Penyakit Periodontal pada Anak.

Penyakti Gingiva disebabkan oleh plak

Gingivitis sering terjadi pada anak-anak dan remaja, mengenai hingga 70% pada anak usia tujuh
tahun. Peradangan umumnya terbatas pada marginal gingiva, kerusakan tulang dan perlekatan
jaringan ikat yang tidak terdeteksi. Meskipun gingivitis tidak selalu menjadi periodontitis,
penanganan penyakit gingiva pada anak-anak sangat penting karena periodontitis bermula dari
gingivitis.
Pada anak-anak, seperti juga pada orang dewasa, penyebab utama gingivitis adalah plak gigi,
disebabkan kebersihan mulut yang buruk. Hubungan antara antara plak dan indeks gingiva, tidak
terlalu terlihat. Meskipun gingivitis sangat tinggi prevelansi pada anak-anak, tetapi keparahannya
tidak separah orang dewasa. Kondisi kebersihan mulut yang Mirip umumnya menghasilkan bentuk
yang kurang parah penyakit pada anak-anak dibandingkan orang dewasa.
Dengan bertambahnya usia anak, kecenderungan mereka untuk terjadinya gingivitis meningkat.
Prevalensi penyakit terendah selama tahun-tahun prasekolah dan memuncak selama masa pubertas.
Peningkatan gingivitis tidak sepenuhnya berkorelasi dengan jumlah plak,tetapi juga pengaruh faktorfaktor lain.

Clinical Features
The most prevalent type of gingival disease in childhood is chronic marginal gingivitis (see Figure 119). The gingival tissues exhibit changes in color, size, consistency, and surface texture similar to
chronic inflammation in the adult. Red, linear inflammation is accompanied by underlying chronic
changes, including swelling, increased vascularization, and hyperplasia. Bleeding and increased
pocket depth are not found as often in children as in adults but may be observed if severe gingival
hypertrophy or hyperplasia occur.[7,40] Chronic gingivitis in children is characterized by loss of collagen
in the area around the junctional epithelium and an infiltrate consisting mostly of lymphocytes, with
small numbers of polymorphonuclear leukocytes, plasma cells, monocytes, and mast cells. Lesions
generally have relatively few plasma cells and resemble the early nondestructive, nonprogressive
lesions seen in adults.

Gambaran Klinis
Jenis yang paling umum dari penyakit gingiva pada anak-anak adalah gingivitis marginal
kronis. Jaringan Gingiva terjadi perubahan dalam warna, ukuran, konsistensi, dan tekstur
permukaan mirip dengan peradangan kronis pada orang dewasa. Merah, peradangan linear
disertai dengan perubahan yang kronis, termasuk pembengkakan, peningkatan vaskularisasi,
dan hiperplasia. Perdarahan dan peningkatan kedalaman poket tidak ditemukan sesering pada
anak-anak seperti pada orang dewasa tetapi dapat diamati jika hipertrofi gingiva parah atau
hiperplasia terjadi. [7,40] gingivitis kronis pada anak-anak ditandai dengan hilangnya kolagen
di daerah sekitar epitel junctional dan infiltrasi sebagian besar terdiri dari limfosit, dengan
sejumlah kecil leukosit polimorfonuklear, sel plasma, monosit, dan sel mast. Lesi umumnya
memiliki relatif sedikit sel plasma dan menyerupai tak rusak, lesi nonprogressive awal
terlihat pada orang dewasa.
Gingivitis in children also differs from adult gingivitis in that the response is
dominated by T lymphocytes, with few B lymphocytes and plasma cells in the
infiltrate. This difference could explain why gingivitis in children rarely progresses

to periodontitis.[29,31,32,35,47]
Gingival histology in children also demonstrates other unique features that may
contribute to a decreased tendency to progress to severe gingivitis. The junctional
epithelium of the primary dentition tends to be thicker than in the permanent
dentition,[9] which is thought to reduce the permeability of the gingival structures to
bacterial toxins that initiate the inflammatory response.
Calculus
Calculus deposits are uncommon in infants and toddlers, but may increase with age. About 9% of 4to 6-year-old children exhibit calculus deposits. By age 7 to 9 years, 18% of children present with
calculus deposits, and by age 10 to 15 years, 33% to 43% have some calculus formation. Within the
category of special needs patients, children with cystic fibrosis have a higher incidence of number of
calculus deposits, which may be caused by increased calcium and phosphate concentrations in their
saliva.[54] Children fed exclusively with gastric or nasogastric tubes show significant calculus buildup
secondary to lack of function and increased oral pH.

