Global burden of oral diseases: emerging concepts, management and interplay with systemic health.

OBJECTIVES: This study presents the global burden of major oral diseases with an exegetical commentary on their current profiles, the critical issues in oral healthcare and future perspectives. METHODS: A narrative overview of current literature was undertaken to synthesise the contexts with critical elaboration and commentary. RESULTS: Oral disease is one of the most common public health issues worldwide with significant socio-economic impacts, and yet it is frequently neglected in public health policy. The oral data extracted from the Global Burden of Disease Study in 2010 (Murray et al, 2012) show that caries, periodontal disease, edentulism, oral cancer and cleft lip/palate collectively accounted for 18 814 000 disability-adjusted life-years; and the global burden of periodontal disease, oral cancer and caries increased markedly by an average of 45.6% from 1990 to 2010 in parallel with the major non-communicable diseases like diabetes by 69.0%. Oral diseases and non-communicable diseases are closely interlinked through sharing common risk factors (e.g. excess sugar consumption and tobacco use) and underlying infection/inflammatory pathways. CONCLUSIONS: Oral disease remains a major public health burden worldwide. It is of great importance to integrate oral health into global health agenda via the common risk factor approach. The long-term sustainable strategy for global oral health should focus on health promotion and disease prevention through effective multidisciplinary teamwork.

Dental Services and Health Outcomes in the New York State Medicaid Program.

Previous reports suggest that periodontal treatment is associated with improved health care outcomes and reduced costs. Using data from the New York State Medicaid program, rates of emergency department (ED) use and inpatient admissions (IPs), as well as costs for ED, IPs, pharmacy, and total health care, were studied to determine the association of preventive dental care to health care outcomes. Utilization of dental services in the first 2 y (July 2012-June 2014) was compared to health care outcomes in the final year (July 2014-June 2015). Costs and utilization for members who did not receive dental services (No Dental) were compared to those who received any dental care (Any Dental), any preventive dental care (PDC), PDC without an extraction and/or endodontic treatment (PDC without Ext/Endo), PDC with an Ext/Endo (PDC with Ext/Endo), or Ext/Endo without PDC (Ext/Endo without PDC). Propensity scores were used to adjust for potential confounders. After adjustment, ED rate ratios were significantly lower for PDC and PDC without Ext/Endo but higher for the Any Dental and Ext/Endo without PDC. IP ratios were lower for all treatment groups except Ext/Endo without PDC. ED costs differed little compared to the No Dental group except for Ext/Endo without PDC. For IPs, costs per member were significantly lower for all groups (-$262.91 [95% confidence interval (CI), -325.40 to -200.42] to -$379.82 [95% CI, -451.27 to -308.37]) except for Ext/Endo without PDC. For total health care costs, Ext/Endo without PDC had a significantly greater total health care cost ($530.50 [95% CI, 156.99-904.01]). Each additional PDC visit was associated with a 3% reduction in the relative risk for ED and 9% reduction for IPs. Costs also decreased for total health care (-$235.64 [95% CI, -299.95 to -171.33]) and IP (-$181.39 [95% CI, -208.73 to -154.05]). In conclusion, an association between PDC and improved health care outcomes was observed, with the opposite association for Ext/Endo without PDC.

Screening for Diabetes Risk Using Integrated Dental and Medical Electronic Health Record Data.

