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 faktor-faktor lain.

Clinical Features

The most prevalent type of gingival disease in childhood is chronic marginal gingivitis (see Figure 11-9). 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 4- to 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 gingivitis—thereby 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 tumbuhGingivitis 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 blockers—drugs used to treat conditions encountered in childhood—result 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.

Non–Plaque-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 ChangesDiabetes Mellitus

Type 1 or insulin-dependent diabetes mellitus occurs more frequently in children and young adults than type 2 or non–insulin-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 DeficienciesLeukemias

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-Lefèvre 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]