Microbiology of Disease
Because the intensity of gingival disease increases as a child develops into adulthood, it is important
to understand the microbiology of disease, which is discussed more fully in Chapter 23. Interestingly,
the composition of the oral microflora also changes as the child matures. [9] Yang et al[55] analyzed
samples of dental plaque in children and reported that 71% of 18- to 48-month-old children were
infected with at least one periodontal pathogen. Sixty-eight percent were infected withPorphyromonas
gingivalis and 20% exhibited Bacteroides forsythus (Tannerella forsythia).[55] A moderate correlation
also has been found between B. forsythus in children and periodontal disease in their mothers. B.
forsythus also has been associated with gingival bleeding in children.

kalkulus
Deposit kalkulus jarang terjadi pada bayi dan balita, namun dapat meningkatkan dengan usia.
Sekitar 9% dari 4 sampai 6 tahun anak pameran deposit kalkulus. Pada usia 7 sampai 9 tahun,
18% dari anak-anak sekarang dengan deposit kalkulus, dan pada usia 10 sampai 15 tahun,
33% sampai 43% memiliki beberapa formasi kalkulus. Dalam kategori pasien berkebutuhan
khusus, anak-anak dengan fibrosis kistik memiliki insiden yang lebih tinggi dari jumlah
deposit kalkulus, yang mungkin disebabkan oleh peningkatan kalsium dan fosfat konsentrasi
dalam air liur mereka. [54] Anak-anak makan secara eksklusif dengan tabung lambung atau
nasogastric menunjukkan kalkulus signifikan penumpukan sekunder kurangnya fungsi dan
meningkatkan pH mulut.
Mikrobiologi Penyakit
Karena intensitas penyakit meningkat gingiva sebagai seorang anak berkembang menjadi
dewasa, penting untuk memahami mikrobiologi penyakit, yang dibahas lebih lengkap dalam
Bab 23. Menariknya, komposisi mikroflora mulut juga berubah sebagai anak dewasa. [9 ]
yang et al [55] menganalisis sampel plak gigi pada anak-anak dan melaporkan bahwa 71%
dari anak-anak usia 18 sampai 48-bulan-tua yang terinfeksi dengan setidaknya satu patogen
periodontal. Enam puluh delapan persen terinfeksi withPorphyromonas gingivalis dan 20%
dipamerkan Bacteroides forsythus (Tannerella forsythia). [55] Sebuah korelasi moderat juga

telah ditemukan antara B. forsythus pada anak-anak dan penyakit periodontal pada ibu
mereka. B. forsythus juga telah dikaitkan dengan gingiva perdarahan pada anak-anak.
In a similar study, 60% of children between 2 and 18 years of age had detectable levels of P.
gingivalis in their plaque and 75% showed similar levels ofActinobacillus actinomycetemcomitans. The
presence of P. gingivalis was most strongly associated with the progression of gingivitis and the onset
of periodontitis in healthy children.[39]
Experimental gingivitis models in children have demonstrated increased subgingival levels
of Actinomyces, Capnocytophaga, Leptotrichia and Selenomonas[15]pathogens that generally are
not seen in adult gingivitisthereby raising interest in their potential role in the etiology of childhood
gingivitis.

Dalam sebuah penelitian serupa, 60% dari anak-anak antara 2 dan 18 tahun memiliki tingkat
terdeteksi P. gingivalis dalam plak dan 75% menunjukkan tingkat yang sama dari Actinobacillus
actinomycetemcomitans. Kehadiran P. gingivalis yang paling kuat terkait dengan perkembangan
gingivitis dan timbulnya periodontitis pada anak-anak yang sehat. [39]
Model gingivitis eksperimental pada anak-anak telah menunjukkan peningkatan tingkat subgingival
dari Actinomyces, Capnocytophaga, Leptotrichia dan Selenomonas [15] -pathogens yang umumnya
tidak terlihat pada orang dewasa gingivitis-sehingga meningkatkan minat dalam peran potensial
mereka dalam penyebab gingivitis masa anak-anak.