Undiagnosed diabetes and prediabetes present a serious public health challenge. We previously reported that data available in the dental setting can serve as a tool for early dysglycemia identification in a primarily Hispanic, urban population. In the present study, we sought to determine how the identification approach can be recalibrated to detect diabetes or prediabetes in a White, rural cohort and whether an integrated dental-medical electronic health record (iEHR) offers further value to the process. We analyzed iEHR data from the Marshfield Clinic, a health system providing care in rural Wisconsin, for dental patients who were ≥21 y of age, reported that they had never been told they had diabetes, had an initial periodontal examination of at least 2 quadrants, and had a glycemic assessment within 3 mo of that examination. We then assessed the performance of multiple predictive models for prediabetes/diabetes. The study outcome, glycemic status, was gleaned from the medical module of the iEHR based on American Diabetes Association blood test cutoffs. The sample size was 4,560 individuals. Multivariate logistic regression revealed that the best performance was achieved by a model that took advantage of the iEHR. Predictors included age, sex, race, ethnicity, number of missing teeth, percentage of teeth with at least 1 pocket ≥5 mm from the dental EHR, and overweight/obesity, hypertension, hyperlipidemia, and smoking status from the medical EHR. The model achieved an area under the receiver operating characteristic curve of 0.71 (95% confidence interval, 0.69-0.72), yielding a sensitivity of 0.70 and a specificity of 0.62. Across a range of populations, informed by certain patient characteristics, dental care team members can play a role in helping to identify dental patients with undiagnosed diabetes or prediabetes. The accuracy of the prediction increases when dental findings are combined with information from the medical EHR. Knowledge Transfer Statement: Prediabetes and diabetes often go undiagnosed for many years. Early identification and care can lead to improved glycemic outcomes and prevent wide-ranging morbidity, including adverse oral health consequences, in affected individuals. Information available in the dental office can be used by clinicians to identify those who remain undiagnosed or are at risk; the accuracy of this prediction increases when combined with information from the medical electronic health record.

Blockade of RAGE suppresses periodontitis-associated bone loss in diabetic mice.

Diabetes is associated with increased prevalence, severity, and progression of periodontal disease. To test the hypothesis that activation of RAGE (Receptor for Advanced Glycation End products) contributes to the pathogenesis of diabetes-associated periodontitis, we treated diabetic mice, infected with the human periodontal pathogen Porphyromonas gingivalis, with soluble RAGE (sRAGE). sRAGE is the extracellular domain of the receptor, which binds ligand and blocks interaction with, and activation of, cell-surface RAGE. Blockade of RAGE diminished alveolar bone loss in a dose-dependent manner. Moreover, we noted decreased generation of the proinflammatory cytokines TNF-alpha and IL-6 in gingival tissue, as well as decreased levels of matrix metalloproteinases. Gingival AGEs were also reduced in mice treated with sRAGE, paralleling the observed suppression in alveolar bone loss. These findings link RAGE and exaggerated inflammatory responses to the pathogenesis of destructive periodontal disease in diabetes.

Modification of in vitro and in vivo immune function by acute inflammatory cells.

The ability of adoptively transferred, syngeneic polymorphonuclear leukocyte-rich (PMNLr) inflammatory cells to influence lymphocyte-mediated cytotoxicity (LMC), complement-dependent cytotoxicity (CDC), and skin allograft survival was studied in a murine model. BALB/c mouse PMNLr, stimulated by i.p. injection of either glycogen (G/PMNLr) or thioglycollate (T/PMNLr), were transferred to other BALB/c mice at the time of primary or secondary immunization with a cellular alloantigen (C57BL/6 spleen cells) or after skin allografting (C57BL/6 tailskin). The metabolic activity of each PMNLr population was determined by measuring glucose utilization in the hexose monophosphate shunt. It appeared that metabolic activity of the T/PMNLr was significantly greater than that of the G/PMNLr. Our results indicate that, while the infusion of G/PMNLr tended to suppress the primary cell-mediated immune response and the secondary humoral immune response, the infusion of T/PMNLr stimulated both of these responses. Furthermore, i.p. infusion of mice with G/PMNLr at a time approximating grafting resulted in prolonged graft survival, but neither T/PMNLr nor syngeneic thymocytes effect graft survival. Our data demonstrate that both cellular and humoral immunity can be modified by acute inflammatory cells. The metabolic status of the acute inflammatory cells seems to be critical in determining their immunoregulatory potential.

Analysis of multiple 2x2 tables with site-specific periodontal data.

Periodontal data typically consist of observations made at multiple sites within each patient. Observations within a patient tend to be positively correlated; hence, standard statistical techniques that assume independence are invalid. Regression techniques for correlated data have been proposed; communicating results from these models, however, is difficult, due to their inherent complexity. Simpler statistical approaches have also been proposed, but many of these methods can be applied only when covariates are specific to the subject, and do not vary from site to site within a subject. In this paper, we present two methods for the analysis of multiple 2x2 tables containing site-specific periodontal data. The methods presented are modifications of the well-known Mantel-Haenszel methods. We illustrate these methods using a subset of data from a clinical trial examining the effects of scaling and root planing on levels of interleukin-1 beta.

