removal of the overgrowth may be recommended.

For patients with 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.

As in any periodontal surgery, scaling and root planing before surgery and meticulous oral hygiene after surgery are essentialto minimize the overgrowth, which can occur as early as 3 to 4 weeks after surgery.

Other drugs that have been reported to induce gingival overgrowth in some patients include

cyclosporin calcium channel blockers valproic acid phenobarbital As with all disorders affecting periodontal

tissues, maintaining excellent oral hygiene is the

primary key to successful therapy.

ASCORBIC ACID DEFICIENCYGINGIVITIS

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 in the absence of local predisposing factors.

The child with scorbutic gingivitis may complain of severe pain, and spontaneous hemorrhage will be evident.

treatment

Severe clinical scorbutic gingivitis is rare in children. However, it may occur in children allergic to fruit

juices when provision of an adequate dietary supplement of vitamin C is neglected . When blood studies indicate a vitamin C deficiency

and exclude other possible systemic conditions, the gingivitis will respond dramatically to the 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.

PERIODONTAL DISEASESIN CHILDREN

Periodontitis, an inflammatory disease of the gingiva and deeper tissues of the periodontium, is characterized by pocket formation and destruction of the supporting alveolar bone.

Bone loss in children can be detected in

bite-wing radiographs by comparing the height of the alveolar bone to the cementoenamel junction.

Distances between 2 and 3 mm can be defined as questionable bone loss and distances greater than 3 mm indicate definite bone loss.

Bone loss is usually between the primary first and second molars.

EARLY-ONSET PERIODONTITIS

In its classification of periodontitis, the American Academy of Periodontology has categorized the earlyonset form under Aggressive Periodontitis.

heterogeneous group of periodontal disease occurring in young individuals who are otherwise healthy.

(1) localized form (localized agressive periodontitis [LAP])

(2) generalized form (generalized agressive periodontitis[GAP])

the prevalence of aggressive periodontitis in adolescent schoolchildren in the United States is 10% in blacks, 5% in Hispanics, and 1.3% in whites.

Boys are more likely to have GAP than girls (ratio of 4.3:1)

Localized aggressive periodontitis

Aggressive periodontitis of the primary dentition can occur in a localized form but usually is seen in the generalized form.

LAP is localized attachment loss and alveolar bone loss only in the primary dentition in an otherwise healthy child.

The exact time of onset is unknown, but it appears to arise around or before 4 years of age, when the bone loss is usually seen on radiographs around the primary molars and/or incisors.

Abnormal probing depths with minor gingival inflammation, rapid bone loss, and minimal to varying amounts of plaque have been demonstrated at the affected sites of the child's dentition.

Abnormalities in host defenses (e.g., leukocyte chemotaxis), extensive proximal caries facilitating plaque retention and bone loss, and a family history of periodontitis have been associated with LAP in children.

Generalized aggressive periodontitis

The onset of (GAP) is during or soon after the eruption of the primary teeth.

It results in severe gingival inflammation and generalized attachment loss, tooth mobility, and rapid alveolar bone loss with premature exfoliation of the teeth .

Testing may reveal a high prevalence of leukocyte adherence abnormalities and an impaired host response against bacterial infections.

Alveolar bone destruction proceeds rapidly, and the primary teeth may be lost by 3 years of age.

Micro-organisms predominating in the gingival pockets include:

Actinobacillus actinomycetemcomitans (Aa) Porphyromonas (Bacteroides) gingivalis, Bacteroides melaninogenicus Prevotella intermedia Capnocytophaga sputigena Fusobacterium nucleatum

Recent findings of Asikainen et al suggest that

the major periodontal pathogens are transmitted among family members.

Often the past medical history of the child reveals a history of recurrent infections. (e.g., otitis media, skin infections, upper respiratory tract infections)

Treatment

Treatment of LAP or GAP depends on early diagnosis, dental curettage, root planing, prophylaxis, oral hygiene instruction, restoration of decayed teeth, removal of the primary teeth that have lost bony support, and more frequent recalls.

Use of antimicrobial rinses (chlorhexidine) and therapy with broad-spectrum antibiotics are effective in eliminating the periodontal pathogens.

Amoxicillin (Augmentin) has been used in children (250-mg liquid three times a day for 10 days).

Treatment of GAP is less successful overall and sometimes requires extraction of all primary teeth.

children affected with LAP or GAP may experience severe periodontitis of the permanent teeth.

LOCALIZED AGGRESSIVE PERIODONTITIS (LOCALIZED JUVENILE PERIODONTITIS) LAP occurs in otherwise healthy children

and adolescents without clinical evidence of systemic disease.

It is characterized by the rapid and severe loss of alveolar bone around more than one permanent tooth, usually the first molars and incisors.

It appears selflimiting, and retrospective data obtained from LAP patients suggest that bone loss around the primary teeth can be an early finding in this disease.

