Periodontal syndromes in children. Ambulatory diagnosis. Tactics dentist.

Periodontal diseases are inflammatory diseases of the supporting structures of the teeth. They are initiated by periodontopathic bacteria and result in progressive destruction and loss of the periodontium. Progression of periodontal disease eventually leads to tooth loss. Periodontal diseases are multifactorial with complex pathogenesis.

Plaque bacteria trigger a host inflammatory response in the gingival tissues. Neutrophils migrate from within the gingival tissues towards the gingival crevice and build a barrier wall against the bacteria. Within the gingival connective tissue, the gingival macrophages and fibroblasts produce inflammatory cytokines (e.g. interleukin-1 and tumor necrosis factor- alpha) that activate collagenases and other degrading enzymes. These enzymes when released and activated destroy the gingival collagen. Lymphocytes are recruited to the gingival lesion to initiate an adaptive immune response and help with containing the infection. With persistence of the microbial infection, the inflammatory changes in the gingival tissues expand apically and reach the alveolar bone. Inflammatory mediators such as interleukin-1, interleukin-6, tumor necrosis factor alpha and prostaglandins induce osteoclasogenesis. Increased inflammatory activity disrupts the normal balance of bone formation/resorption and results in alveolar bone loss.

Periodontal disease is a serious and morbid oral condition among Down-syndrome (DS) affected individuals. Gingivitis and periodontitis start early in life and their severity increases with age. Periodontal disease advances rapidly in DS individuals and is characterized by severe gingival inflammation, loss of periodontal attachment and radiographic alveolar bone loss. Heavy amounts of plaque and calculus are often present. Periodontal disease is an important cause of tooth loss among DS individuals.

The exact reason (or reasons) for this increased susceptibility to periodontitis is (are) not known. Understanding the pathogenesis of periodontitis in DS individuals would greatly help with the management and control of the destructive process associated with the disease and help DS affected individuals retain their teeth hopefully throughout their lifetime.

Previously researchers have investigated factors usually associated with periodontitis such as subgingival plaque microbial composition, immune and inflammatory responses individually in DS affected individuals. The individual factors investigated were never collectively evaluated together to provide an overall understanding of the pathogenesis of periodontitis in individuals with DS. The objective of this chapter is to review in a systematic fashion all the involved factors previously reportedtogether to generate a hypothetical collective model of the pathogenesis of periodontal disease in individuals with DS. Such a model would enhance our understanding of periodontal disease development/progression in this vulnerable group, would help with disease management, would identify gaps in knowledge, and would provide enlightenment for future research endeavors.

In this review I have searched the available dental/medical literature for studies investigating the main factors suspected in the increased susceptibility to periodontitis in DS individuals. I have summarized the main findings from these studies and used this information to generate a hypothetical model of the pathogenesis of periodontitis in DS individuals.

Periodontal disease is a common problem among DS individuals with an estimated prevalence between 58% and 96% for those under 35 years of age. The disease starts early in life and progresses with age eventually leading to tooth loss. Periodontal disease in DS individuals adversely impacts on the quality of their life. The increased prevalence and severity of periodontal disease in DS individuals inspired many researchers to investigate the various factors that might be involved.

Periodontal diseases are initiated by bacterial plaque build-up in the dentogingival region. It is well documented that DS individuals have difficulty with maintaining adequate oral hygiene levels and thus tend to harbor high levels of bacterial plaque on their teeth. In addition, DS individuals following oral hygiene instructions have reduced ability to master adequate plaque control. It was often surmised that mental disability associated with DS is an important factor in their reduced ability to maintain adequate oral hygiene and consequently increases their susceptibility to periodontitis. Our group recently showed in a multivariate model including traditional risk factors for periodontitis combined with mental disability that loss of periodontal attachment in DS individuals was not associated with mental disability. Thus other factors associated with DS might be involved.

It is well documented that DS is associated with immune deficiencies and host response impairment. Infections, in particular respiratory infections are an important cause of death in DS individuals. The most likely reason for this increased susceptibility to infection and reduced immunity in DS individuals is an increased dosage of a protein product or products encoded by chromosome 21. Several proteins important in immune function are encoded on chromosome 21. Examples include superoxide dismutase (SOD), carbonyl reductase (NADPH) and integrin beta-2 (CD18). Increased SOD and NADPH production is associated with increased oxidative stress and tissue injury in DS individuals. Aberrant expression of CD18 integrin on immune cell surfaces in DS individuals may be associated with altered lymphocyte function. The IL10RB component of the IL-10 receptor (involved with resolution of inflammation) is encoded by chromosome 21 and its function may be altered in DS individuals. In addition, it seems that interleukin-1 (IL-1) is upregulated indirectly by some chromosome 21 based genes. IL-1 is an important immune/inflammatory mediator. Its increased production in DS individuals was associated with brain tissue damage.

Since periodontitis is initiated by bacterial infections, indeed it is conceivable that altered immunity in DS individuals may be the primary reason for their increased susceptibility to periodontal infections. Perhaps reduced immunity in DS individuals would make it easier for virulent periodontopathic microbial species to colonize their subgingival plaque. If true, such elevated microbial presence, unchallenged and unchecked, would induce an intense inflammatory reaction within the gingival tissues. Increased gingival inflammation within the gingival tissues would lead to elevated production of degrading enzymes and alter bone remodeling. The end result of these inflammatory induced changes would be the loss and destruction of the periodontium and eventually tooth loss. Several studies (microbiological, immune and inflammatory) attempted to investigate these hypotheses.

Barr-Agholme et al. reported increased presence of Aggregatibacter (Actinobacillus)actinomycetemcomitans, Capnocytophaga and Porphyromonas gingivalis in subgingival plaque ofadolescents with DS. A. Actinomycetemcomitans was detected in 35% of patients with DS compared to 5% in the healthy, age and sex matched controls. The authors suggested that this increased frequency of A. actinomycetemcomitans indicated an altered microbial composition in the subgingival plaque of DS patients as compared to healthy controls. Amano et al.. found various periodontal disease-causing bacteria present in very young DS patients. The authors reported that various periodontopathic bacteria could colonize the teeth in the very early childhood of DS patients. Pathogens in DS patient’s subgingival plaque were detected with far greater frequency than in the age-matched controls. This may be the reason why these DS patients have such intense gingival inflammation. The authors concluded that periodontopathic pathogens establish a presence at a very early age, and that certain bacteria, like P. gingivalis, play a key role in the initiation of gingival inflammation.

Sakellari et al. evaluated seventy DS patients, 121 age-matched healthy individuals and 76 patients with cerebral palsy. Full-mouth recordings of clinical periodontal parameters were assessed and subgingival plaque samples were taken from the Ramfjord teeth and analysed for 14 species using "checkerboard" DNA-DNA hybridization. They reported that important periodontal pathogens colonize these subjects earlier and at higher levels compared with age-matched healthy individuals and patients with cerebral palsy.

Reuland-Bosma et al. compared subgingival microflora in DS adult patients to other mentally retarded individuals. Despite advanced periodontitis in DS patients, no differences in the prevalence of distinct suspected periodontopathic bacteria were established between the DS patients and the control group. The authors concluded that host factors are the most likely explanation for the advanced periodontal disease associated with DS patients.

Amano et al. took subgingival plaque specimens from 67 DS young adults and 41 age-matched systemically healthy individuals with mental disabilities (MD). The prevalence of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola, Prevotella intermedia, Prevotella nigrescens, Capnocytophaga ochracea, Capnocytophaga sputigena, Campylobacter rectus, and Eikenella corrodens, were investigated in subgingival plaque samples using a polymerase chain reaction method. The authors found no significant differences in the bacterial profiles between the groups.

The cited microbiological studies indicate early colonization of important periodontal pathogens in children and adolescents with DS. However, the microbial subgingival profile of adult DS individuals is not different from matched non-DS individuals. Perhaps reduced immunity in young DS individuals facilitates early colonization in comparison to young non-DS individuals with normal immunity. With age, and a combination of long-term exposure to pathogens and changes in immune response, non-DS individuals may also be susceptible to colonization by periodontal pathogens. However, despite lack of differences in microbial profiles between adult DS and non-DS individuals, adult DS individuals still show greater loss of periodontal attachment. This suggests that the host response to the same bacteria is different between DS and non-DS individuals. It seems that the immune-inflammatory response in DS is more intense resulting in greater tissue damage. The following studies will investigate this claim.

IMMUNE DYSFUNCTION STUDIES

As we said earlier, DS is associated with immune dysfunction. Various studies investigated different components of the immune system in relation to periodontitis in DS patients. These studies mainly focused on neutrophil function, the gingival immune cellular response and antibody production against periodontopathic bacteria.

NEUTROPHIL FUNCTION STUDIES

Izumi et al. found a faulty neutrophil chemotaxis in DS patients. The authors reported that DS patients had significantly lower chemotaxis compared to healthy controls. Since the neutrophils are the main cells involved in the first line of host defense in a bacterial invasion, having a defective neutrophil chemotaxis can lead to the progression of periodontitis. Significant correlations were identified between the amount of bone loss and the age and chemotactic index of the DS patients. The authors found that the rate of periodontal destruction was dependent on the degree of defective chemotaxis.

Yavuzyilmaz et al. evaluated clinical parameters, chemotaxis and random migration of neutrophils in 15 patients with DS and 15 healthy subjects. Signs of more severe gingival inflammation were present in the DS group. The random migration and chemotaxis of neutrophils were significantly decreased in comparison with the control group.

Zaldivar-Chiapa examined patients with DS to evaluate the effectiveness of surgical and non-surgical periodontal therapies and to assess their neutrophil immunological status. The population consisted of 14 DS patients, 14 to 30 years old. Surgical and non-surgical periodontal therapies were compared in a split-mouth design. Clinical periodontal parameters were recorded at baseline, post-treatment, 6 months, and 1 year. Neutrophil chemotaxis, phagocytic activity, and production of super-oxide anion were compared between DS patients and healthy controls. Both surgical and non-surgical therapies showed a significant improvement in all the clinical parameters compared to baseline. Neutrophil chemotaxis, phagocytic activity, and production of super-oxide anion were significantly decreased in the DS patients. The authors concluded that the neutrophil impairment does not seem to affect the clinical response to therapy.

All the presented studies showed deficient neutrophil chemotaxis in DS subjects. The reason for impaired neutrophil chemotaxis in DS individuals may be secondary to increased oxidative stress associated with trisomy of chromosome 21. Oxidative stress may impair internal cell function and disrupt chemotaxis. One study positively correlated such reduced chemotaxis with measures of periodontitis. Another study gave hope that despite reduced neutrophil chemotaxis, periodontal therapy aiming at reducing plaque and correcting periodontal architecture is still helpful.

GINGIVAL IMMUNE CELLULAR RESPONSE

Sohoel et al. examined the composition of mononuclear cells in the gingival inflammatory infiltrate in DS patients with marginal periodontitis. The authors reported that DS patients had a higher number of cells in the cellular infiltrate of chronic marginal periodontitis (CMP) compared to normal patients. There were also an increased number of CD22+ cells (B lymphocytes), CD3+ cells, CD4+ cells, CD8+ cells, and CD11+ cells (macrophages). There was also a significantly higher CD4+/CD8+ ratio in DS patients when compared to the normal controls, which could indicate active tissue destruction. This study concluded that DS patients have a more pronounced and altered gingival cellular immune response when compare to controls.

