Childhood periodontal diseases

Periodontal diseases can be grouped broadly into gingivitis and periodonti-tis, and each can be further divided according to the disease characteristics (e.g., chronic, aggressive) and the contributing factors, including related systemic conditions and disorders [39]. On the basis of histopathology, gingivitis is characterized by inflammation confined to the gingiva, and peri-odontitis denotes destruction of periodontal tissues that involve the gingiva, the periodontal ligament, root cementum and the supporting bone (alveolar bone) (Fig. 1). From the epidemiological aspect, gingivitis is more prevalent in childhood than periodontitis.

The periodontal diseases are well recognized to be initiated by some selected microorganisms, so-called periodontopathic microorganisms, in subgingival plaque and/or supragingival plaque adjacent to gingival crevice. It is also evident that the onset and progress of these inflammatory diseases are based on the balance between the periodontopathic microorganisms and the host-defense against them (host-parasite relationship) [40]. In other words, the children with related systemic conditions and/or disorders could be easily afflicted with periodontal diseases. Thus, the host-defense as well as periodontopathic bacteria play an important role in the outcome of childhood periodontal diseases.

The following sections address: (i) clinical and etiological aspects of childhood periodontal diseases, (ii) pathogenic bacteria, (iii) onset of peri-odontal diseases - host-parasite relationship, and (iv) transmission of peri-odontal bacteria.

Clinical and etiological aspects of childhood periodontal diseases

Plaque-induced gingivitis without other local contributing factors is a bac-terially elicited inflammation of the marginal gingiva, and is the most common gingivitis among children as well as adults. Etiological involvement of supragingival plaque in the gingivitis has been demonstrated by the pioneer experiments by Loe and coworkers [41]. They showed that the increase in severity of gingivitis was directly proportional to the amount of accumulated supragingival plaque, and that gingivitis was eliminated by the removal of the bacterial plaque. The early finding of a strong cause-and-effect relationship between the amount of plaque and the severity of gingivitis has led to a major emphasis on prevention of gingivitis by the reduction in amount of plaque. From the standpoint of the etiological model of 'host-parasite relationship in periodontal diseases', however, the plaque-induced gingivitis appears to be a typical periodontal disease in that the increased virulence of periodontopathic bacteria surpasses the host defense. Therefore, the gingivitis cannot be cured only by the reduction in amount of plaque, but by the elimination of pathogens in the plaque. In fact, a recent study demonstrates that there is no correlation between plaque amounts and severity of periodontal inflammation in children with deciduous dentition [42]. In this report, it has been also indicated that clinical manifestations of gingivitis are more severe in adults than in children and adolescents, whereas the accumulation of dental plaque are almost equal between them. Since periodontal bacteria appear to inhabit the child's oral cavity as described below, these observations suggest that the host defense in childhood is more effective in opposing the periodontal pathogens than that of adults, resulting in prevention of the onset and/or progression of gingivitis. However, it should be remembered that the children with related systemic conditions and/or disorders could be easily afflicted with periodontal diseases. Thus, steroid-addicted subjects, young people during pubertal development, patients with endocrine disorders and juvenile diabetes mellitus patients may suffer from gingivitis (e.g., drug-influenced gingivitis, puberty-associated gingivitis and diabetes mellitus-associated gingivitis) due to a decline or alterations in host defenses.

Prevalence of periodontitis is extremely low in childhood, compared to that in adults. In a population-based study of 3896 Swedish children (7-9 years old), it was found that only 32 children (0.8%) exhibited alveolar bone loss [43]. Since the sulcular epithelium around temporary (deciduous) tooth is thicker than that of a permanent tooth, a likely explanation of the difference in prevalence may be that the host defense could more efficiently prevent an invasion of periodontal bacteria to the gingival epithelium in children with deciduous dentition than in adults with permanent dentition. However, the fact that periodontitis is also a rare disease even in children with mixed and permanent dentitions suggests other preventive factors. The host defense seems more effective in arresting the developing of periodon-titis in children for some reason.