Endorphinergic modulation of immune function: potent action of the dipeptide glycyl-L-glutamine.

Glycyl-L-glutamine (GLG), the carboxy terminal dipeptide of B-endorphin, inhibits brainstem neuronal activity. It also occurs along with B-endorphin in pituitary secretory vesicles suggesting a neurosecretory role for this dipeptide. We have evaluated potential immunoregulatory actions of this compound using the Phytohemaglutinin (PHA) blastogenesis and the concanavalin A (ConA) suppressor cell induction assays. GLG in low doses (10(-12) M) enhanced the response of human lymphocytes to PHA induced blastogenesis, however; with higher doses of the dipeptide (10(-7) M) immunosuppression was consistently observed. In the suppressor cell induction assay, when GLG was used together with ConA, we observed a dose-dependent inhibition of suppressor activity. These results clearly indicate that GLG produces a dose dependent bidirectional modulation of at least two indicies of immune function, and confirm the presence of a second pituitary peptide with the potential for potent immunomodulatory action.

Beta-endorphin modulates human immune activity via non-opiate receptor mechanisms.

Here we report that Beta-endorphin is a potent and efficacious suppressor of phytohemagglutinin induced T-lymphocyte blastogenesis when human leukocytes are exposed early in the course of mitogenic activation. This suppression becomes more difficult to observe, however, if blastogenesis is established by prior exposure to mitogen. Suppression by Beta-endorphin is not blocked by pretreatment with the opiate antagonist naloxone. These results, therefore, suggest that neuroendocrine modulation of human immune expression may be a peripheral physiological function of Beta-endorphin which is mediated by mechanisms distinct from traditional opiate receptors.

The accurate diagnosis of oral lesions in human immunodeficiency virus infection. Impact on medical staging.

OBJECTIVE: To compare identification of oral candidiasis (OC) and oral hairy leukoplakia (OHL) by medical examiners and oral/dental examiners and to assess the impact of these diagnoses on the medical staging of the human immunodeficiency virus (HIV). DESIGN: Retrospective analysis of data collected by medical and oral/dental examiners at the baseline examination of a prospective study. SETTING: Homosexual men and men and women who were parenteral drug users residing in New York City, enrolled in a longitudinal cohort study. SUBJECTS: A total of 245 individuals participated in this study. MAIN OUTCOME MEASURES: The diagnoses of OC and OHL as recorded in the medical and oral/dental charts were analyzed retrospectively for the same medical and oral/dental evaluation visits. The medical staging of HIV infection based on that evaluation was analyzed concomitantly. RESULTS: Among homosexual men, the oral/dental examiners diagnosed OC in 11% of the individuals and the medical examiners in 4%. In the same cohort, OHL was diagnosed by the oral/dental examiners in 14% of the individuals and by the medical examiners in 8%. Among the parenteral drug users the oral/dental examiners diagnosed OC in 29% of the individuals while the medical examiners made this diagnosis in 11%. In the same cohort, OHL was diagnosed by the oral/dental examiners in 9% of the individuals and by the medical examiners in 2%. The OC and OHL diagnoses affected the medical staging of 12% of the HIV-positive homosexual men and of 22% of the HIV-positive parenteral drug users. Forty percent of the HIV-positive homosexual men and 79% of the HIV-positive parenteral drug users with stage-defining oral lesions were not properly identified by the medical examiners. CONCLUSIONS: Specific training and a comprehensive oral examination have a significant impact on the diagnoses of OC and OHL, and on the medical staging of individuals with HIV infection.

Effects of supernatants of polymorphonuclear neutrophils recruited by different inflammatory substances on mitogen responses of lymphocytes.