Sohoel et al. (1995 ) investigated the expression of HLA class II antigens in chronic marginal periodontitis (CMP) in patients with DS. Variations in the expression of HLA class II antigens on antigen-presenting cells play an important role in immune regulation. The results of this study indicated an increased frequency of HLA class II antigens in the gingival tissues of CMP DS patients when compared to controls. There were significantly higher numbers of CD1a+ cells and ratios of HLA-DR+/CD1a+ cells and HLA-DP+/CD1a+ cells in the DS group compared to the control group. The authors concluded that there is a highly activated immune response in DS patients.

The same investigators investigated gamma/delta T lymphocytes in gingival tissues of DS individuals. The T-cell receptor (TCR) of gamma/delta T lymphocytes is different from the alpha/beta TCR. The gamma/delta TCR binds to antigens that are intact proteins and antigens that are not presented within class I or class II histocompatibility molecules. The gamma/delta T lymphocytes usually reside within epithelial tissues and encounter antigens on the surface of epithelial cells. The researchers reported that the percentage of gamma/delta T lymphocytes in the gingival tissues of DS subjects was less than 1%.

The presented studies showed an intense presence of a variety of immune cells within the gingival tissues of DS patients with periodontitis. Increased production of HLA class II antigens on the surfaces of antigen producing cells suggests that the cells are locally engaged in specific immune responses. The low presence of gamma/delta T lymphocytes may increase the vulnerability to microbial noxious agents.

ANTIBODY/IMMUNOGLOBULIN PRODUCTION

These studies investigated specific antibodies against periodontopathic bacteria in serum and saliva.

Santos et al. determined the circulating antibody titers to Aggregatibacter (Actinobacillus) actinomycetemcomitans (Aa) in sera of DS and normal patients. Eleven DS patients with periodontitis (pocket depth > 4 mm), five DS patients with gingivitis (inflammation and pocket depth < or = 3 mm), and 10 non-DS healthy subjects had blood drawn and analyzed for antibody response to Aa. The authors noted significant differences between the control group and the DS groups (p = 0.05), with the DS periodontal group having the highest response, followed by the DS gingivitis and normal controls, respectively.

Morinushi et al. obtained sera from 75 DS subjects (aged 2 to 18 years) and their gingival health assessed using a modified gingival inflammation index (PMA Index). Antibody titers to Porphyromonas gingivalis, Prevotella intermedia, Treponema denticola, Fusobacterium nucleatum, Selenomonas sputigena, Actinobacillus actinomycetemcomitans, and Streptococcus mitis were determined using a micro-ELISA. The average antibody titers to A. actinomycetemcomitans, S. mitis, and F. nucleatumexceeded those of the normal adult reference serum pool. In addition, IgG antibody titers to P. gingivalis, A actinomycetemcomitans, F. nucleatum, S. sputigena, and S. mitis correlated significantly with the modified PMA scores.

Barr-Agholme et al. investigated the clinical periodontal conditions and salivary immunoglobulins in patients with DS. The results showed an altered distribution of IgG subclasses in saliva, with an increased amount of IgG1 in DS patients compared to controls. This is in agreement with other studies that show increased IgG1 in DS patients. On the contrary, the proportion of IgG2, IgG3, and IgG4 subclasses in saliva did not differ between the 2 groups. Also, in DS patients with bone loss, it was noted that they have an increased level of sIgA, compared to those DS patients without bone loss.

Chaushu et al. assessed age-related changes in the salivary-specific humoral immunity of DS subjects. Parotid and whole saliva were collected from a young group of DS, an older group of DS individuals and compared to two age-matched groups of healthy volunteers. The levels of total IgA, and specific antibodies to three common oral pathogens (Porphyromonas gingivalis, Aggregatibacter (Actinobacillus) actinomycetemcomitans and Streptococcus mutans) were analyzed. The median secretion rates of the specific antibodies in whole and parotid saliva were 70-77% and 34-60% (respectively) lower in young DS individuals as compared to young controls and farther 77-100% and 75-88% (respectively) lower in old DS compared to young DS.

The presented studies were somewhat controversial and indicated different antibody responses between saliva and serum in DS individuals. While in saliva the antibody response was low in DS individuals, in serum the antibody responses to several periodontopathic bacteria were elevated. The low antibody responses in saliva were associated with decreased salivary flow in DS individuals. The low salivary antibody activity may facilitate the colonization of periodontal pathogens in DS individuals. The elevated antibody titers in DS serum corroborate the gingival immune cellular activity described previously. It demonstrates that DS individuals despite known immune deficiencies are capable of mounting a humoral specific immune response. Such antibodies would find their way into the gingival tissues and fluid and help with containing the microbial damage. Increased antibody levels in gingival tissues may also accentuate the gingival inflammatory response through complement activation.

INFLAMMATORY RESPONSE STUDIES

Inflammatory response studies focused on inflammatory mediators and degrading enzymes in gingival crevicular fluid.

STUDIES INVESTIGATING INFLAMMATORY MEDIATORS

Barr-Agholme et al. investigated the levels of prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) in gingival crevicular fluid (GCF). GCF was collected from both DS patients and healthy controls. They found the mean level of PGE2 in GCF was significantly higher in the DS patients as compared to the controls. This finding suggests an alteration in arachidonic acid metabolism in DS patients. The mean level of IL-1β in the GCF was not significantly higher in the DS patients as compared to the healthy controls. Perhaps the reason the IL-1β levels did not differ between the groups, despite the fact that the gingival inflammation was more severe in the DS group, may be because PGE2 has been reported to down-regulate the production of IL-1β. This issue has not been revisited since and indeed is worthy of further investigation.

Tsilingaridis et al. determined the levels of PGE2, LTB4, and MMP-9 in GCF from 18 Down syndrome patients and from 14 controls matched with respect to age and degree of gingival inflammation. Clinical periodontal parameters were recorded including probing depth (PD) and bleeding on probing (BOP). The mean levels of PGE2, LTB4, and MMP-9 were significantly (P<0.05) higher in GCF from Down syndrome patients compared to controls. When comparing the two groups, the correlation coefficients for LTB4 to BOP and PD, respectively, as well as for MMP-9 to BOP significantly differed between Down syndrome and controls (P<0.05).

STUDIES INVESTIGATING DEGRADING ENZYMES

Halinen et al. characterized the periodontal status of 9 non-institutionalized DS children 9 to 17 years old relative to their age-matched systemically and periodontally healthy controls. Clinical periodontal parameters were recorded. They also assessed the collagenase and gelatinase activities in the gingival crevicular fluid (GCF) and saliva samples collected from DS patients and from the controls. The endogenously active collagenase and total collagenase activities were slightly higher in GCF of DS children compared to healthy controls. Western blot demonstrated that GCF collagenase of DS patients was human neutrophil collagenase (MMP-8 or collagenase-2). Salivary collagenase in DS was high when compared to controls but of the same MMP-8 type as in control saliva.

Komatsu et al. examined both the amount present and the enzyme activity of matrix metalloproteinases (MMP-2) in the gingival tissues of Down syndrome patients and controls. The authors reported that there was a significantly higher production of MMP-2 in the cultured gingival fibroblasts of the Down syndrome patients when compared with the controls. In addition, the mRNA expressions of membrane-type I metalloproteinases (MTI-MMP) and MMP-2 were markedly different when the cultured fibroblasts of the DS patients were compared to the controls. This would indicate that the increased amount of active MMP-2 produced in DS could be linked to the simultaneous expression of MTI-MMP, which could also be connected to the cause of periodontal disease that is seen in a majority of DS patients.

Yamazaki-Kubota et al. investigated levels of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-8 (MMP-8) in gingival crevicular fluid (GCF) and detection of periodontopathic bacteria from subgingival plaque. Samples of GCF and plaque were isolated from central incisors. Levels of MMPs were evaluated by enzyme-linked immunosorbent assay, and periodontopathic bacteria were detected by polymerase chain reaction. Levels of MMP-2 and MMP-8 in DS patients were higher than those in healthy control subjects. In the DS group, increases in these MMPs were observed in GCF from patients with good oral hygiene and absence of bleeding on probing. The detection rate of periodontopathic bacteria in DS patients was higher than that in the control subjects. Surprisingly, MMP-2 levels in sites harbouring Porphyromonas gingivalis or Aggregatibacter (Actinobacillus) actinomycetemcomitans were lower than in those without these microorganisms.

The cited studies indicate increased matrix metalloproteinase activity in the gingival tissues of DS individuals. The presence of MMP-8 suggests that neutrophils in their frustration to reach their target pathogens release their enzymes extracellularly. Matrix metalloproteinases are involved in the breakdown of the extracellular matrix. Their increased activity in the gingival tissues of DS individuals explains the gingival tissue loss and associated clinical signs (increased probing depth and loss of attachment) described. In addition the increased levels of prostaglandin E2 in combination with increased activity of MMP-9 suggests increased osteoclastic activity and explains the increased alveolar bone loss described in DS individuals.

A hypothesized model of the pathogenesis of periodontitis in Down syndrome

The presented articles viewed collectively suggest the following sequence of events in the pathogenesis of periodontitis in DS. Decreased salivary flow accompanied by reduced salivary antibody production and defective neutrophil chemotaxis facilitates early microbial colonization in the dentogingival region and makes it easier for periodontal pathogens to gain a foothold. The heavy microbial presence initiates a strong gingival immune/inflammatory response characterized by the presence of high numbers of macrophages and lymphocytes in the gingival tissues. Antigen presenting cells are active in initiating adaptive immunity (as evidenced by the increased expression of HLA Class II antigens on inflammatory cells) and eventually the production of a strong humoral antibody response. The specific antibodies may help with containing the microbial infection. In addition, macrophages and other gingival resident cells (fibroblasts) seem to be engaged in high production of degrading enzymes. Frustrated neutrophils may release their degrading enzymes extracellularly into the gingival tissues. Tissue injury releases arachidonic acid metabolites (prostaglandins). The degrading enzymes and prostaglandins are involved with periodontal tissue destruction.

Hypothesized model of periodontitis pathogenesis in Down syndrome.

Conclusions

In summary I have attempted to use the available periodontal literature on periodontitis in DS to construct a hypothesized model of the pathogenesis of the disease. Periodontitis in DS individuals is characterized by an intense and persistent immune/inflammatory response. Viewing this body of literature as a temporal sequence of events suggests that therapies aiming at reduction of microbial colonization could greatly benefit DS individuals by reducing the immune/inflammatory response and associated inflammatory mediators and degrading enzymes. The model also may suggest future therapies such as host response modulation. Strikingly absent from the model is information related to core immune/inflammatory abnormalities associated with DS such as increased oxidative stress, altered integrin expression (and associated altered lymphocyte function), altered IL-10 receptor expression (and possible impact on resolution of inflammation), and increased IL-1 production and their relation to periodontal disease. Further studies are needed to resolve these gaps in knowledge, and to access the implications for everyday periodontal care of this periodontally vulnerable population

Treatment of parodontitis. General principles.