Eruption Gingivitis
Gingivitis associated with tooth eruption is so common that the term eruption gingivitis has come into
common use. Tooth eruption per se does not cause gingivitis; however, inflammation associated with
plaque accumulation around erupting teeth, perhaps secondary to discomfort caused by brushing
these friable areas, may contribute to gingivitis. [9] The gingiva around erupting teeth may appear
reddened because gingival margins have not yet keratinized fully and sulcus development is
incomplete (Figure 11-10).

Figure 11-10 Eruption gingivitis complicated with s

evere marginal gingivitis secondary to the illustrated poor oral hygiene.

Gingivitis gigi tumbuh

Gingivitis yang berhubungan dengan erupsi gigi sangat umum bahwa gingivitis letusan istilah telah
datang ke dalam penggunaan umum. Erupsi gigi per se tidak menyebabkan gingivitis; Namun,
peradangan yang terkait dengan akumulasi plak di sekitar gigi tumbuhnya , mungkin sekunder untuk
ketidaknyamanan yang disebabkan oleh menyikat daerah-daerah gembur, dapat menyebabkan
radang gusi. [9] gingiva sekitar gigi tumbuhnya mungkin muncul memerah karena margin gingiva
belum keratin sepenuhnya dan pengembangan sulcus adalah tidak lengkap (Gambar 11-10).

Exfoliating and severely carious primary teeth often contribute to gingivitis caused by plaque
accumulation secondary to pain during brushing or food impaction in areas of tooth destruction. As a
normal part of exfoliation, the junctional epithelium migrates under the resorbing tooth, increasing
pocket depth and potentially creating a niche for pathogenic bacteria. [9] The discomfort of chewing on
severely infected teeth often leads to unilateral chewing on the unaffected side.

Puberty Gingivitis
As mentioned previously, the incidence of marginal gingivitis increases as a child matures, peaking at
9 to 14 years of age, then decreasing slightly after puberty.[9]Gingival disease that behaves in such a

manner is often referred to as pubertal (or puberty) gingivitis. Chapters 9 and 27 continue the
discussion of this condition.
The most frequent manifestation of puberty gingivitis is bleeding and inflammation in interproximal
areas. Inflammatory gingival enlargement may also be noted in both males and females and generally
subsides after puberty[38] (Figure 11-11).

Figure 11-11 Pubertal gingival inflammation and enlargement secondary to poor oral hygiene and
hormonal influences. Little or no calculus was found when the child's teeth were scaled. This most often
clears with improved oral hygiene and natural stabilization of estrogen and testosterone levels.

The altered gingival response during this developmental stage is thought to be the result of hormonal
changes that magnify the vascular and inflammatory response to dental plaque [9,40] and modify
reactions of dental plaque microbes.[19]

Drug-Induced Gingival Enlargement

Gingival enlargement, discussed in Chapter 9, may result from the use of certain drugs.
Cyclosporine, phenytoin, and calcium channel blockersdrugs used to treat conditions encountered
in childhoodresult in a higher prevalence of gingival enlargement. Although complicated by the
plaque levels along the gingival margin, this form of gingival disease has features that are not typical
of chronic marginal gingivitis.[40]

Gingival Changes Related to Orthodontic Appliances

Gingival enlargement can be related to the presence of fixed orthodontic appliances, which
complicate plaque removal (Figure 11-12). Gingival changes can occur within 1 to 2 months of
appliance placement, are generally transient, and only rarely produce long-term damage to
periodontal tissues.[17] The fact that most orthodontic treatment is provided to individuals during
puberty when they are subject to the inflammatory changes associated with puberty gingivitis may
exacerbate the observed effect.

Figure 11-12 Chronic marginal gingivitis secondary to orthodontic therapy and inadequate oral
hygiene. Improved hygiene coupled with chlorhexidine mouthwash may help to reduce the inflammation
in this patient.

Mouth Breathing
Mouth breathing and lip incompetence, or an open mouth posture, are often associated with
increased plaque and gingival inflammation.[17] The area of inflammation is often limited to the gingiva
of the maxillary incisors. There is often a clear line of demarcation in which the gingiva is uncovered
by the lip (Figure 11-13).