Two different substances, glycogen and thioglycollate, were used to recruit early peritoneal exudate cells (4h). In the acute phase of the inflammatory response the cellular infiltrate is large, and the predominant cell (greater than 95%) is the polymorphonuclear neutrophil. Supernatant had differing effects on lymphocyte responses to the mitogens PHA and LPS, also carried out in serum-free media, depending on recruiting substance and time of culture. While glycogen-recruited PMN supernatant (GPMN-S) always enhanced splenocyte responses to PHA, thioglycollate-recruited cells (TPMN-S) did not produce an enhancing factor until the cells had been in culture for 24 h. Whereas GPMN-S enhanced the splenocyte response to LPS only after 1 or 4 h of culture, TPMN-S failed to have any significant effect. Thymocyte responses to PHA were facilitated by all supernatants. Dilution of the soluble PMN factors resulted in a suppressive effect on splenocyte responses to both PHA and LPS, regardless of whether PMN were recruited by the thioglycollate or glycogen or of the time of cell incubation. These results indicate that PMN-rich cell populations of different types of activity are recruited by glycogen and thioglycollate and that these cells produce factors capable of potentiating, enhancing, or suppressing responses to T- or B-cell mitogens by normal syngeneic lymphocytes.

The host response in gingival crevicular fluid: potential applications in periodontitis clinical trials.

Traditional clinical variables of periodontal pathology have only limited value as indicators for future disease progression in patients with adult periodontitis. Consequently, other aspects of the periodontal lesion are being examined for their diagnostic utility. Analysis of the host response in gingival crevicular fluid (GCF) is among the most intensely studied of these new diagnostic approaches. Specific indicators of the humoral immune response, cellular immune response, and acute inflammatory response have been identified in GCF. The relationship of indicators of the humoral immune response to active periodontal disease is equivocal. Specific indicators of the cellular immune response in GCF may ultimately prove to be important diagnostically, but the relationship of any specific marker to active periodontal disease has not been reported. In contrast, the acute inflammatory response in GCF has been extensively studied and a number of factors appear to be associated with an increased risk for future disease progression. Indicators of enhanced polymorphonuclear leukocyte activity, (lysosomal beta-glucuronidase, lysosomal collagenase), prostaglandin E2, and an indicator of acute tissue destruction (the cytoplasmic enzymes aspartate aminotransferase) have been associated with the occurrence of clinical attachment loss. An example of the application of a GCF marker in a periodontitis clinical trial is provided by describing the relationship of lysosomal beta-glucuronidase in GCF at baseline and 2 weeks following root planing and scaling to the occurrence of disease activity during the following 6 months. Persistently elevated levels of this enzyme were related to clinical attachment loss. The positive, negative, and total predictive values for beta-glucuronidase as an identifier of clinical attachment loss were 86%, 71%, and 76%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Risk indicators for future clinical attachment loss in adult periodontitis. Tooth and site variables.

In an earlier report, we examined the relationship of patient-derived clinical and epidemiological variables to the risk for future clinical attachment loss (CAL) in chronic adult periodontitis. We determined that the extent of the patient's existing periodontal disease as measured by mean attachment loss (MAL) and the patient's age were the most important patient-derived risk indicators for CAL among those factors evaluated. In this study, we examined the tooth and site variables that were associated with CAL. Seventy-five patients with chronic adult periodontitis were followed for 6 months. Clinical data at baseline, including attachment level and probing depth, were obtained from six sites per tooth. The hazard rate for CAL at all sites was 2.0%, and 4.1% of teeth displayed at least one site with CAL. Mandibular and maxillary molars and maxillary premolars displayed the highest incidence of CAL (6.1%, 5.6%, 5.5%, respectively), while maxillary anterior teeth (1.8%) and mandibular premolar teeth (2.1%) demonstrated the lowest incidence. The greatest number of sites demonstrating CAL had an existing attachment level of 4 to 7 mm and a probing depth of less than or equal to 5 mm. When the data were converted to hazard rates, however, an increase in hazard rate was seen with increasing existing attachment loss or probing depth. When MAL was considered, patients with mild and moderate periodontitis demonstrated a relatively low incidence of CAL at sites with less than or equal to 7 mm of existing attachment loss. Patients with severe periodontitis exhibited greater hazard rates for sites with 0 to 3, 4 to 5 and 6 to 7 mm of existing attachment loss.(ABSTRACT TRUNCATED AT 250 WORDS)

Inflammatory and immune mediators in crevicular fluid from HIV-infected injecting drug users.