The term 'early-onset periodontitis' has now been renamed to 'aggressive periodontitis'. Early-onset periodontitis represents a group of highly destructive periodontitis in young subjects that includes prepubertal, juvenile and rapidly progressive periodontitis. Prepubertal periodontitis develops just after eruption of temporary teeth in such subjects. Juvenile periodontitis starts from puberty in late teens to 20s, and rapidly progressive periodontitis has been characterized as a highly destructive periodontitis that usually has an onset before 35 years of age. However, the age-dependent classification of this type of periodontitis is neither adequate nor practical in either the etio-logical or the clinical aspect, since the scientific basis for using the patient's age of disease onset as a classification division of periodontitis is lacking, and similar dysfunction/malfunction in host-defense mechanisms can be observed in most of the early-onset periodontitis patients. Thus, the highly destructive forms of periodontitis have been renamed to aggressive periodontitis. The former 'prepubertal periodontitis' and 'juvenile periodontitis' are categorized into two forms based on the localization of lesions: one is a localized type in which severe periodontal destructions are limited to first molars and incisors, and the other is generalized (defused) type in which destruction of the periodontal tissue widely progresses in all teeth. Clinical manifestations of the localized type of this periodontitis (localized aggressive periodontitis) are as following: accumulation of the dental plaque is usually limited and gingival inflammation is rarely observed, although resorption of alveolar bone occurs. A likely explanation of the localization to first molars and incisors is that these are the teeth with greater probability for being at risk when the disease started, as other teeth had not yet erupted. On the other hand, extensive alveolar bone resorption and significant gingival inflammation with severe plaque accumulation are commonly observed in generalized type of the aggressive periodontitis (generalized aggressive periodontitis).

Etiological factors reported as being associated with aggressive peri-odontitis include the specific bacterial pathogens, especially Actinobacillus actinomycetemcomitans for localized aggressive periodontitis, and functional abnormalities of peripheral blood polymorphonuclear leukocytes (PMNL) [44]. The PMNL is the principal cell of the gingival crevicular exudate.

Chediak Higashi Syndrome Oral
Figure 2. Gingival inflammation and periodontal destruction in a patient with Chediak-Higashi syndrome.

PMNL come into direct contact with plaque bacteria in the gingival crevice and actively phagocytose them. The protective function of PMNL in human periodontal diseases is demonstrated by the fact that patients with PMNL disorders, e.g., Chediak-Higashi syndrome (Fig. 2) [45, 46], lazy leukocyte syndrome [47], cyclic neutropenia [48], chronic granulomatous disease [49] and diabetes mellitus [50, 51], have usually rapid and severe, aggressive peri-odontitis. Quantitative analyses using a flow cytometer revealed that about 50% of the patients with localized and generalized aggressive periodon-titis, but not chronic periodontitis (formerly adult periodontitis), exhibited depression of phagocytic function of peripheral blood PMNL (Tab. 2) [52]. The depressed phagocytic responses could be due to cell-associated

Table 2. Prevalence of the periodontitis patients exhibiting depressed phagocytic function of peripheral blood PMNLa

Aggressive periodontitis

Localized type

Generalized type

Chronic periodontitis

% Phagocytosis

53% (8/15)b

46% (6/13)

6% (3/52)

d-Phagocytosis

67% (10/15)

46% (6/13)

6% (3/52)

aPhagocytic function was assessed by means of the percentage of phagocytosing cells (% Phagocytosis) and the degree of phagocytosis by one PMNL (d-Phagocytosis). Depressed phagocytic function was defined when 2 SD below the mean of those in healthy subjects. bPatients exhibiting depressed phagocytic function/total patients.

aPhagocytic function was assessed by means of the percentage of phagocytosing cells (% Phagocytosis) and the degree of phagocytosis by one PMNL (d-Phagocytosis). Depressed phagocytic function was defined when 2 SD below the mean of those in healthy subjects. bPatients exhibiting depressed phagocytic function/total patients.