Using digital imaging techniques and electronic image processing, the clinician can even "quantify" bone loss or gain by using digital image subtraction techniques. This chapter discusses the need for radiographic images, the desirable image characteristicsfor optimum hard tissue assessment, the techniques available, digital imaging techniques, and possible future trends for periodontal radiographic imaging.

IMAGE REQUIREMENTS

Unlike imaging for dental caries, which demands high-contrast images, the periodontal image demands different image characteristics. For one thing, the image should have a longer scale of contrast—that is, to be able to show many more shades of gray than the caries image. Subtle bone changes at the alveolar crest, demonstration of calculus deposits, and the extent of horizontal bone loss are sometimes lost in a high-contrast image. Vertical-, rather than horizontal-oriented, bitewings often are preferred and demand different image detector placement.  shows the difference between a cavity-detecting radio-graphic image and one used for periodontal assessment.  shows two scales of contrast, one with few grays and one with many.

Unfortunately, most x-ray generators currently sold have fixed kV (kilovoltage) settings (usually 70 kV) that preferentially produce high-contrast images for caries detection. Fortunately, the newer image receptors, such as storage phosphor plates and solid-state detectors (CCD or CMOS), discussed later in this chapter may help the clinician to compensate for this shortcoming. shows before and after views of a digital image subjected to electronic image processing to enhance periodontally induced disease changes.

In the periodontal assessment, there is a critical need for ideal image geometry to reflect the most accurate horizontal bone levels. Properly positioned bitewing and periapicalradiographs for this task require a paralleling technique using appropriate positioning devices. The paralleling technique further requires the image receptor to be positioned away from the teeth, especially in the maxillary arch, so that the arch curvature and shape does not orient the film or image receptor improperly.  showswhat happens when a maxillary image receptor is placed too close to the teeth.

These errors, called "foreshortening" and "elongation," can lead to distortion of the true bone levels. This is much more common in the "bisecting-angle" technique than with the paralleling technique.

Figure 9-1.

The accurate assessment of "bone height" is essential to successful periodontal disease management. Unfortunately, there are many technical errors attributable toradiographic image acquisition that can affect the appearance of the bony structures, and thus the clinician's assessment. "Radiographic bone height" may be different from "actual bone height" because of vertical angulation errors present in poorly positioned films. Radiography is only "shadow casting," and the operator can cast the "shadow" of the bone higher on the radiographic image than is truly present. This is especially true of periapical as opposed to bitewing images. Exposure geometry is extremely important and, if not compensated for, can lead to serious errors in radiographic interpretation and, consequently, diagnosis. Ritchey and Orban 1 studied the effect of varying exposure geometry on the radiographic appearance of bony defects in dried specimens. Radiographic images at various vertical angulations provided radically different views of the defects. By varying vertical angulation from a baseline of 0 degrees (right angle to the long axis of the tooth) to ±25 degrees, for example, significant furcal radiolucencies could be made to appear larger or to disappear entirely.

Figure 9-3.

RADIOGRAPHIC IMAGE TYPES AND TECHNIQUES

There are three basic intraoral radiographic techniques to consider for assessment of the bone status in patients with clinical features of periodontitis. This discussion is limited to features of the images created using these techniques, rather than the techniques themselves. (Refer to contemporary textbooks on oral and maxillofacial radiology for explanation of the actual positioning techniques.) The standard techniques for radiographic assessment of the patient with suspected periodontal bone loss are:

1. Horizontal bitewing

2. Vertical bitewing

3. Periapical

Horizontal Bitewing Technique

Bitewing radiographs are probably the most important images for establishing the true radiographic picture of the alveolar bone height in most patients with periodontal disease. With the teeth in a close approximation of their normal occlusion, the angulation used (positive 7 to 10 degrees) is favorable to projecting the image of both the maxillary and mandibular posterior teeth in their most parallel orientation. Well positioned, well exposed, horizontal bitewings will give excellent image geometry and will result in the most accurate diagnostic images of the teeth and crestal bone (Fig. 9-6). Horizontal bitewings are usually ordered when the patient has suspected "mild to moderate" horizontal bone loss, as determined by the clinical examination.

If properly positioned, the clinician should expect to see:

1. Superimposition of the buccal and lingual/palatal cusps

2. A sharp or well-defined alveolar crestal margin

3. No horizontal "overlap" between adjacent teeth (i.e., "open" interproximal spaces without overlap in the contact areas)

Figure 9-6. Crest is visible in both arches, but it is close to the edge of the film between the mandibular premolars. The root trunks of the molar teeth are not entirely visible.

Vertical Bitewing Technique

Vertical bitewings are useful if the patient has demonstrated deep probing depths on clinical examination and the clinician expects the patient to have moderate to severehorizontal bone loss. Some clinicians prefer vertical bitewings over horizontal bitewings for the majority of patients with any signs of alveolar bone loss. The operator should be cautioned about two potential problems during image acquisition. The first is that the image receptor (film) oriented vertically will impinge more readily on the palatal curvature because of the increased height of the receptor (film). This is especially true if the patient has a relatively shallow palatal vault. This impingement may lead to image distortion. The second is that vertical orientation reduces the image information in an anterior-posterior dimension because the receptor is narrower in the horizontal direction in this orientation. Thus, there may be an additional vertical image required for complete coverage of the structures being examined. Figure 9-7 shows examples of vertical bitewing radiographs.

Periapical Technique

Periapical radiographs make excellent supplemental images for periodontal bone level determination and are essential for assessing the crown-to-root ratio, root morphology, periodontal ligament spaces, and periapical status. The two types of images discussed, bitewing and periapical, are complementary and both image sets most likely will be necessary for patients with periodontal problems. However, applying selection criteria principles, periapical images are not mandatory on every patient. The patient with simple gingivitis and no evidence of attachment loss may not require periapical images. If the bitewing images are properly exposed and assessed, they will indicate the need for prescribing additional periapical radiographs in many cases. That being said, bitewing images are unable to provide information that may be critical to diagnosis and treatment planning, such as the position of important anatomic structures (e.g., mandibular nerve, floor of the maxillary sinus) and the presence or absence of periapical lesions. If suchinformation is needed, the selection criteria would dictate that the clinician order the appropriate periapical radiographs.

Figure 9-7.

Note that a greater amount of alveolar bone is visible compared with the horizontal bitewing shown in Figure 9-6. The root trunks of the molar teeth are visible in their entirety. However, because the film is oriented vertically, there is less visibility anteroposteriorly. Thus, an additional vertical bitewing would be needed on each side to see all the posterior teeth.

RADIOGRAPHIC INTERPRETATION AS APPLIED TO THE PERIODONTAL PATIENT

Use and Limitations

It is not possible to render a definitive periodontal diagnosis by means of a radiograph.5 For example, consider the patient with advanced periodontitis who has had a good clinical response to adequate and appropriate therapy. The patient may well have minimal probing depths, but the radiographic bone levels will likely remain largely unchanged after treatment. It will be impossible to determine whether that individual requires further treatment by examining posttreatment radiographs alone. Conversely, serial radiographs taken at baseline (pretreatment) and at subsequent appointments may reveal ongoing bone loss and, therefore, will be indispensable, but only in the context of supplementing the findings from the clinical examination.

Another obvious example is the endodontically involved mandibular molar that reveals radiolucency in the furcation region. Probing may reveal no increase in probing depth or clinical attachment loss—that is, there has been no apical migration of the epithelial attachment and the sulcus is not continuous with the furcation area. This is strictly anendodontic problem unless and until the sulcus becomes continuous with the furcation (see Chapter 30). Nevertheless, the radiographic image may mimic the appearance of significant furcation involvement caused by periodontal destruction.

The caveat needs to be borne in mind then that the radiographic appearance may be deceptive in that (1) bone loss may be more advanced than indicated by the radiograph, (2) a radiograph taken at one point in time says nothing about disease activity or progress, but only represents a history of tissue destruction, and (3) radiographs cannot be used as a surrogate measure of probing depth (or any aspect of the clinical examination). Despite these limitations, however, radiographs are absolutely necessary in the proper diagnosis and treatment of periodontitis. There is much information that can be obtained only from radiographs5,6: root length and morphology, root trunk dimensions, crown-to-root ratio, an approximate idea of bone destruction, coronal extent of the interdental septum, some sense of the bony topography, and anatomic structures that may be of interest when planning therapy (e.g., mental foramen, mandibular canal, maxillary sinus, nasal cavity). Similarly, there are a number of parameters that cannot be assessed using conventional radiography5,6: periodontal probing depth or attachment levels, morphology of bony defects (although this may be suggested), soft-to-hard tissue relation, toothmobility, and bony topography on the buccal and lingual surfaces of the teeth.7

Interdental Septum and Crestal Lamina Dura

One of the areas of chief interest in the periodontal examination is the interdental septum. The interdental septum, or septal bone, is located between the roots of adjacent teeth. It is therefore more clearly visualized than bone that is located on the buccal or lingual aspect of the tooth (the latter being partially obscured by the superimposed image of the root). The shape of the interdental septum is a function of the morphology of the contiguous teeth. Teeth that are quite convex on the approximating surfaces (i.e., "cup-shaped") will give rise to a wider interdental space in the mesiodistal dimension. This will result in flatter, broader septa of larger mesiodistal width. Teeth that present with a flatter, less convex interproximal profile will tend to produce narrower interdental spaces. This results in formation of a "septal peak" and is most commonly seen in the anterior regions.

Loss of this architecture results in "blunting" or loss of septal height and may indicate early periodontitis (although evidence of clinical attachment loss will precederadiographically evident bone loss). Figure 9-8 shows early and more advanced blunting of the septal crests.

Figure 9-8.

A, Early loss of the septal peak between the mandibular incisors. B, More advanced loss of the septal peak. As bone loss occurs, the clinician can see that the distance between the alveolar crest and the cementoenamel junction increases.

The normal shape of the crowns of the posterior teeth gives rise to a relatively flat alveolar crest and this, in turn, results in a rather flat interdental image on the bitewing radiograph. The thin, radiopaque line at the top of the crest, which is continuous with the lamina dura adjacent to the periodontal ligament (PDL), is known as the crestal laminadura (Fig. 9-9). It has been suggested that loss of the crestal lamina dura may correspond to periodontal disease activity. However, failure to visualize the crestal lamina dura with conventional imaging may occur in a high percentage of interproximal sites, and thus may be regarded as within normal limits.8 Greenstein and co-workers9 report that the crestallamina dura is not significantly related to any of a number of clinical periodontal parameters. While the absence of the crestal lamina is not indicative of current or impending disease activity, there is evidence to suggest that the presence of a crestal lamina dura may be associated with clinical stability.8 Increased density of the crestal lamina dura has been reported after successful periodontal therapy.10 Normally, the alveolar crest meets the lamina dura at a right angle. However, when teeth are tipped, the appearance of thecrestal lamina may mimic a vertical bone defect.

Because of the improper vertical angulation or orientation of the tipped tooth, the CEJ is positioned inferiorly relative to the adjacent tooth. This creates the impression of a vertical bony defect when in reality there is no bony defect. A similar "CEJ discrepancy" can occur as a simple anatomic variation from normal. Some people have a mesial tilt to the posterior teeth that can result in the appearance of vertical defects adjacent to the mesial surfaces of multiple teeth. Figure 9-9 provides for anexplanation of this phenomenon. Ritchey and Orban11 report that lines drawn between the adjacent CEJs should parallel the crestal lamina dura, and this simple test will readily distinguish true vertical defects from "pseudo-defects" caused by tooth angulation.