Gingival crevicular fluid (GCF) levels of the polymorphonuclear leukocyte (PMN) lysosomal enzyme beta-glucuronidase (beta G), the pro-inflammatory cytokine interleukin 1 beta (IL-1 beta), and immunoglobulins (IgA, IgG, and IgM) were examined in 16 HIV seropositive (HIV+) and 10 HIV seronegative (HIV-) injecting drug users (IDU). Each subject received a periodontal examination including assessment of probing depth, attachment level, bleeding on probing, and plaque and calculus accumulation. GCF was collected from the mesial surfaces of premolar and molar teeth using filter paper strips. Although HIV+ subjects had a significantly lower number of peripheral blood CD4+ T cells/mm3 compared to HIV- subjects, there were no significant differences in mean probing depth, percentage of sites exhibiting bleeding on probing, or plaque and calculus accumulation between HIV- and HIV+ subjects. When the GCF components were analyzed, we found no significant differences between HIV- and HIV+ subjects in GCF levels of beta G, IL-1 beta, IgA or IgM, but GCF levels of IgG were significantly increased in HIV+ subjects. When sites were categorized by probing depth, no differences in the levels of beta G, IgA, IgG, and IgM existed between sites with probing depth < or = 3 mm compared to sites with probing depth > or = 4 mm in both HIV- and HIV+ IDU. However, levels of IL-1 beta in GCF were increased in the deeper sites (> or = 4 mm) in HIV+ IDU when compared to sites with PD < or = 3 mm. Analyzing GCF constituents in relation to the CD4 cell number, no differences were found between subjects with < or = 400 or > 400 CD4 cells/mm3 with respect to the levels of IL-1 beta, IgG, and IgM. However, the level beta G was significantly decreased in the HIV+ IDU with < or = 400 CD4 cells when compared to those with > 400 CD4 cells/mm3, while levels of IgA were significantly higher in HIV+ subjects with < or = 400 CD4 cells/mm3. Our results suggest that levels of IgG, and in immunodeficient subjects IgA were increased in GCF of HIV+ IDU while decreased levels of beta G were found in immunodeficient HIV+ IDU. These findings may be local manifestations of systemic alterations and suggest that analysis of GCF may provide insight into the immune and inflammatory responses of HIV-infected individuals to periodontal microorganisms.

Development of a biochemical profile for gingival crevicular fluid. Methodological considerations and evaluation of collagen-degrading and ground substance-degrading enzyme activity during experimental gingivitis.

The potential application of gingival crevicular fluid (GCF) analysis to periodontal diagnosis has been examined for more than 25 years. Unfortunately, the information available has not provided the clinician with a more sensitive means of diagnosing periodontal disease or an effective means of monitoring periodontal therapy. A careful review of the literature on GCF, however, suggests that discrepancies occur in the method of GCF collection, the use of GCF for analysis from pooled or isolated crevicular locations, the method of analyzing the samples and the way in which the data is reported. Studies in our laboratory have suggested a technique for GCF analysis that collects GCF from individual crevices with a filter paper strip inserted for a standard time, determines the volume of GCF collected with a calibrated electronic meter and elutes the material into a larger volume of diluent. This approach allows for detection of site-to-site and patient-to-patient differences in GCF volume while providing sufficient samples to analyze GCF for multiple constituents. We have used this approach to evaluate GCF for vertebrate forms of the enzymes collagenase (latent and active forms), beta-glucuronidase and arylsulfatase during the development of experimental gingivitis in man. Interproximal and midradicular areas were studied. Our results indicate that during the 4 weeks of the gingivitis, the absolute amount of active collagenase in GCF increased 550% at the interproximal sites and 190% in the midradicular sites, and the per cent of active collagenase increased from 15 to 71% at the interproximal sites, and from 16 to 36% at the midradicular sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Infantile agranulocytosis with survival into adolescence: periodontal manifestations and laboratory findings. A case report.