Reported estimates of the prevalence of LAP range from 0.1% to 1.5% with a bilaterally symmetric pattern of bone loss in a geographically diverse adolescent population.

The prevalence in the black population is greater, at 2.5%.

Clinically, LAP patients have little or no tissue inflammation and very little supragingival dental plaque or calculus.

Progression of bone loss is three to four times faster than in adult periodontitis.

The probable causative microbial species are Aa or Aa in combination with porphyromonas-like species.

A variety of neutrophil defects have been reported in patients with LAP: abnormalities in peripheral blood neutrophil ( polymorphonuclear leukocyte) chemotaxis and in some cases in monocyte chemotaxis.

Also, anomalies of phagocytosis, bacterial activity, leukotriene B4 generation, and other defects have been reportedsome believe the mode

Transmission is: autosomal recessive Xlinked dominant mode.

GENERALIZED AGRESSIVE PERIODONTITIS (GENERALIZED JUVENILE PERIODONTITIS)

The generalized form occurs at or around puberty in older juveniles and young adults. It often affects the entire periodontium of the dentition.

Because of its wide distribution and rapid rate of alveolar bone destruction, the generalized form of EOP also is known by the terms

generalized juvenile periodontitis (GJP), severe periodontitis, and rapidly progressive periodontitis.

Affected teeth harbor more nonmotile, facultative, anaerobic, gram-negative rods (especially Porphyromonas gingivalis) in GAP than in LAP.

The localized and generalized forms of AP are distinctly different radiographically and clinically. Neutrophils in GAP patients have suppressed

chemotaxis. Individuals with GAP exhibit marked periodontal

inflammation and have heavy accumulations of plaque and calculus.

Loe and Brown reported a 0.13% prevalence of GAP among adolescents in the United States.

TREATMENT

Successful treatment of AP depends on early diagnosis, use of antibiotics against the infecting microorganisms, and provision of an infection-free environment for healing.

Treatment of AP both the localized and generalized types, includes surgery and

the use of tetracyclines (sometimes in combination with metronidazole).

Treatment of GAP is often less predictable.

In patients with LAP, Aa organisms penetrate into the crevicular epithelium.

Treatment with antibiotics alone, such as a 2-week course of doxycycline (a synthetic tetracycline), has been shown to reduce the Aa population.

Surgical removal of infected crevicular epithelium and debridement of root surfaces during surgery while the patient is on a 14-day course of doxycycline hyclate (1 g per day) is considered the best effective treatment modality.

Rams, Keyes, and Wright described the Keyes technique as effective in treating LAP.

The treatment involves meticulous scaling and root planing of all teeth, with concomitant irrigation to probing depth of saturated inorganic salt solutions and 1% chloramine T.

In addition, they recommended administration of systemic tetracycline (1 g per day) for 14 days.

Patient home care treatment included daily application of a paste of sodium bicarbonate and 3% hydrogen peroxide and inorganic salt irrigations.

PREMATURE BONE LOSS IN THE PRIMARYDENTITION

Advanced alveolar bone loss associated with systemic disease occurs in children and adolescents as well as adults.

Local factors (periodontitis, trauma, and infection secondary to caries) account for the majority of cases of premature bone loss.

Systemic disease

hypophosphatasia, Papillon-Lefevre syndrome, histiocytosis X, agranulocytosis, leukocyte adherence deficiency, neutropenias, leukemias, diabetes mellitus, scleroderma, fibrous dysplasia, acrodynia, Down syndrome, and Chediak-Higashi syndrome.

Diabetes mellitus

Occur in both insulin-dependent and noninsulin- dependent diabetes mellitus. Impaired immune function. 10% to 15% of teenagers with insulin-dependent diabetes mellitus have significant periodontal disease. Poor metabolic control increases the risk of

periodontitis, and untreated periodontitis in turn worsens metabolic control of diabetes.

Down Syndrome

Plaque levels are high in these patients, but the severity of periodontal destruction exceeds that

attributable to local factors alone. Various minor immune deficits, particularly in

neutrophil function, have been identified and may be responsible for the increased susceptibility to periodontitis.

Severe recession in the mandibular anterior region associated with a high frenum attachment is also common in Down syndrome.

Hypophosphatasia

The disease is characterized by improper mineralization of bone caused by deficient alkaline phosphatase activity in serum, liver, bone, and kidney (tissue nonspecific).

Increased levels of urinary phosphoethanolamine are also seen.

lethal autosomal recessive infantile type (I), autosomal recessive milder juvenile type (II) and the autosomal dominant adult type (III).

Early exfoliation of the primary teeth is usually associated with the juvenile type (II), although such a history may also be present in the adult type (III).

The early loss of teeth is the result of defective cementum formation, which in turn results in a weakened attachment of tooth to bone.