Radiographic Evidence of Bone Loss

A number of investigators, using dried jaw specimens, have determined that significant amounts of bone must be removed before bone loss is visible on conventional radiographs. Ortman and co-workers12 used dried specimens with artificially created bone defects and report that radiographic examination tends to underestimate the artificial bone loss when 30% or less of the bone was removed. Bender and Seltzer13 found that mandibular lesions created with a bur were not visible until some cortical bone was removed. Ramadan and Mitchell14 determined that significant amounts of bone removal in their dried specimens did not consistently produce changes in the radiographic images.

In clinical studies on actual patients, most investigators have found that radiographic images tend to underestimate bone loss as compared with clinical measurements.15–20The amount by which this loss is underestimated has been variously reported as 1.2,21 1.3,18 and 2.3 mm.17 This is important for the clinician to keep in mind, because the radiographic examination is likely to give a "best case scenario." Treatment plans, therefore, should account for the potential to find more significant bone loss during surgical therapy. In one recent study, radiographic images significantly underestimated bone levels when compared with direct measurements made during surgery.22 Some workers also have reported that this tendency is more pronounced in untreated than treated sites.18 Lastly, it has been shown that clinical changes (i.e., clinical attachment loss) precede radiographic changes.23One of the primary problems in radiographic examination is the lack of consistency among serial radiographs taken under normal clinical conditions.24 Relatively smallchanges in film positioning can result in large changes in bone appearance. Lesions can appear or disappear. Generally, changes in bone height have been determined by comparing the distance from the CEJ to the alveolar crest at two different time points (e.g., before and after some type of treatment). If a certain amount of loss is detected, then the label of "bone loss" can be affixed. Given the variations in consistency, various thresholds of bone loss have been described, ranging from greater than 1 mm to greater than 3 mm.25,26 The lack of consistency is not to suggest that the radiograph is useless or ineffective in the diagnosis of periodontal disease. Although clinical attachment loss is often more advanced than would be indicated by the radiograph, the latter is often a good approximation of the former. Prichard6 suggests that the radiograph should be a "critic" of the clinical examination, and further cautions that if there is a pronounced lack of congruity between what is seen radiographically and the results of the clinical examination, then a reason must be sought so that these conflicting data can be reconciled. An example might be a patient with good home care and a history of previous periodontal therapy. Periodontal probing reveals minimal probing depths with little recession. The radiographs, however, reveal significant horizontal bone loss. The most obvious reason for this seeming anomaly is the presence of a long junctional epithelial attachment subsequent to the previous periodontal intervention. In this case, repair took place and health was restored, but complete regeneration of the attachment apparatus, including the alveolar bone, did not occur.

The opposite condition may also be observed. For example, a patient presents for routine examination and a 10-mm pocket is detected on the distolingual aspect of themandibular right second molar; however, there is no radiographic evidence of a bone defect at this site. Again, there is a simple explanation: the dense (i.e., radiopaque) buccal and lingual cortical plates in this molar region are superimposed on the defect image, thereby preventing it from being seen on the radiograph. In the event of such inconsistency between clinical and radiographic examinations, however, it is prudent to reexamine the site (or sites) clinically to ensure that pathology has not been overlooked.

Patterns of Bone Loss and Defect Morphology

A distinction often is made between "horizontal" bone loss and "vertical" bone loss.

Horizontal bone loss is the symmetric loss of bone on both the mesial and distal surfaces of contiguous teeth such that the bony architecture appears to be rather flat. This is in contrast to vertical bone defects, which have a funnel-shaped appearance and plunge apically on one tooth surface, whereas there is little or no bone loss on the contiguous tooth surface (Fig. 9-10).

One variant of this pattern is the so-called hemiseptal defect in which significant bone loss has occurred on the proximal surface of one tooth, to the extent that both buccaland lingual cortical plates have been destroyed, but the bone level on the adjacent tooth surface is at a relatively normal level (or at least has not experienced the same degree of loss).6 Thus, roughly one half of the interdental septum is lost, giving rise to the term hemiseptal. These defects (also known as "one-wall" defects because they have only one bony wall facing the involved tooth surface) are among the most challenging to treat. (See Chapter 23.)

Figure 9-10.

Periapical radiograph of lower left posterior sextant showing multiple vertical defects. The most prominent is on the distal aspect of tooth #21. Note the more coronal position of the bony crest on the mesial of tooth #20 compared with the distal of #21. This radiograph also demonstrates radiographic suggestion of calculus on the mesial of tooth #18,mesial of #19, and distal of #21. A radiolucent area suggestive of bone loss also is noted in the furcation of tooth #19.

The most common type of periodontal osseous defect is the two-walled interdental crater, which is located between adjacent posterior teeth. (See Chapter 23.) The walls referred to represent the buccal and lingual bony walls. The presence of buccal and lingual bony walls, with their cortical bone intact, often prevents these defects from being clearly visualized by conventional radiography. The threewalled defect is the type of bony defect most amenable to regeneration. Like the two-walled crater, this defect may be difficult to visualize on the radiograph, because the buccal and lingual walls remain intact and obscure the radiographic image of the defect.When the clinician examines a radiographic series of the entire mouth, some patterns of bone loss are strongly suggestive of certain disease entities. Recognition of patterns of bone loss is valuable in establishing a diagnosis and formulating a treatment plan. For example, in determining whether a diagnosis of generalized or localized disease will be made, the radiographs may be of significant value. This is particularly true of localized aggressive periodontitis (previously referred to as "localized juvenile periodontitis")27 (see Chapter 2). This clinical entity is essentially defined by involvement of some or all of the first molars and incisors, with little involvement of other teeth.

Periodontal Ligament Space

The periodontal ligament space often can be discerned on routine radiographs as a thin radiolucent line interposed between the root and the radiopaque line that outlines the root. This radiopaque line (which is not consistently visible in all projections) is the image of the cribriform plate or alveolar bone proper. This radiographic image is known as thelamina dura, which is continuous with the crestal lamina dura (discussed earlier), which is the radiopaque line at the most superior aspect of the interdental septum (see Fig. 9-9). The width of the PDL has been considered important in the diagnosis of various conditions, including occlusal trauma (see Chapter 29). However, the PDL width varies with varying tube/film geometry and exposure conditions and with root morphology.28 Thus, it has not been demonstrated that PDL width can be measured consistently and reliably with conventional radiographs. Nonetheless, various authorities have suggested that a widened PDL space is suggestive of occlusal trauma.29 Specifically, occlusal trauma may be manifested as a widening of the PDL space or may present as a funneling of the coronal aspect of the PDL space. Widening of the periodontal ligament space also is seen in vertical root fractures,30,31 in progressive systemic sclerosis (scleroderma),32–34 and occasionally as a manifestation of periapical pathology.

Furcation Defects

Loss of bone in the furcation areas of molar teeth may occur as a result of periodontitis, endodontic infection, root perforation during dental procedures, or occlusal trauma. These changes are most readily seen in the mandibular molar region. Because most mandibular molars have only two roots, one mesial and one distal, any loss of bone where the roots meet the crown is normally detected easily (see Fig. 9-10 and Fig. 9-11). There is a radiolucent appearance in the furcation, and the clinician often can follow the bone level from the interproximal areas to the furcation.

Because most maxillary molars have three roots, early change in their furcation areas are more difficult to assess. Bone loss in the facial furcation may occasionally be detected on radiographs, but the superimposition of the palatal root makes such detection difficult. Defects occurring between the mesiobuccal and palatal roots and between thedistobuccal and palatal roots often are easier to detect radiographically.

Lesions involving these mesial and distal furcations often are manifested by the presence of furcation "arrows"35 (Fig. 9-12). Approximately 30% to 55% of grade 2 or 3furcation involvements have a furcation arrow present on the radiograph. Thus, although the furcation arrow is a useful tool to complement the clinical examination, it should not be relied on as a lone diagnostic tool to detect mesial and distal maxillary molar furcation defects, because many furcations with bone loss do not demonstrate a furcation arrow. Conversely, the presence of the furcation arrow had a high degree of specificity (relatively few false-positives)—that is, furcation areas without bone loss rarely showed a furcationarrow on the radiograph.

Radiograph demonstrates distinct radiolucency in the furcation region of the mandibular first molar, suggestive of furcal bone loss. Note also the appearance of heavy calculus deposits. The roots of the first molar are relatively divergent, whereas the roots of the second molar are in close proximity. Tests with a high specificity often are clinically useful.36 In such a test, the results are almost always negative (e.g., no furcation arrow present on the radiograph) when the condition being assessed (e.g., furcation involvement) is absent. If a furcation arrow is present on the radiograph, there is a high likelihood that a furcation involvement is present. This is of particular interest in the case of the mesial and distal maxillary molar furcations, which are difficult to evaluate clinically because of their interproximal location. Therefore, it is suggested that the clinician compare the radiographic appearance of the maxillary molars with the clinical findings. If furcation arrows are present, but the examination reveals no furcation involvement, it may be prudent to reevaluate those sites clinically.

11. Periodontal diseases in children - P. A. Heasman and P. J. Waterhouse

11.1 INTRODUCTION

Periodontal diseases comprise a group of infections that affect the supporting structures of the teeth: marginal and attached gingiva; periodontal ligament; cementum; and alveolar bone.  Acute gingival diseases⎯primarily herpetic gingivostomatitis and necrotizing  gingivitis⎯are ulcerative conditions that result from specific viral and bacterial infection. Chronic gingivitis, however, is a non-specific inflammatory lesion of the marginal gingiva which reflects the bacterial challenge to the host when dental plaque accumulates in the gingival crevice. The development of chronic gingivitis is enhanced when routine oral hygiene practices are impaired. Chronic gingivitis is reversible if effective plaque control measures are introduced. If left untreated the condition invariably converts to chronic periodontitis, which is characterized by resorption of the supporting connective tissue attachment and apical migration of the junctional epithelia. Slowly progressing, chronic periodontitis affects most of the adult population to a greater or lesser extent, although the early stages of the disease are detected in adolescents. Children are also susceptible to aggressive periodontal diseases that involve the primary and permanent dentitions, respectively, and present in localized or generalized forms. These conditions, which are distinct clinical entities affecting otherwise healthy children, must be differentiated from the extensive periodontal destruction that is associated with certain systemic diseases, degenerative disorders, and congenital syndromes. Periodontal tissues are also susceptible to changes that are not, primarily, of an infectious nature. Factitious stomatitis is characterized by self-inflicted trauma to oral soft tissues and the gingiva are invariably involved. Drug-induced gingival enlargement is becoming increasingly more prevalent with the widespread use of organ transplant procedures and the use of long-term immunosuppressant therapy. Localized enlargement may occur as a gingival complication of orthodontic treatment. A classification of periodontal diseases in children is given in 604HTable 11.1.