A case of infantile agranulocytosis with survival into adolescence is presented. The polymorphonuclear leukocyte is considered an important source of lysosomal enzymes in gingival crevicular fluid, and evaluation of connective tissue-degrading enzymes in the fluid was performed. The activity of beta-glucuronidase, a ground substance-degrading enzyme that may serve as a marker for polymorphonuclear leukocytes, was markedly reduced in the fluid compared to samples from systemically healthy adults with periodontitis. The activities of the ground substance-degrading enzyme arylsulfatase, and collagenase, were in the low-normal range. The plaque microbiology, as characterized by dark-field microscopy and selective culturing, was consistent with advanced periodontitis. A review of the medical history revealed a series of bacterial infections since infancy. Improvement in the systemic health of the patient occurred at about the age of 15, and the intake of antibiotics to control infections was correspondingly reduced after this time. An exacerbation of the patient's periodontal disease, as evaluated by loss of alveolar bone on radiographs, occurred 1 to 2 years later. The progression of periodontal disease observed in this patient was apparently associated with the withdrawal of antibiotics administered for control of systemic (nonoral) infections.

Immunoglobulin isotypes in gingival crevicular fluid: possible protective role of IgA.

In order to simultaneously assess the local humoral immune and polymorphonuclear leukocyte (PMN) responses in periodontal disease, IgG, IgM, and IgA, as well as the PMN lysosomal enzyme beta-glucuronidase (beta G), were examined in gingival crevicular fluid (GCF) from patients with varying degrees of periodontal pathology. Evaluations were made before and after conservative therapy (scaling and root planing). Thirty patients with varying degrees of periodontal pathology, ranging from mild inflammatory gingivitis to moderate periodontitis, were studied. GCF was collected from the mesial surfaces of all teeth. The presence of the 3 immunoglobulin isotypes was determined by enzyme linked immunosorbent assays (ELISA), while total beta G activity in GCF was determined by a fluorometric assay. Clinical parameters were obtained from 6 sites per tooth. Our data indicate that prior to treatment, total beta G activity is strongly related to the severity of periodontal disease as measured by mean probing attachment level (AL; r = 0.89; P < .005), mean probing depth (PD; 4 = 0.89; P < .0005) and percentage of sites exhibiting bleeding on probing (% BOP; r = 0.49; P < .005). Following treatment, no statistically significant relationship of disease severity and beta G is found. The concentrations of IgG and IgM in GCF do not follow a specific pattern when related to disease severity. In contrast, prior to treatment the concentration of IgA is negatively correlated to mean AL (r = -0.54; P < .005), mean PD (r = -0.59; P < .005), and % BOP (r = -0.47, P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid loss of alveolar bone associated with nonprecious alloy crowns in two patients with nickel hypersensitivity.

In recent years there has been a dramatic increase in the use of nonprecious alloy and porcelain crowns in clinical dentistry. The alloy in these restorations frequently contains a high percentage (greater than 70%) of nickel. Most cases of metal hypersensitivity are related to nickel, and clinical manifestations of the hypersensitivity are the result of a cellular (T lymphocyte) immune response. In this report, we review the cases of two women who demonstrated significant loss of alveolar bone about nickel-rich nonprecious alloy and porcelain crowns. The loss of alveolar bone occurred within 18 months after placement of the restorations. Both individuals displayed a positive patch test to a nickel preparation. These findings suggest that a Type IV hypersensitivity reaction may have accounted for the rapid loss of alveolar bone. Though the majority of individuals treated with nonprecious alloy and porcelain crowns apparently tolerate these restorations quite well, greater care is urged in case selection.

Development of a risk profile for periodontal disease: microbial and host response factors.