The teeth are affected in the order of formation, so that those that form the earliest are most likely to be involved and the most severely affected.

There currently is no treatment for the disease, but the dental prognosis for the permanent teeth is good.

Typically the primary incisors are exfoliated before the age of 4 years, the other primary teeth are affected to varying degrees, and the permanent dentition is normal.

CHERUBISM (FAMILIAL FIBROUS DYSPLASIA)

A symmetric or asymmetric enlargement of the jaws may be noted at an early age.

Teeth in the involved area are frequently exfoliated prematurely as a result of the loss of support or root resorption or, in permanent teeth, as a result of an interference in the development of roots.

ACRODYNIA

The exposure of young children to minute amounts of mercury is responsible for a condition referred to as acrodynia or pink disease.

Ointments and medications are the usual sources of the mercury.

Dental amalgam restorations do not cause acrodynia.

The clinical features of the disease include fever, anorexia, desquamation of the soles and palms (causing them to be pink), sweating, tachycardia, gastrointestinal disturbance, and hypotonia.

The oral findings include inflammation and ulceration of the mucous membrane, excessive salivation, loss of alveolar bone, and premature exfoliation of teeth.

HYPOPHOSPHATEMIA (FAMILIAL OR X-LINKEDHYPOPHOSPHATEMIC RICKETS OR VITAMIN D RESISTANT RICKETS)

hypophosphatemia is the most common inherited abnormality of renal tubular transport.

Clinical: short stature and bowing of the lower extremities in affected boys.

Premature tooth exfoliation is sometimes also a feature.

in the absence of PHEX enzymatic activity, osteopontin — a mineralization-inhibiting protein found in the extracellular matrix of bone— may accumulate in the bone to contribute to the osteomalacia. {Sodek, J; et al (2000). "Osteopontin". Critical Reviews in Oral Biology and Medicine 11 (3): 279–303.}

Other dental manifestations often include apical radiolucencies, abscesses, and fistulas associated with

pulp exposures in the primary and permanent teeth. The pulp exposures relate to the pulp horns extending to

the dentinoenamel junction or even to the external surface of the tooth. The thin, hypomineralized enamel is abraded easily,

which exposes the pulp. Dentin dysplasia , interglobular dentin. Absent or abnormal lamina dura.

Leukocyte Adhesion Deficiency

Leukocyte adhesion deficiency (LAD) is a rare,

recessive genetic disease. In LAD, the CD 18 surface protein on

leukocytes is defective or absent resulting in poor migration to infection sites and impaired phagocytic function.

This leaves patients susceptible to bacterial infections, including periodontitis.

Due to the high incidence of skin abscesses, recurrent otitis media, pneumonitis, and other bacterial infections of soft tissues, a diagnosis is usually made before dental symptoms appear.

Dental symptoms are manifested early in the primary dentition.

Bone loss is rapid around nearly all teeth, and inflammation is marked.

In the dental literature LAD has sometimes been called generalized prepubertal periodontitis.

Neutropenia

Several different forms of neutropenia, including cyclic neutropenia, have been associated with oral symptoms in children.

Neutropenia can be diagnosed by a finding of depressed neutrophils on a differential blood count.

Periodontal therapy consists of rigorous local measures to control plaque, but patients are seldom able to maintain the level of oral hygiene necessary to prevent disease.

Papillon-Lefevre Syndrome Papillon-Lefevre syndrome is a rare disease that has

as a symptom the onset of severe periodontitis in the primary or transitional dentition.

It is a genetic disorder that is easily identified on clinical examination by the finding of hyperkeratosis of the palms of the hands and soles of the feet.

Severe inflammation and rapid bone loss are characteristic of the periodontitis.

The exact cause of periodontal disease in PLS has not been found, but it has been attributed to decrease neutrophil phagocytosis (Rathi, 2002).

Histiocytosis

Langerhans cell histiocytosis (LCH), previously known as histiocytosis X.

Rare disorder of childhood with typical presentation as infiltration of bones, skin, liver, and other organs by histiocytes.

In 10% to 20% of cases, the initial infiltrates occur in the oral cavity, usually in the mandible.

Typical findings are gingival enlargement,ulceration, mobility of teeth with alveolar expansion, and discrete, destructive lesions of bone that can be observed on radiographs.

Teeth may be left "floating in air" and eventually exfoliated.

The lesions of histiocytosis may initially be mistaken for localized aggressive periodontitis.

Therapy consists of local measures such as radiation and surgery to remove lesions and systemic chemotherapy for disseminated disease.

Leukemia

AML, but not usually ALL, may present with gingival enlargement caused by infiltrates of leukemic cells.

The lesions are bluish red and may

sometimes invade bone.

In addition to the gingival lesions, the patient may have fever, malaise, gingival or other bleeding, and bone or joint pain.