11.2 ANATOMY OF THE PERIODONTIUM IN CHILDREN

Marginal gingival tissues around the primary dentition are more highly vascular and contain fewer connective tissue fibres than tissues around the permanent teeth. The epithelia are thinner with a lesser degree of keratinization, giving an appearance of increased redness that may be interpreted as mild inflammation. Furthermore, the localized hyperaemia that accompanies eruption of the primary dentition can persist, leading to swollen and rounded interproximal papillae and a depth of gingival sulcus exceeding 3 mm. During eruption of the permanent teeth the junctional epithelium migrates apically from the incisal or occlusal surface towards the cementoenamel junction (CEJ). While the epithelial attachment is above the line of maximum crown convexity, the gingival sulcus depth often exceeds 6 or 7 mm, which favours the accumulation of plaque. When the teeth are fully erupted, there continues to be an apical shift of junctional epithelium and the free gingival margins. Stability of the gingiva is achieved at about 12 years for mandibular incisors, canines, second premolars, and first molars. The tissues around the remaining teeth continue to recede slowly until about 16 years. Thus the gingival margins are frequently at different levels on adjacent teeth that are at different stages of eruption. This sometimes gives an erroneous appearance that gingival recession has occurred around those teeth that have been in the mouth longest. A variation in sulcus depths around posterior teeth in the mixed dentition is common. For example, sulcus depths on the mesial aspects of Es and 6s are greater than those on the distal of Ds and Es, respectively. This is accountable to the discrepancy in the horizontal position of adjacent CEJs due to the difference in the occlusoapical widths of adjacent molar crowns. The attached gingiva extends from the free gingival margin to the mucogingival line minus the sulcus depth in the absence of inflammation. Attached gingiva is necessary to maintain sulcus depth, to resist functional stresses during mastication, and to resist tensional stress by acting as a buffer between the mobile gingival margin and the loosely structured alveolar mucosa. The width of attached gingiva is less variable in the primary than in the permanent dentition. This may partly account for the scarcity of mucogingival problems in the primary dentition. The periodontal ligament space is wider in children, partly as a consequence of thinner cementum and alveolar cortical plates. The ligament is less fibrous and more vascular. Alveolar bone has larger marrow spaces, greater vascularity, and fewer trabeculae than adult tissues, features that may enhance the rate of progression of periodontal disease when it affects the primary dentition. The radiographic distance between the CEJ and the healthy alveolar bone crest for primary canine and molar teeth ranges from 0 to 2 mm. Individual surfaces display distances of up to 4 mm when adjacent permanent or primary teeth are erupting or exfoliating, respectively, and eruptive and maturation changes must be considered when radiographs are used to diagnose periodontal disease in children. When such changes are excluded, a CEJ-alveolar crest distance of more than 2 mm should arouse suspicion of pathological bone loss in the primary dentition.

Key Points

Anatomy:

• junctional epithelium;

• marginal gingiva;

• attached gingiva;

• alveolar bone.

11.3 ACUTE GINGIVAL CONDITIONS

11.3.0 Introduction

The principal acute gingival conditions that affect children are primary herpetic gingivostomatitis and necrotizing ulcerative gingivitis. The latter is most frequently seen in young adults, but it also affects teenagers.

11.3.1 Primary herpetic gingivostomatitisHerpetic gingivostomatitis is an acute infectious disease caused by the herpesvirus hominis. The primary infection is most frequently seen in children between 2 and 5 years of age, although older age groups can be affected. A degree of immunity is transferred to the newborn from circulating maternal antibodies so an infection in the first 12 months of life is rare. Almost 100% of urban adult populations are carriers of, and have neutralizing antibodies to, the virus. This acquired immunity suggests that the majority of childhood infections are subclinical. Transmission of the virus is by droplet infection and the incubation period is about 1 week. The child develops a febrile illness with a raised temperature of 100-102 °F

(37.8-38.9 °C). Headaches, malaise, oral pain, mild dysphagia, and cervical

lymphadenopathy are the common symptoms that accompany the fever and precede the onset of a severe, oedematous marginal gingivitis. Characteristic, fluid-filled vesicles appear on the gingiva and other areas such as the tongue, lips, buccal, and palatal mucosa. The vesicles, which have a grey, membranous covering, rupture spontaneously after a few hours to leave extremely painful yellowish ulcers with red, inflamed margins (605HFig. 11.1 (a) and (b)). The clinical episode runs a course of about 14 days and the oral lesions heal without scarring. Very rare but severe complications of the infection are aseptic meningitis and encephalitis. The clinical features, history, and age group of the affected children are so characteristic that diagnosis is rarely problematic. If in doubt, however, smears from recently ruptured vesicles reveal degenerating epithelial cells with intranuclear inclusions. The virus protein also tends to displace the nuclear chromatin to produce enlarged and irregular nuclei. Herpetic gingivostomatitis does not respond well to active treatment. Bed rest and a soft diet are recommended during the febrile stage and the child should be kept well hydrated. Pyrexia is reduced using a paracetamol suspension and secondary infection of ulcers may be prevented using chlorhexidine. A mouthrinse (0.2%, two to three times a day) may be used in older children who are able to expectorate, but in younger children (under 6 years of age) a chlorhexidine spray can be used (twice daily) or the solution applied using a sponge swab. In severe cases of herpes simplex, systemic acyclovir can be prescribed as a suspension (200 mg) and swallowed, five times daily for 5 days. In children under 2 years the dose is halved. Acyclovir is active against the herpesvirus but is unable to eradicate it completely. The drug is most effective when given at the onset of the infection.

Key PointsHerpetic gingivostomatitis⎯clinical:

• primary/recurrent;

• viral;

• vesicular lesions;

• complications rare.Key Points

Herpetic gingivostomatitis⎯treatment:

• symptomatic;

• rest and soft diet;

• paracetamol suspension;

• acyclovir.

After the primary infection the herpesvirus remains dormant in epithelial cells of the host. Reactivation of the latent virus or reinfection in subjects with acquired immunity occurs in adults. Recurrent disease presents as an attenuated intraoral form of the primary infection or as herpes labialis, i.e. the common 'cold sore' on the mucocutaneous border of the lips (606HFig. 11.2). Cold sores are treated by applying acyclovir cream (5%, five times daily for about 5 days).607H

Fig. 11.1 Ulcerative stage of primary herpetic gingivostomatitis:(a) palatal gingiva; (b) lower lip mucosa. 608H

Fig. 11.2 Herpetic 'cold sore' at the vermilion border of the lower lip. 11.3.2 Necrotizing ulcerative gingivitis Necrotizing ulcerative gingivitis (NUG) is one of the commonest acute diseases of the gingiva. In the United States and Europe, NUG affects young adults in the 16-30 age range with reported incidence figures of 0.7-7%. In developing countries, NUG is prevalent in children as young as 1 or 2 years of age when the infection can be very aggressive leading to extensive destruction of soft and hard tissues (609HFig. 11.3). Epidemic-like occurrences of NUG have been reported in groups such as army recruits and first-year college students. These outbreaks are more likely to be a consequence of the prevalence of common pre-disposing factors rather than communicability of infection between subjects. Clinical features NUG is characterized by necrosis and ulceration, which first affect the interdental papillae and then spread to the labial and lingual marginal gingiva. The ulcers are 'punched out', covered by a yellowish-grey pseudomembranous slough, and extremely painful to the touch (610HFig. 11.3). The acute exacerbation is often superimposed upon a pre-existing gingivitis, and the tissues bleed profusely on gentle probing. The standard of oral hygiene is usually very poor. A distinctive halitosis is common in established cases of NUG, although fever and lymphadenopathy are less common than in herpetic gingivostomatitis. The clinical course of NUG is such that the acute stage enters a chronic phase of remission after 5-7 days. Recurrence of the acute condition is inevitable, however, and if this acute-chronic cycle is allowed to continue then the marginal tissues lose their contour and appear rounded. Eventually, the inflammation and necrosis involve the alveolar crest and the subsequent necrotizing periodontitis leads to rapid bone resorption and gingival recession. Progressive changes are also a consequence of inadequate or incomplete treatment.

Aetiology

A smear taken from an area of necrosis or the surface of an ulcer will reveal numerous dead cells, polymorphonuclear leucocytes, and a sample of the micro-organisms that are frequently associated with NUG. Fusiform bacteria and spirochaetes are both numerous and easy to detect. A fusospirochaetal complex has been strongly implicated as the causative organisms in NUG. Other Gram-negative anaerobic organisms including Porphyromonas gingivalis, Veillonella species, and Selenomonasspecies have been detected, which suggests that NUG could be a broad anaerobic infection. A viral aetiology has also been suggested, primarily because of the similarity between NUG and known viral diseases. The restriction of the disease to children and young adults, for example, may infer that older subjects have undergone seroconversion (and are thus immune) as a consequence of clinical or subclinical viral infection in earlier life. The recurring episodes of the disease may also be explained by a viral hypothesis. The ability to undergo latent infection that is subject to reactivation is a characteristic of the herpesvirus. The argument for the implication of a virus in NUG is therefore valid and novel, although a specific virus has yet to be isolated from oral lesions. Predisposing factors Poor oral hygiene and a pre-existing gingivitis invariably reflect the patient's attitude to oral care. Many young adults with NUG are heavy smokers. The effect of smoking on the gingiva may be mediated through a local irritation or by the vasoconstrictive action of nicotine, thus reducing tissue resistance and making the host more susceptible to anaerobic infection. Smoking is obviously not a predisposing factor in young children. In underdeveloped countries, however, children are often undernourished and debilitated, which may predispose to infection. Outbreaks of NUG in groups of subjects who are under stress has implicated emotional status as an important predisposing factor. Elevated plasma levels of corticosteroids as a response to an emotional upset are thought to be a possible mechanism. It is conceivable that all the predisposing factors have a common action to initiate or potentiate a specific change in the host such as lowering the cell-mediated response. Indeed, patients with NUG have depressed phagocytic activity and chemotactic response of their polymorphonuclear leucocytes. Key Points

Necrotizing ulcerative gingivitis⎯clinical:

• yellow-grey ulcers;

• fusospirochaetal infection;

• possible viral aetiology;

• well-established predisposing factors.

Treatment

It is important at the outset that the patient is informed of the nature of NUG and the likelihood of recurrence of the condition if the treatment is not completed. Smokers should be advised to reduce the number of cigarettes smoked. A soft, multitufted  brush is recommended when a medium-textured brush is too painful. Mouthrinses may be recommended but only for short-term use (7-10 days). Rinsing with chlorhexidine (0.2% for about 1 min) reduces plaque formation, while the use of a hydrogen peroxide or sodium hydroxyperborate mouthrinse oxygenates and cleanses the necrotic tissues. Mechanical debridement should be undertaken at the initial visit. An ultrasonic scaler with its accompanying water spray can be effective with minimal discomfort for the patient. Further, if NUG is localized to one part of the mouth, local anaesthesia of the soft tissues can allow some subgingival scaling to be undertaken. In severe cases of NUG, a 3-day course of metronidazole (200 mg three times a day) alleviates the symptoms, but the patients must be informed that they are required to reattend for further treatment. Occasionally, it is necessary to surgically recontour the gingival margin (gingivoplasty) to improve tissue architecture and facilitate subgingival cleaning.

Key Points

Necrotizing ulcerative gingivitis⎯treatment:

• intense oral hygiene;

• remove predisposing factors;

• mechanical debridement;

• metronidazole.