Advances in our understanding of the relationship between the microbial challenge and the host response in periodontal disease have led to the search for pathogenesis-based risk indicators or risk factors for disease progression. This evaluation is based on analysis of non-invasive or minimally invasive samples that allow measurement of the subgingival plaque microflora or the host response in gingival crevicular fluid (GCF), serum, or saliva. Studies conducted by us have indicated that in GCF, persistently elevated levels of beta-glucuronidase (beta G, a marker for primary granule release from polymorphonuclear leukocytes) are associated with clinical attachment loss in patients with periodontitis. This finding has been confirmed in a multicenter trial. We have also observed that a statistically significant positive correlation exists between beta G in GCF and measures of the subgingival microbial challenge, but the correlation was less than 0.5, suggesting variations in the host response to the challenge. Furthermore, beta G levels in GCF were inversely correlated with the IgG serum antibody titer to a panel of periodontal pathogens, suggesting the essentially protective function of the systemic humoral response in periodontal disease. Data in the literature support this concept. In addition, recent studies of the relationship of antibody isotypes in GCF to progression of clinical attachment loss have suggested that IgA in GCF has a protective function. This may relate to the lack of complement activation by IgA. Alternately, the development of IgA antigen-specific responses are T-cell dependent, and reductions in local levels of IgA may indicate a decrease in T-helper cell function. These data have allowed development of strategies for identifying individual risk profiles for patients with periodontal disease based on the host response to the microbial challenge. With identification of these risk indicators/risk factors for active periodontal disease, the next challenge is to provide clinicians with access to the tests and analyses that are required for this approach to periodontal diagnosis. Improved patient management should result from the incorporation of these tests into clinical practice.

Risk indicators for future clinical attachment loss in adult periodontitis. Patient variables.

We studied patient-derived variables to identify individuals at risk for future clinical attachment loss (CAL). Seventy-five patients with chronic adult periodontitis were followed for 6 months and clinical and epidemiological parameters collected at baseline were related to CAL. Clinical parameters were obtained from 6 sites per tooth and whole-mouth averages were calculated. Epidemiologic parameters were obtained by questionnaire and interview. After the baseline examination, patients were treated with root planing and scaling. Thirty-one patients (41.3%) demonstrated greater than or equal to 1 site with CAL of greater than or equal to 2.5 mm, while 16 patients (21.3%) demonstrated CAL at greater than or equal to 2 sites. Epidemiological factors such as gender, health status, marital status, education, and occupation were not associated with CAL. In contrast, baseline mean attachment level, age, baseline mean probing depth, baseline mean recession, percentage of sites exhibiting bleeding on probing, and the number of missing teeth were related to CAL. Using logistic modelling, we found that baseline attachment level was the primary risk indicator for post-treatment CAL. Nineteen percent of the patients with baseline attachment levels less than 4.0 mm, 50% of the patients with 4.0 to 4.9 mm, and 85% (P less than .005) of the patients with greater than or equal to 5.0 mm exhibited CAL. The age of the patient was also a major risk indicator for CAL, and was independent of baseline attachment levels. Eighty-nine percent of the 60 to 69 year old patients demonstrated CAL, compared to only 35% of patients between the ages of 30 and 59 (P less than or equal to .005).(ABSTRACT TRUNCATED AT 250 WORDS)

An analysis of peripheral blood and salivary polymorphonuclear leukocyte function, circulating immune complex levels and oral status in patients with inflammatory bowel disease.

In an earlier case report, we described a 28-year-old man with active Crohn's disease and rapidly progressive alveolar bone loss, who presented with enhanced peripheral blood polymorphonuclear leukocyte activity as assessed by phagocytosis and lysis of a target bacterium. To assess the significance of this finding, peripheral blood polymorphonuclear leukocytes (PMN) from thirty patients with active or inactive inflammatory bowel disease (IBD) were examined for spontaneous and stimulated hexose monophosphate shunt (HMS) activity. Analysis revealed the PMN from active IBD patients displayed greater metabolic activity than PMN from inactive IBD patients, which in turn were more active than PMN from normal subjects. Since circulating immune complex (CIC) levels might be of importance in the in vivo activation of PMN, analysis of serum CIC levels via polyethylene glycol 6000 precipitation was carried out. This indicated that active IBD patients had higher levels of CIC activity then inactive IBD patients. Ten of these patients were evaluated for spontaneous HMS activity by salivary PMN. As compared to controls, comparable numbers of salivary PMN from IBD patients displayed an average of 45% less activity than control salivary PMN. Analysis of the oral status of 10 IBD patients referred to the Peter Bent Brigham Dental Clinic indicated that two patients had overt oral pathoses apparently attributable to IBD. These two patients also had the highest CIC levels observed in the 30 serum samples tested.