defect(s) of the PMNL, and therefore it remains unchanged after periodon-tal treatments, suggesting that the depression of PMNL phagocytosis in both types of aggressive periodontitis may not be a transient phenomenon associated with the local periodontal status. In contrast, the capacity of the PMNL to mount intracellular oxidative burst reaction was much higher in both types of aggressive periodontitis and chronic periodontitis than that in the control [53]. On an individual basis, the elevated capacity of oxidative burst showed a significant positive correlation to clinical periodontal parameters, and decreased to normal levels after periodontal treatments. These findings suggest that the PMNL with marked increase in oxidative metabolic capability ('primed' PMNL) could be a significant component of the host defense to not only aggressive but also chronic periodontitis, as seen in other systemic bacterial infections [54]. Thus, the host defense, especially by PMNL, plays an important role in the outcome of childhood periodontitis. Nevertheless, the association of the unique and specific pathogens must be taken account in the pathogenesis of childhood periodontitis. The functional abnormalities of PMNL is implicated in the pathogenesis of both forms of aggressive periodontitis (localized and generalized), but the clinical manifestations of the two periodontitis are clearly distinguishable, as described above. Furthermore, the prominence of A. actinomycetemcomitans is cited as a feature in only the localized type.

Pathogenic bacteria

Although the pathogens of periodontal diseases were presumed to be microorganisms habiting in the dental plaque, none of periodontopathic bacteria were identified until the late 1970s. The main reason is because these bacteria are obligatory anaerobes and do not, or hardly, proliferate under the conventional aerobic culture conditions. Therefore, a development and prevalence of anaerobic culture methods were required to isolate and identify the periodontopathic bacteria. Clinical and basic studies, including animal trials, have recently revealed that some selected microorganisms that colonize in subgingival plaque in gingival crevice, the so-called periodontopathic microorganisms, can cause periodontal diseases. Several groups of periodontopathic bacterial species are considered to be responsible for each form of clinical manifestations of the periodontal diseases. These include Gram-negative obligatory anaerobic rods: P. gingivalis, Prevotella intermedia, Prevotella nigrescens and Tannerella forsythensis (formerly Bacteroides forsythus); Gram-negative facultative anaerobic rods: A. actinomycetemcomitans, Capnocytophaga spp., Campyrobacter rectus and Eikenella corrodens; and oral spirochetes: Treponema denticola (Tab. 3).

P. gingivalis is considered to be a major pathogen of chronic periodon-titis in adults and generalized (but not localized) aggressive periodontitis [55]. This microorganism possesses several virulence factors for periodon-topathogenicity, including fimbriae, proteolytic enzymes and lipopolysac-charide (LPS) [56]. Fimbriae of P. gingivalis are involved in the attachment with the host cells; they specifically bind to salivary component proteins of proline-rich protein (PRP) and proline-rich glycoprotein (PRGP) [57]. In addition, they significantly interact with extracellular matrix proteins, fibro-nectin and laminin [58, 59]. Therefore, P. gingivalis cells can bind to tooth surface and upper gingival sulcus, which are covered with saliva. Although a deeper portion of the gingival sulcus is not contaminated with saliva, P. gingivalis can bind sulcular epithelial cells via interaction with extracellular matrix proteins and may invade sulcular epithelial cells (Fig. 1). It has been also reported that the fimbriae exhibit a variety of biological and immuno-logical activities in the infectious process [60].

Large amounts of the proteolytic enzymes of gingipains and collagenase are produced by P. gingivalis, and these proteases have the abilities to destroy periodontal tissue directly or indirectly [61, 62]. Furthermore, since P. gingivalis is asaccharolytic, proteolytic dipeptides are uptaken and used as an energy source. Ammonia, propionate and butyrate produced from amino acids can disrupt the host immune system and be toxic against the gingival epithelium. LPS from the outer membrane of the bacteria also elicits a wide variety of responses that may contribute to inflammation and host defense. At established periodontal disease lesions, infiltration of inflammatory lymphocytes, especially B cells and plasma cells, are significant [63], and this event seems to correlate with the polyclonal or oligoclonal B cell activation by P. gingivalis LPS [56, 64].