Figure 11-13 Patient with gingivitis secondary to compulsive mouth breathing secondary to allergic
rhinitis. This is a typical gingival response to chronic desiccation in adolescent patients. This was
originally diagnosed as allergic gingivitis by the patient's pediatrician because it subsided when he
gave the patient antihistamines. Of course, the antihistamines simply allowed him to breathe through
his nose so he could keep his mouth closed.

NonPlaque-Induced Gingival Lesions

Intraoral soft tissue lesions may be encountered in the pediatric population as in the adult population.
The six most common pediatric intraoral lesions are primary herpetic gingivostomatitis, recurrent
herpes simplex, recurrent aphthous stomatitis, candidiasis, angular cheilitis, and geographic tongue.
[40]
Most of these lesions present without significant difference between the pediatric and adult
population. Two have specific pediatric considerations.

Primary Herpetic Gingivostomatitis

Primary herpetic gingivostomatitis is an acute-onset viral infection that occurs early in childhood, with
a heightened incidence from 1 to 3 years of age (see Chapter 10). In children with primary herpetic
infections, 99% are symptom-free or have symptoms that are attributed to teething. The remaining 1%
can develop significant gingival inflammation and ulceration of the lips and mucous
membranes[24,40] (Figure 11-14).

Figure 11-14 Acute herpetic gingivostomatitis in an 18-month-old child. Several active lesions still exist
on the tongue. The gingiva demonstrates the typical red, swollen appearance associated with the
herpes virus. The infection is mostly limited to the attached gingiva, tongue, palate, and lips. It is most
important to control hydration with bland, nonacetic fluids. Hospitalization may be necessary for
rehydration in severe cases.

Candidiasis
Candidiasis results from an overgrowth of Candida albicans, usually after a course of antibiotics or as
a result of congenital or acquired immunodeficiencies. It is far less common in the child than the adult
and is rarely associated with a healthy child.[12]
Although gingivitis is considered to be nearly universal in children over the age of 7 years, [15,40] frank
periodontal disease with loss of periodontal attachment and supporting bone is far less common in the
pediatric population than in adults.[15] The incidence of disease begins increasing between age 12 to
17 years, but the prevalence of severe attachment loss involving multiple teeth remains low at 0.2% to
0.5%.[15] When comparing the different presentations of periodontal disease, chronic periodontitis has
been shown to be more prevalent in adults and aggressive periodontitis is more common in children
and adolescents.[15]
See Chapters 16, 17, and 18Chapter 16 Chapter 17 Chapter 18 for detailed descriptions of the
different types of periodontal disease.

Aggressive Periodontitis
Aggressive periodontitis is addressed in greater detail in Chapter 18. Because of the relatively early
presentation of disease, which occurs around the time of puberty, former classifications include
mention of developmental stage: early onset periodontitis, prepubertal periodontitis, and juvenile
periodontitis.[15,40] The currently accepted designation of aggressive periodontitis may be further
broken down into two forms: localized or generalized.
Localized aggressive periodontitis is defined as interproximal attachment loss on at least two
permanent first molars and incisors, with attachment loss on no more than two teeth other than first
molars and incisors.[15]
In young individuals, localized aggressive periodontitis is more common than the generalized form.
Prevalence of the localized form has been reported to range from 0.1% to 15%, with most studies
estimating less than 1%. Black and Hispanic individuals are reported to have a higher prevalence [2,15];

some studies suggest a higher prevalence in Asian children as well. [2,48] Of relevance to the pediatric
population is the finding that the classic presentation of localized aggressive periodontitis may be
preceded by signs of bone loss around teeth in the primary dentition. [15]
The generalized form of aggressive periodontitis, which is defined as a generalized interproximal
attachment loss, including at least three teeth that are not first molars and incisors is rare in children.
The onset of this form of periodontitis generally occurs after the initiation of adolescence. The general
prevalence is 0.13% in 14 to 17 year olds[15]; however, individuals with Down syndrome demonstrate a
higher prevalence.[3,14,43] A purported genetic influence in the overall disease process suggests that
any signs of disease in a child with a family history of generalized aggressive periodontitis should be
investigated further.
Several studies have suggested the involvement of A. actinomycetemcomitans[2,28,48] and P.
gingivalis[2] in the pathogenesis of aggressive periodontitis, with the former found at higher levels in
children with the localized form and the latter at higher levels in the generalized form. Both of these
pathogens are relatively rare in healthy children, with a prevalence of 4.8%, but are elevated in
children with periodontitis, with a reported prevalence of 20%. [41]