611H

Fig. 11.3 A 5-year-old Ethiopian boy with necrotizing ulcerative gingivitis.

11.4 CHRONIC GINGIVITIS

National Surveys (1973, 1983, and 1993) of children's dental health in the United Kingdom show that the prevalence of chronic gingivitis increases steadily between the ages of 5 and 9 years and is closely associated with the amount of plaque, debris, and calculus present (612HFig. 11.4). For example, in 1993, 26% of 5-year-olds had some signs of gingivitis, and the proportion increased to 62% at the age of 9. The prevalence of gingivitis peaks at about 11 years and then decreases slightly with age to 15 years. In terms of gingivitis, there has been no improvement over the decades between surveys. Indeed, in 1993, between 11 and 14% more children of all ages between 6 and 12 years had signs of gingivitis when compared with 1983. These differences were not maintained with increasing age, however, as 52% of 15-yearolds had gingivitis in 1993 compared with 48% in 1983. Furthermore, there were no differences between 1983 and 1993, in the proportion of 15-year-olds with pockets between 3.5 and 5.5 mm (9 and 10%, respectively). These data suggest that the gingival condition of children in the United Kingdom has deteriorated over the 10 years between 1983 and 1993, whereas the periodontal status of 15-year-olds has not changed. Certainly, changes in gingival health do not mirror the dramatic improvement in the prevalence of caries over the same period. Children's mouths tended to be cleaner in 1983 than in 1973. This trend was reversed by 1993 when between 10 and 20% more children of all ages had plaque deposits. Levels of calculus were similar in both surveys. The onset of puberty and the increase in circulating levels of sex hormones is one explanation for the increase in gingivitis seen in 11-year-olds. Oestrogen increases the cellularity of tissues and progesterone increases the permeability of the gingival vasculature. Oestradiol also provides suitable growth conditions for species of black pigmenting organisms which are associated with established gingivitis. Histopathology.The inflammatory infiltrate associated with marginal gingivitis in children is analogous to that seen in adults during the early stages of gingival inflammation. The dominant cell is the lymphocyte, although small numbers of plasma cells, macrophages, and neutrophils are in evidence. Research findings have not yet determined unequivocally whether the lymphocyte population is one of unactivated B cells or is T-cell dominated. The relative absence of plasma cells, which are found in abundance in more established and advanced lesions in adults, confirms that gingivitis in children is quiescent and does not progress inexorably to involve the deeper periodontal tissues.

Key Points

Chronic gingivitis:

• plaque-associated;

• lymphocyte-dominated;

• complex flora;

• linked to the onset of puberty.

Microbiology

The first organisms to colonize clean tooth surfaces are the periodontally harmless, Gram-positive cocci that predominate in plaque after 4-7 days. After 2 weeks, a more complex flora of filamentous and fusiform organisms indicates a conversion to a Gram-negative infection, which, when established, comprises significant numbers of Capnocytophaga, Selenomonas, Leptotrichia, Porphyromonas, and Spirochaete spp. These species are cultivable from established and advanced periodontal lesions in cases of adult periodontitis. This suggests that the host response (rather than the subgingival flora) confers a degree of immunity to the development of periodontal disease in children, thus preventing spread of the contained gingivitis to deeper tissues. Manual versus powered toothbrushesThe treatment and prevention of gingivitis are dependent on achieving and maintaining a standard of plaque control that, on an individual basis, is compatible with health. Toothbrushing is the principal method for removing dental plaque, and powered toothbrushes now provide a widely available alternative to the more conventional, manual toothbrushes for cleaning teeth. There is considerable evidence in the literature to suggest that powered toothbrushes are beneficial for specific groups: patients with fixed orthodontic appliances⎯for whom there is also evidence that powered toothbrushes are effective in reducing decalcification; children and adolescents; and children with special needs. It remains questionable whether children who are already highly motivated with respect to tooth cleaning will benefit from using a powered toothbrush. It is possible that,particularly  in children, any improved plaque control as a consequence of using a powered toothbrush may result from a 'novelty effect' of using a new toothbrush rather than because the powered toothbrush is more effective as a cleaning device. A systematic review evaluating manual and powered toothbrushes with respect to oral health has made some important conclusions. Compared to manual toothbrushes, rotating/oscillating designs of powered toothbrushes reduced plaque and gingivitis by 7-17% although the clinical significance of this could not be determined. Powered brushes, therefore, are at least as effective and equally as safe as their manual counterparts with no evidence of increased incidence of soft tissue abrasions or trauma. No clinical trials have looked at the durability, reliability, and relative cost of powered and manual brushes so it is not possible to make any recommendation regarding overall toothbrush superiority. 613H

Fig. 11.4 Chronic marginal gingivitis in a 10-year-old girl.

11.5 DRUG-INDUCED GINGIVAL ENLARGEMENT

11.5.0 Introduction

Enlargement of the gingiva is a well-recognized unwanted effect of a number of drugs. The most frequently implicated are phenytoin, cyclosporin, and nifedipine (614HFig. 11.5). 615H

Fig. 11.5 Drug (phenytoin)-induced gingival enlargement in a 12-year-old boy.

11.5.1 PhenytoinPhenytoin is an anticonvulsant used in the management of epilepsy. Gingival enlargement occurs in about 50% of dentate subjects who are taking the drug, and is most severe in teenagers and those who are cared for in institutions. The exact mechanism by which phenytoin induces enlargement is unclear. The gingival enlargement reflects an overproduction of collagen (rather than a decrease in degradation), and this may be brought about by the action of the drug on phenotypically distinct groups of fibroblasts that have the potential to synthesize large amounts of protein. Phenytoin-induced enlargement has been associated with a deficiency of folic acid, which may lead to impaired maturation of oral epithelia.

11.5.2 Cyclosporin

Cyclosporin is an immunosuppressant drug that is used widely in organ transplant patients to prevent graft rejection. Approximately 30% of patients taking the drug demonstrate gingival enlargement, with children being more susceptible than adults. The exact mechanism of the drug in causing enlargement is unknown. There is evidence to suggest both a stimulatory effect on fibroblast proliferation and collagen production as well as an inhibitory effect on collagen breakdown by the enzyme collagenase.

11.5.3 Nifedipine

Nifedipine is a calcium-channel blocker that is used in adults for the control of cardiovascular problems. It is also given to post-transplant patients to reduce the nephrotoxic effects of cyclosporin. The incidence of gingival enlargement in dentate subjects taking nifedipine is 10-15%. The drug blocks the calcium channels in cell membranes⎯intracellular calcium ions are a prerequisite for the production of collagenases by fibroblasts. The lack of these enzymes could be responsible for the accumulation of collagen in the gingiva. Clinical features of gingival enlargement.The clinical changes of drug-induced enlargement are very similar irrespective of the drug involved. The first signs of change are seen after 3-4 months of drug administration. The interdental papillae become nodular before enlarging more diffusely to encroach upon the labial tissues. The anterior part of the mouth is most severely and frequently involved so that the patient's appearance is compromised. The tissues can become so abundant that oral functions, particularly eating and speaking, are impaired. Enlarged gingiva is pink, firm, and stippled in subjects with a good standard of oral hygiene. When there is a pre-existing gingivitis the enlarged tissues compromise an already poor standard of plaque control. The gingiva then exhibit the classical signs of gingivitis (616HFig. 11.5).

Key Points

Gingival enlargement:

• drug-induced;

• collagen accumulation;

• surgical treatment;

• superimposed gingivitis.

Management of gingival enlargement

A strict programme of oral hygiene instruction, scaling, and polishing must be implemented. Severe cases of gingival enlargement inevitably need to be surgically excised (gingivectomy) and then recontoured (gingivoplasty) to produce an architecture that allows adequate access for cleaning. A follow-up programme is essential to ensure a high standard of plaque control and to detect any recurrence of the enlargement. As the causative drugs need to be taken on a long-term basis, recurrence is common. When a phenytoin-induced enlargement is refractory to long-term treatment, the patient's physician may be requested to modify or change the anticonvulsant therapy to drugs such as sodium valproate or carbamazepine, which do not cause gingival problems. There is no alternative medication to cyclosporin, however, and the patients inevitably require indefinite oral care.

11.6 TRAUMATIC GINGIVITIS (GINGIVITIS ARTEFACTA/FACTITIOUS

GINGIVITIS)

Gingivitis artefacta has minor and major variants. The minor form results from rubbing or picking the gingiva using the fingernail, or perhaps from abrasive foods such as crisps, and the habit is usually provoked by a locus of irritation such as an area of persistent food packing or an already inflamed papilla (617HFig. 11.6). The lesions resolve when the habit is corrected and the source of irritation is removed. The injuries in gingivitis artefacta major are more severe and widespread and can involve the deeper periodontal tissues (618HFig. 11.7 (a)). Other areas of the mouth such as the lips and tongue may be involved and extraoral injuries may be found on the scalp, limbs, or face (factitious dermatitis) (619HFig. 11.7 (b)). The lesions are usually viewed with complete indifference by the patient who is unable to forward details of their time of onset or possible cause.The treatment of these patients, other than the dressing and protection of oral wounds, does not lie with the dentist. Psychological reasons for inflicting the lesions may be complex and obscure. A psychological or psychiatric consultation, rarely welcomed either by older children or their parents, is necessary if the patient is to be prevented from ultimately inflicting serious damage upon themselves.

Key Points

Gingivitis artefacta:

• minor/major;

• self-inflicted;

• habitual;

• psychological.620H

Fig. 11.6 Traumatic gingival injury inflicted by the fingernail (arrowed) that

has been teased from the gingival crevice of 1|. (Reproduced with kind permission of the Editor, British Dental Journal and Mr P. R. Greene, General Dental Practitioner, Manchester.) 621H

Fig. 11.7 (a) Generalized, self-inflicted ulceration of the attached gingiva and extensive loss of attachment around |6. (b) Ulcerative lesion at the hairline on the scalp. The lesions were produced by rubbing with a fingernail. (Reproduced with kind permission of the Editor, Journal of Periodontology.)

11.7 MUCOGINGIVAL PROBLEMS IN CHILDREN

In adults much attention has focused on whether recession is more likely to occur locally where there is a reduced width of keratinized gingiva (KG). Conversely, of course, gingival recession inevitably leads to a narrowing of the zone of KG. It is, therefore, often difficult to determine unequivocally whether a narrow zone of KG is the cause or the effect of recession. A narrow or finite width of KG is compatible with gingival health, providing the tissues are maintained free of inflammation and chronic, traumatic insult. A wider zone of KG is considered more desirable to withstand gingival inflammation, trauma from mastication, toothbrushing, and forces from muscle pull. Anterior teeth with narrow zones of KG are frequently encountered in children, as the width of KG varies greatly during the mixed dentition. For example, when permanent  teeth erupt labially to their predecessors they frequently appear to erupt through alveolar mucosa with a complete absence of KG (622HFig. 11.8). When the tooth has fully erupted an obvious width of KG is present. The width of KG alone should not be the sole indicator of potential sites of gingival recession in children. The position of a tooth in the arch is a better guide as studies have shown that, of those permanent incisors with recession, about 80% are displaced labially. Aggravating factors such as gingivitis or mechanical irritation from excessive and incorrect toothbrushing further increase the likelihood of recession. Gingival recession is also a common periodontal complication of orthodontic therapy when labial tipping of incisors is undertaken. When roots move labially through the supporting envelope of alveolar bone the potential for recession increases. When gingival recession occurs in children, a conservative approach to treatment should be adopted. The maximum distance from the gingival margin to the CEJ should be recorded. Overenthusiastic toothbrushing practices are modified and a scale and polish given if necessary. The recession must then be monitored carefully until the permanent dentition is complete. Longitudinal studies of individual cases have shown that, as the supporting tissues mature, the gingival attachment tends to creep spontaneously in a coronal direction to cover at least part of the previously denuded root surface. This cautious approach is preferred to corrective surgicalintervention to increase the width of KG.