A. actinomycetemcomitans was originally isolated from a localized aggressive periodontitis patient [65], and has been recognized to be involved in this type of aggressive periodontitis, since early experiments indicated the positive relationship between the periodontal destruction and the high levels of serum antibodies to the bacteria. The reported virulent factors of the bacteria include LPS and an exotoxin, leukotoxin, which has cellular toxicity against human PMNL and monocytes. However, substantial evidence demonstrates that not all A. actinomycetemcomitans can produce leukotoxin,

Table 3. Prevalence of periodontopathy microorganisms in plaque and saliva from children (119 children aged 2-15 years)

Periodontopathic microorganisms

Detection ratio (%)

Plaque only

Saliva only

Both

Porphyromonas gingivalis

1.5

3.0

0.6

Prevotella intermedia

0.6

2.4

0.3

Prevotella nigrescens

26.2*

11.3

5.7

Tannerella forsythensis

6.3

15.5*

2.4

Actinobacillus actinomycetemcomitans

10.1

38.7*

30.4

Capnocytophaga ochracea

7.4

34.8*

40.8

Capnocytophaga sputigena

12.5

33.0*

33.6

Eikenella corrodens

15.5

25.6*

10.7

Campyrobacter rectus

21.4

16.4

11.6

Treponema denticola

0

0.6

0

*Significantly higher detection ratio between plaque and saliva samples by Fisher's exact probability test (p < 0.01).

*Significantly higher detection ratio between plaque and saliva samples by Fisher's exact probability test (p < 0.01).

and leukotoxin-non-producing strains of the bacteria were also recovered from localized aggressive periodontitis patients [66]. Furthermore, recent studies using a PCR detection method revealed that the prevalence rate of the microorganism was relatively high even in periodontally healthy children; it was greater than 50% in saliva, and 30% in subgingival plaque of Japanese children (2-15 years old) [67, 68]. Thus, A. actinomycetemcomitans appears to be an early colonizer in the human oral cavity. However, the accumulation of the bacteria to a critical amount in plaque may contribute as the predisposing factor for the onset and/or progression of localized aggressive periodontitis especially in children with systemic risk factors such as functional impairments/abnormalities of PMNL.

In addition to the two periodontopathic bacteria described above, Capnocytophaga sputigena, C. ochracea, E. corrodens, Campylobacter rectus, P. intermedia, P. nigrescens, T. forsythensis and T. denticola have been proposed as possible periodontophatic pathogens in some types of periodonti-tis, although most of these bacteria can be often or occasionally detected in the plaque microflora of periodontally healthy children [67].

Onset of periodontal diseases - Host-parasite relationship

The onset of periodontal diseases, especially periodontitis, is based on the balance in host-parasite relationship in gingival crevices. The gingival crev ice (sulcus) is a groove between the tooth surface and the sulcular epithelium that extends from the free surface of the junctional epithelium to the level of the free gingival margin. The junctional epithelium forms a collar around the tooth. The gingival crevice is bathed in saliva that contains a lot of antibiotic agents, such as lysozyme, lactoferrin, peroxydase and secretory IgA. In addition, the sulcular epithelium acts as a physical barrier against intruders. Furthermore, serum antimicrobial components consecutively exude to the gingival crevice through the junctional epithelium, termed gingival crevicular fluid (GCF). GCF originates from plasma exudates, and thus contains IgG, IgA, complements and cellular elements. It is noted that 95% of the cellular elements are PMNL and the remainder are lymphocytes and monocytes, even in the GCF from clinically healthy gingival crevice [40]. This suggests that PMNL in plasma emigrate actively to gingival crevices and play an important role in the localized host defense within the gingival crevice.