Chronic Periodontitis
Chronic periodontitis, formerly known as adult periodontitis or chronic adult periodontitis, is one of the
most prevalent forms of periodontitis. It is characterized by a slow to moderate rate of progression
that may include periods of rapid destruction.[15] Although the disease can appear in children and
adolescent populations secondary to retained plaque and calculus, it is far less prevalent than in
adults.[15]
Similar to the adult version that is discussed in greater detail in Chapter 16, chronic periodontitis may
occur in children in the localized form in which less than 30% of dentition is affected, as well the
general form, in which more than 30% of the dentition is affected.
Although the microbiology of this disease is discussed in Chapters 16 and 23, it is important to note
that recent studies suggest a familial transmission of certain bacteria associated with chronic
periodontitis. Strains such as T. forsythensis, P. intermedia, and P. nigrescens are found more often in
the children of individuals who have been shown to harbor these types. [53] Both F. nucleatum and/or P.
gingivalis have been noted at significant levels in children of similarly affected parents. [11,25] Levels of
these strains have been observed to increase with age, suggesting that P. gingivalis and B.
forsythus might serve as early markers in the screening of periodontal disease. [11,28,51] Thus, even
though chronic periodontitis may not be highly prevalent in children, early colonization may
underscore the importance of early detection, particularly for those at elevated risk for adult forms of
the disease.

Gingival Manifestation of Systemic Disease in Children

Systemic diseases resulting in periodontitis occur more frequently in children than adults. [2] Chapter
27 discusses some of the general systemic diseases and disorders that impact periodontal health.
Many diseases, however, are expressed differently in children than in adults and therefore merit
special mention.
Acute necrotizing gingivitis (Figure 11-15) is very rarely seen except in cases of primary or secondary
immune suppression, Down syndrome, or severe malnutrition. [16,23,43] The breath is fetid, and the child
complains of pain and discomfort when eating (see Chapter 10).

Figure 11-15 Acute necrotizing ulcerative gingivitis in a preschool child.

Endocrine Disorders and Hormonal Changes

Diabetes Mellitus
Type 1 or insulin-dependent diabetes mellitus occurs more frequently in children and young adults
than type 2 or noninsulin-dependent diabetes mellitus. As in the diabetic adult, gingival inflammation
and periodontitis are more prevalent in affected children than in unaffected individuals. [40,44] Clinical
consequences include premature tooth loss and impaired immune response to the oral flora. The
severity of periodontal disease is worse in children with poor metabolic control.
Although destructive changes are rather rare in healthy children, periodontal destruction can be
observed in diabetic children, usually appearing around the time of puberty and becoming
progressively worse as children mature into adulthood. Disease prevention and fastidious oral
hygiene measures should be highly promoted.[27]

Hematologic Disorders and Immune Deficiencies

Leukemias
Leukemia is the most common type of cancer in children. Acute lymphocytic leukemia accounts for
the majority of cases in children under the 7 years of age. Leukemia must be considered in the
differential diagnosis for children who present with the hallmark features of acute gingival
enlargement, ulceration, bleeding, and infection. [1]

Leukocyte (Neutrophil) Disorders

As mentioned in Chapter 27, neutrophil disorders impair defenses against infections, making afflicted
individuals susceptible to severe periodontal destruction. Many neutrophil disorders are genetic,
including some forms of neutropenia, Chediak-Higashi syndrome, leukocyte adhesion deficiency, and
Papillon-Lefvre syndrome. Therefore diagnosis of the systemic disorder generally will have occurred
before any signs of periodontal destruction appear. Since periodontal changes are difficult to reverse
in children with neutrophil disorders, disease management includes oral hygiene measures,
mechanical debridement, antimicrobial therapy, and supportive care for resultant tissue destruction or
tooth loss. Treatment success is unpredictable as a result of the impact of systemic disease. [15]

Congenital Anomalies
Down syndrome is another congenital condition that would be diagnosed before expression of
periodontal disease. Afflicted individuals experience a high prevalence of severe aggressive
periodontitis in early adulthood. The disease process is thought to be related to some kind of host
susceptibility resulting in an exaggerated immune-inflammatory response rather than a reaction to a
specific causative microbe.[3,4,16]