Key Points

Gingival recession:

• narrow keratinized gingiva;

• local trauma;

• post orthodontics;

• conservative treatment approach.

623H

Fig. 11.8 Lower central incisors that have erupted somewhat labially to the partially erupted There is only a minimal width of keratinized gingiva buccal to the .

11.8 CHRONIC PERIODONTITIS

A number of epidemiological studies (624HTable 11.2) have investigated the prevalence of chronic periodontitis in children. The variation in prevalence between studies is considerable and attributable to different methods of diagnosing attachment loss and the use of different cut-off levels to determine disease presence. Some workers use intraoral radiographs to measure from the CEJ to the alveolar crest, while others use a periodontal probe to determine clinically the distance from the CEJ to the base of the periodontal crevice or pocket. Radiographic studies on children with a primary or a mixed dentition indicate that loss of attachment is uncommon under the age of 9 years. A microscopic examination of the root surfaces of 200 extracted molars, however, demonstrated a mean attachment loss of 0.26 mmon two-thirds of the surfaces on 94% of teeth. Clinically, such small changes are insignificant and difficult to detect. Cut-off levels at which disease is diagnosed in adolescents have been set at 1, 2, or 3 mm. Larger cut-off values provide more stringent criteria for the detection of  attachment loss and consequently the disease appears less prevalent. An exception to this trend was seen in a study of 602, 14-15-year-olds in the United Kingdom; 51.5% of the subjects were diagnosed as having periodontal disease determined by a CEJ⎯alveolar crest distance of 3 mm. Additional radiographic features were also used, namely an irregular contour of the alveolar crest and a widened, coronal periodontal ligament space. Such observations may result from minor tooth movements following eruption of the second molars and consolidation of the occlusion, or from remodelling of bone after orthodontic treatment. It is, therefore, likely that 51.5% is a considerable overestimate of disease prevalence in this age group. If a cut-off value of 2 mm is deemed acceptable, the majority of studies put the prevalence of disease in adolescents at 1-11%. This suggests that chronic adult periodontitis initiates and progresses during the early teenage years. Observations made with respect to periodontal disease in children include:

• When loss of attachment occurs at interproximal sites it is a consequence of pathological change and correlates closely with the presence of subgingival calculus;

• The prevalence of periodontal destruction correlates positively with DMF (decayed, missing, and filled) teeth or surfaces. This suggests either, that carious or broken down surfaces predispose to plaque accumulation, or perhaps more likely, that in the absence of oral health care, periodontal disease and caries progress independently;

• When the loss of attachment occurs on buccal or palatal surfaces, it is more often associated with trauma from an incorrect toothbrushing technique than with an inflammatory response.

Key Points

Loss of attachment:

• plaque-induced;

• trauma-induced;

• detected radiographically;

• decayed, missing, and filled (teeth) link.

11.9 RISK FACTORS FOR PERIODONTAL CONDITIONS AND DISEASES

11.9.0 Introduction

A risk factor can be defined as a state or occurrence that increases the probability of an individual developing a disease. Risk factors for periodontal disease can be classified as local or general. Local factors, for example, an instanding lateral incisor, may serve to compromise local plaque control by hindering effective cleaning and resulting in dental plaque accumulation. On the other hand, general risk factors, such as an inherited disorder may predispose an individual to periodontal disease despite a good level of plaque control. It is important to understand that if a child possesses a risk factor for periodontal disease, it does not necessarily follow that the child will develop the condition. Conversely, a patient may appear to have no risk factors, but the disease may develop subsequently. Bearing this in mind, risk factors (both local and general) should be considered when assessing, diagnosing, treating, and maintaining child patients with periodontal disease.

 11.9.1 Local risk factors

These can be grouped simply into four areas. There may be overlap between these areas.

• Malocclusions.

• Following traumatic dental injuries.

• Plaque retentive factors.

• Ectopic eruption

Malocclusions

An instanding or rotated tooth may be difficult to clean and can cause increased plaque retention. A traumatic occlusion may result in direct damage to the periodontal support. Angle's Class II division ii malocclusions with increased and complete overbites may predispose to damage of the gingiva palatal to the upper incisor teeth. Similarly, severely retroclined upper incisor teeth may damage the labial gingiva of the lower teeth. Following a traumatic dental injury Luxation, intrusion and avulsion injuries all result in varying degrees of damage to the periodontal ligament and if severe, alveolar bone. This results in increased tooth mobility which is managed by providing the affected teeth with a splint. If a traumatised tooth is left in a severely mobile state or in traumatic occlusion, the periodontal ligament fibres will not heal and further damage may ensue. Plaque retentive factorsThere is a multitude of plaque retentive factors which may serve to compromise the health of the periodontium. They may be naturally occurring (in the case of a dental anomaly) or be iatrogenic.

Examples of dental anomalies include:

• Erupted supernumerary teeth (localized malocclusion).

• Invaginated odontomes. • Talon cusps.

• Pitted, grooved amelogenesis imperfecta (with sensitivity).

• Enamel pearls or root grooves.

Examples of iatrogenic factors include:

• Orthodontic appliances.

• Partial dentures.

• Ledges and overhangs on poorly fitting preformed metal crowns.

• Ledges and overhangs from intracoronal restorations.

11.9.2 General risk factors

General risk factors for periodontal disease may have a genetic basis, with certain inherited conditions possessing periodontal manifestations (e.g. Papillon Lefevre Syndrome). The genetic conditions are dealt with previously in this chapter. There are also metabolic, haematological, and environmental risk factors within the general category. A full discussion of each is outwith the scope of this chapter, so the two most prevalent examples of general risk factors, diabetes mellitus and smoking will be discussed. Diabetes mellitusChildren with Type I diabetes with poor diabetic control are at risk of developing periodontal disease. The link appears not to be directly with the level of plaque control but to the presence of systemic complications, such as retinal and renal problems. The overall severity of periodontal disease may increase with increasing duration of the diabetes. There are a number of factors which may contribute to a child's risk status. They may be inherited or secondary to high levels of blood glucose (hyperglycaemia).

These can be outlined as:

• Defective polymorphonuclear leucocyte function (chemotaxis, phagocytosis, and adherence);

• Disordered collagen metabolism (gingival fibroblasts produce less collagen and the polymorphonuclear leucocytes produce more of the enzyme collagenase than in nondiabetics). This results in poor wound healing;

• The hyperglycaemic state may favour certain inflammatory mediators and increase oxygen radical production by macrophages. Tobacco smoking Smoking is now thought to be a significant environmental risk factor for periodontal disease. Smokers have 3-6 times the level of periodontal disease when compared with non-smokers and young people are thought to be more vulnerable. Often, the signs of disease are masked because nicotine and other tobacco products cause vasoconstriction, reducing the blood supply to the gingivae and lowering the tendency to bleed. There are a number of smoking-related mechanisms pertaining to smoking as a risk factor for periodontal disease. These include:

• Increased prevalence of some periodontal pathogens;

• Reduction in the levels of salivary IgA;

• Reduction in effective phagocytosis;

• Alterations in the numbers of certain T cell populations.

If an individual stops smoking this will allow an improved response to the

management of periodontal disease, but the time taken for this 'recovery' to occur is unclear. The underlying defect associated with general risk factors is compromised phagocytosis and or chemotaxis. The importance of polymorphonuclear leucocyte (neutrophil) function to the host response is also demonstrated in less common conditions such as the neutropaenias (see page 252).

11.10 PERIODONTAL COMPLICATIONS OF ORTHODONTIC

TREATMENT

11.10.0 Introduction

Orthodontic treatment in adolescents, particularly with fixed appliances, can pre- dispose to a deterioration in periodontal health and a number of well-recognized complications.

11.10.1 Gingivitis

Access for interproximal toothbrushing is reduced considerably during fixed appliance therapy and the accumulation of plaque induces gingivitis (625HFig. 11.9). The problem is compounded when teeth are banded rather than bonded as periodontal health is more easily maintained when the gingival sulcus is not encroached upon by metal bands. When supragingival plaque deposits are present on teeth that are being repositioned  orthodontically, the type of movement used may play an important part in the development of periodontal problems. Supragingival plaque deposits are shifted into a subgingival location by tipping movements. Conversely, bodily movements are less likely to induce a relocation of supragingival plaque. 626H

Fig. 11.9 Chronic marginal gingivitis associated with fixed appliance therapy.

11.10.2 Gingival enlargement

The anterior palatal gingiva and mucosa have a propensity for enlargement when tissues are 'rolled up' between incisors that are being retracted and the fixed anterior margin of the acrylic plate of a removable appliance (627HFig. 11.10 (a) and (b)). Generally, however, these changes tend to be transient and resolve when appliances are removed. 628H

Fig. 11.10 (a) Gingival enlargement on the palatal aspect of retracted maxillary incisors. (b) Appliance in situ. (Reproduced by kind permission of Mr N. E. Carter, Consultant in Orthodontics, Newcastle.)

11.10.3 Attachment and bone loss

The mean, annual rate of coronal attachment loss during appliance therapy ranges from 0.05 to 0.30 mm, which compares favourably with figures for the mean annual attachment loss in untreated populations. A well-recognized complication of orthodontic tooth movement is apical root resorption, particularly when excessive forces are used (629HFig. 11.11). Such changes must also be regarded as loss of attachment, albeit at an apical rather than a coronal site. 630H

Fig. 11.11 Apical root resorption of 321|123 following orthodontic treatment.

(Reproduced by kind permission of Dr I. L. Chapple, Professor of Periodontology, Birmingham, UK.)

11.10.4 Gingival recession

The response of the facial periodontal tissues to labial tooth movement in anterior segments is unpredictable. Labial movement of incisors is sometimes associated with gingival recession. The risk of recession is greater when the alveolar bone plate is thin or where dehiscences or fenestrations in the bone exist.

11.10.5 Trauma

Direct local irritation of the soft tissues by components of a fixed appliance can be minimized if due care and attention is exercised during bonding, banding, and placement of wires and elastics. If chronic irritation of the gingiva does occur then a localized, acute inflammatory reaction will quickly follow. This may develop further into a region of gingival enlargement or a fibrous epulis that is superimposed upon a burrowing infrabony lesion.

Key Points

Orthodontic problems:

• gingivitis;

• enlargement;

• root resorption;

• gingival trauma.