Although the colonization of periodontopathic bacteria in gingival crevice does not necessarily induce infection that causes destruction of the periodontium, the acquisition of the putative pathogens is a prerequisite process for developing periodontal diseases. In adults, periodontopathic bacteria are detected from periodontally healthy sites as well as diseased sites, although the number of the microorganisms is generally lower than that in diseased sites [55, 69]. In children, however, less information is available on periodontopathic bacterial infection in their plaque. Our recent longitudinal investigations by means of PCR method using the periodon-topathic bacterial species-specific primers for 16S rRNA genes indicated that seven out of ten bacteria, i.e., C. rectus, E. corrodens, A. actinomy-cetemcomitans, Capnocytophaga ochracea, C. sputigena, T. forsythensis and P. nigrescens were frequently found in both subgingival plaque and saliva from 119 periodontally healthy children (2-15 years old) [67]. In contrast, P. gingivalis, T. denticola and P. intermedia were rarely detected in plaque and saliva from children. These findings indicate that the colonization of many putative periodontopathic bacteria can occur quite early in childhood without development of periodontal diseases, and may become common members in the microflora of plaque and saliva in children. However, the oral infection/colonization of P. gingivalis, T. denticola and/or P. intermedia could be an occasional and transient phenomenon. The child's oral cavity is assumed to be possibly colonized by P. gingivalis based on the premise that the bacteria specifically interact with the saliva proteins, PRP and PRGP, and with extracellular matrix proteins of the sulcular epithelium as in the adult's oral cavity. Therefore, the low prevalence rate of P. gingivalis, T. denticola and P. intermedia observed in the study suggest that the child host-defense of antibiotic components in saliva and GCF efficiently prevent the initial colonization and/or proliferation of these periodontal pathogens, resulting in the arrest of periodontal diseases in healthy children. Regarding other putative periodontopathic bacteria including C. rectus, E. corrodens,

A. actinomycetemcomitans, C. ochracea, C. sputigena, T. forsythensis and P. nigrescens, the pathogenic role in periodontal diseases is still not clear. Together with the observation in adults that a relatively lower, but significant, number of the periodontopathic bacteria are detected from periodon-tally healthy gingival crevices, it is likely that the initially colonized bacteria having pathogenic potentials are efficiently controlled by the host-defense mechanisms so that they do not to reach a critical level of accumulation in the healthy gingival crevice. If the host-defense is not efficient, as is the case in children with functional impairments/abnormalities of PMNL, the bacteria with no or little pathogenic potentials could be a factor that governs the periodontopathic potential. In fact, the children with Down's syndrome often develop severe early-onset of periodontal diseases. These subjects demonstrate an early decline in the host-defense ability including malfunction of PMNL due to premature senescence. Our microbial observation in children with Down's syndrome indicated that the seven putative periodon-topathic bacteria (C. rectus, E. corrodens, A. actinomycetemcomitans, C. ochracea, C. sputigena, T. forsythensis and P. nigrescens) were detected with greater frequency in Down's syndrome patients than in healthy control children [70]. Furthermore, the cluster group characterized by the additional infections with P. gingivalis, T. denticola and P. intermedia to the seven putative periodontopathic bacteria showed the highest severity in periodontal parameters, suggesting that this particular predisposing condition probably permits the colonization of these periodontopathic bacteria and allows their growth, resulting in the onset of periodontal diseases in these children.

Transmission of periodontal bacteria

Periodontal diseases are caused by dental plaque bacteria, and thus can be classified as infectious diseases by indigenous bacteria. It has been demonstrated that children whose parents were colonized by the BANA-positive periodontpathic species including P. gingivalis, T. denticola, and T. forsythensis were 9.8 times more likely to be colonized by these species, and children whose parents had clinical evidence of periodontitis were 12 times more likely to be colonized the species [71]. Concordance in colonization of T. forsythensis, P. intermedia and P. nigrescens within children and their parents was also observed in Japanese families [72]. In addition, vertical transmission of A. actinomycetemcomitans was reported in families from Finland [73], and was estimated between 30% and 60% in the Netherlands [74]. Compared with A. actinomycetemcomitans, the case of P. gingivalis is still controversial; vertical as well as horizontal transmission was speculated in a study of 564 members of American families [75], whereas vertical (parents-to-children) transmission has rarely been observed in the Netherlands [74], in Finland [73], and in the research of 78 American subjects [76]. In the later reports, since horizontal transmission of P. gingivalis between adult family members was considerable, it was suggested that P. gingivalis commonly colonizes in an established oral microbiota. According to these observations, vertical and horizontal transmission of periodontal pathogens may be controlled by periodontal treatment involving elimination of the pathogen in diseased individuals and by oral hygiene instructions.

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