11.11 AGGRESSIVE PERIODONTAL DISEASES

11.11.0 Introduction

Aggressive periodontal diseases comprise a group of rare, but rapidly progressing infections that affect the primary and permanent dentitions. The disorders are associated with a more specific microbial challenge and an inherent defect in the host's immunological response. The nature of these diseases can lead to premature tooth loss at an early age. Prompt diagnosis is essential if treatment is to be successful, and the periodontal status must be monitored regularly to ensurethat the treated disease remains quiescent. Aggressive periodontal diseases were previously known as early-onset diseases, namely, prepubertal and juvenile periodontitis. A classification system for periodontal diseases and conditions published in 1999 effectively combined these two diseases into one⎯aggressive periodontitis (see Further Reading). This classification, which is used in this chapter, removed the arbitrary age limitations that were previously inferred by terms such as prepubertal, juvenile, and even adult periodontitis. It is now recognized that aggressive periodontitis can affect the primary and permanent dentitions both in localized and generalized forms.

11.11.1 Primary dentition (prepubertal periodontitis)

The disease may present immediately after the teeth have erupted. In the generalized form the gingiva appear fiery red, swollen, and haemorrhagic. The tissues become hyperplastic with granular or nodular proliferations that precede gingival clefting and extensive areas of recession. Gross deposits of plaque are inevitable as the soft tissue changes make it difficult to maintain oral hygiene. The disease progresses extremely rapidly, with primary tooth loss occurring as early as 3-4 years of age. The entire dentition need not be affected, however, as the bone loss may be restricted to one arch. Children with generalized disease are susceptible to recurrent general infections, principally otitis media and upper respiratory tract infections. Localized disease progresses more slowly than the generalized form and bone loss characteristically affects only incisor-molar teeth. Plaque levels are usually low, consequently soft tissue changes are minimal with gingivitis and proliferation involving only the marginal tissues. The predominant micro-organisms that have been identified are aggressive periodontopathogens: Actinobacillus actinomycetemcomitans,Porphyromonas gingivalis, Fusobacterium nucleatum, and Eikenella corrodens. This suggests that there is an infective component to the disease, although defects in the hosts' response have also been identified. Profound abnormalities in chemotaxis and phagocytosis of polymorphonuclear neutrophils and monocytes are frequently reported in these patients. These immunological defects are heritable risk factors that help to define phenotypically the disease entity. Conversely, they may also be associated with more serious and life-threatening conditions, and thus a full medical screen is indicated. Oral hygiene instruction, scaling, and root planing should be undertaken at frequent intervals. Bacterial culturing of the pocket flora identifies specific periodontopathogens. If pathogens persist after oral debridement, an antibiotic such as metronidazole or amoxycillin (amoxicillin) should be given systemically after sensitivity testing, as a short course over 1-2 weeks. Generalized disease responds poorly to treatment. Some improvement has been achieved following a granulocyte transfusion in a patient with a defect in neutrophil function. Extraction of involved teeth has also produced an improvement in neutrophil chemotaxis, which suggests that the defect may be induced by certain organisms in the periodontal flora. Furthermore, in severe cases of generalized periodontitis, extraction of all primary teeth (and the provision of a removable prosthesis) can limit the disease to the primary dentition. Presumably, anaerobic pathogens are unable to thrive in the absence of teeth. When the permanent teeth erupt, bacterial culturing of the subgingival flora ensures that reinfection is detected early.

Key Points

Primary dentition (prepubertal periodontitis):

• localized/generalized;

• aggressive pathogens;

• intense treatment.

11.11.2 Permanent dentition (juvenile periodontitis)

In the permanent dentition, aggressive periodontitis involves severe periodontal destruction with an onset around puberty. The localized form occurs in otherwise healthy individuals, with destruction classically localized and around the first permanent molars and incisors, and not involving more than two other teeth. Generalized periodontitis also occurs in otherwise healthy individuals but involves more than 14 teeth, that is, being generalized to an arch or the entire dentition. Some reports have monitored children suffering from aggressive periodontitis of the primary dentition to find that,at around puberty, the disease became generalized to involve the entire dentition. EpidemiologyStudies show a prevalence of about 0.1% in developed countries and about 5% in underdeveloped nations, although some variation may be due to different methods of screening and different criteria used to define the disease. The disease is clearly more prevalent in certain ethnic groups. In the United Kingdom an epidemiological study of 7266 schoolchildren in Coventry and Birmingham showed an overall prevalence of 0.02% in Caucasians, 0.2% in Asians, and 0.8% in the AfroCaribbean population. There was no difference in prevalence between males and females, which does not concur with the data of many earlier epidemiological studies of the disease which reported a female to male ratio of 3 : 1.

Clinical and radiographic featuresThe age of onset is between 11 and 15 years. The clinical features are pocket formation and loss of attachment associated with the permanent incisors and first molar teeth. The radiographic pattern of bone loss is quite distinctive. Bilateral angular bone defects are identified on the mesial and, or distal surfaces of molars (631HFig. 11.12 (a) and (b)). Angular defects are sometimes seen around the incisors, although the very thin interproximal bone is resorbed more evenly to give a horizontal pattern of resorption. The bone loss around the molars can be detected on routine bitewing radiographs. The interpretation of the films must be made with a sound knowledge of the patient's dental history, however, as localized angular defects are found adjacent to teeth with overhanging or deficient interproximal restorations, and teeth that have tilted slightly (632HFig. 11.13). The gingiva can appear healthy when the levels of plaque are low, but a marginal gingivitis will be present if a good standard of plaque control is not evident. The generalized form may also present at puberty. Severe generalized bone loss is the characteristic feature (633HFig. 11.14). The pattern may be a combination of angular and horizontal resorption producing an irregular alveolar crest. When patients have good plaque control the degree of bone resorption is not commensurate with the level of oral hygiene. The more generalized nature of the disease predisposes to multiple and recurrent abscess formation which is a common presenting feature. Invariably, one of the presenting signs is tooth migration or drifting of incisors. Tooth movement is not necessarily a consequence of advanced disease as drifting may occur when only a fraction of a tooth's periodontal support is lost. Conversely, extensive bone loss can occur with no spontaneous movement of teeth and the subject may only be alerted to the problem when a minor traumatic episode, such as a blow to the mouth during a sporting activity, causes unexpected loosening of teeth. Bacteriology and pathogenesis.The subgingival microflora comprises loosely adherent, Gram-negative anaerobes including Eikenella corrodens, Capnocytophaga spp., and Prevotella intermedia. The most frequently implicated organism is Actinobacillus actinomycetemcomitans, which has been found in over 90% of patients. Sufferers also have raised IgG titres to A. actinomycetemcomitans, but levels of the bacteria fall significantly following successful treatment of the condition.

Key Points

Permanent dentition (Juvenile periodontitis):

• onset around puberty;

• localized/generalized;

• Actinobacillus actinomycetemcomitans;

• neutrophil chemotaxis defect.

The extreme pathogenicity of A. actinomycetemcomitans is due to its ability to invade connective tissues and the wide range of virulence factors that it produces. These include a potent lipopolysaccharide that induces bone resorption, collagenase, an epitheliotoxin, a fibroblast-inhibiting factor, and a leucotoxin that kills neutrophils and so dampens the host's first line of defence against bacterial challenge. About 70% of patients have defects in neutrophil chemotaxis and phagocytosis. The chemotactic defect is linked to reduced amounts of cell-surface glycoproteins and is transmitted as a dominant trait. About 50% of siblings of patients who have both aggressive periodontitis and chemotactic defects, also demonstrate impaired neutrophil function. Treatment.A combined regimen of regular scaling and root planing with a 2-week course of systemic tetracycline therapy (250 mg, four times daily) has been used extensively in the management of this condition. A. actinomycetemcomitans is sensitive to tetracycline, which also has the ability to be concentrated up to 10 times in gingival crevicular fluid when compared with serum. More recently, a combination of metronidazole (250 mg) and amoxicillin (amoxycillin) (375 mg), three times a day for 1 week, in association with subgingival scaling, has also been found to be effective. Amore radical approach is to undertake flap surgery so that better access is achieved for root cleaning, and the superficial, infected connective tissues are excised. An antimicrobial regimen can also be implemented in conjunction with a surgical approach.

Key Points

Permanent dentition (juvenile periodontitis)⎯treatment:

• plaque control;

• mechanical debridement;

• systemic antimicrobials;

• periodontal surgery. 634H

Fig. 11.12 (a) Clinical appearance of a 13-year-old girl with localized aggressive periodontitis. (b) Radiographic appearance of vertical bone loss on the mesial aspect of 6|. (Reproduced by kind permission of Mr D. G. Smith, Consultant in Restorative Dentistry, Newcastle upon Tyne). 635H

Fig. 11.13 Radiographic view of |7 that has erupted and tipped mesially into the |6 extraction site. The contour of the bone crest on the mesial of |7 gives the impression of a vertical bony defect. 636H

Fig. 11.14 Aggressive periodontitis with generalized bone loss in a 16-year-old male.

11.11.3 Genetic factors and aggressive diseases

The increased prevalence of aggressive periodontitis in certain ethnic groups and within families strongly suggests that susceptibility to these diseases may be influenced by a number of genetic determinants. Furthermore, genetic factors are implicated in the pathogenesis of the diseases as many affected patients have functionally defective neutrophils. The mode of transmission has not been determined unequivocally. The apparent  increased incidence in females suggests an X-linked dominant mode of inheritance with reduced penetrance. The association with females, however, may reflect epidemiological bias as females are more likely to seek dental attention. Large family studies of subjects with aggressive periodontitis suggest an autosomal-recessive pattern of inheritance. The role of hereditary components in periodontal diseases has been supported by the link with specific tissue markers. The major histocompatibility complex (MHC) determines the susceptibility of subjects to certain diseases. Class I and II genes in the MHC encode for specific human leucocyte antigens (HLA I and II), which account for individual variation in immunoresponsiveness. There are clear associations between HLA serotypes and diabetes mellitus and rheumatoid arthritis. A strong link between an HLA serotype and aggressive diseases has still to be determined, although a mild association between the HLA-A9 antigen and aggressive periodontitis has been found.

Genetic components of periodontitis:

• family associations;

• ethnic associations;

• major histocompatibility complex link;• link with syndromes.

PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DISEASE

Introduction

The genetic basis for aggressive periodontitis in particular is substantiated by the definite association between the condition and a number of rare inherited medical conditions and syndromes (637HTable 11.1). The pattern of inheritance reflects a single gene disorder, commonly involving inherited defects of neutrophils, enzyme reactions, or collagen synthesis.

Papillon-Lefevre syndrome (PLS)

This syndrome is characterized by palmar-plantar hyperkeratosis, premature loss of primary and permanent dentitions, and ectopic calcifications of the falx cerebri. Some patients show an increased susceptibility to infection. The syndrome is an autosomalrecessive trait with a prevalence of about 1-4 per million of the population. Consanguinity of parents is evident in about one-third of cases. Rapid and progressive periodontal destruction affects the primary dentition with an onset at about 2 years. Exfoliation of all primary teeth is usual before the permanent successors erupt and patients may be edentulous by the mid to late teens. Cases of a late-onset variant of PLS have also been described in which the palmarplantar and periodontal lesions are relatively mild and only become evident in the permanent dentition. An extensive family dental history supported by clinical, laboratory, and radiographic examinations confirms the diagnosis.