One-year follow-up of the immune profile in serum and selected sites of generalized and localized aggressive periodontitis.

BACKGROUND: The local and systemic immunological profiles of important inflammatory mediators in the localized (LAgP) and generalized (GAgP) forms of aggressive periodontitis are still unknown, as well as the effect of periodontal therapy on these parameters. The aim of this prospective study was to evaluate clinical and immune responses of patients with AgP undergoing nonsurgical treatment. MATERIAL AND METHODS: Eighteen patients with GAgP, 10 with LAgP and 10 healthy participants were included in this study. AgP participants were submitted to scaling and root planing plus systemic antibiotics (amoxicillin and metronidazole). At baseline and 1-year follow-up were measured clinical parameters, such as probing depth [PD] and clinical attachment loss [CAL], and the levels of 10 immunological mediators (GM-CSF, M-CSF, MCP-1, ICAM-1, CXCL8, IL-1ß, TNF-α, IL-17, IL-4, and IL-10) in the gingival crevicular fluid (GCF) of selected sites [AgP forms: PD ≥ 6 mm or the deepest, bleeding on probing (BoP) and bone loss measured by periapical radiography; healthy individuals: PD ≤ 3 mm, no BoP, no bone loss] and serum. RESULTS: After periodontal treatment both forms of AgP presented a significant reduction of PD and CAL, an increase of GM-CSF, ICAM-1, MCP-1, TNF-α, IL-17, IL-4, and IL-10 in the GCF, as well as of GM-CSF and IL-4 in the serum, and a reduction in the serum concentration of IL-1ß. Serum levels of M-CSF, ICAM-1, and MCP-1 remained significantly below those found in healthy individuals in both forms of AgP even after therapy. An increase in the systemic or local levels of MCP-1, ICAM-1 and the anti-inflammatory profile (IL-4, IL-10) was correlated with an improvement in clinical parameters of LAgP patients. Also, a local reduction of IL-1ß levels in both forms of AgP was correlated with an increase in the clinical attachment gain. CONCLUSION: Nonsurgical periodontal therapy was successful in improving clinical parameters and modulating the immune response in both forms of AgP. However, this therapeutic approach does not seem to affect the deficient level of important serum mediators involved in mechanisms of cell transmigration.

Local IL-10 level as a predictive factor in generalized aggressive periodontitis treatment response.

Generalized aggressive periodontitis (GAgP) presents a reduced response to non-surgical therapy. However, it is not clear if the initial clinical, microbiological or immunological characteristics are impacting the worse response to treatment. This study aimed to identify the predictive value of clinical, microbiological and immunological patterns on the clinical response to therapy in GAgP patients. Twenty-four GAgP patients were selected, and gingival crevicular fluid (GCF) and subgingival biofilm were collected. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia levels were evaluated by qPCR, and IL-1ß and IL-10 concentration by ELISA. Twelve patients were treated with SRP (scaling and root planning), and twelve with SRP plus 375 mg amoxicillin and 250 mg metronidazole (8/8 hours, 7 days) (SRP + AM). The clinical changes (Probing Pocket Depth [PPD] reduction and Clinical Attachment Level [CAL] gain) 6 months post-treatment were correlated to the initial clinical, inflammatory and microbiological variables using stepwise logistic regression (α = 5%). CAL gain at 6 months was 1.16 ± 0.77 for SRP and 1.74 ± 0.57 mm for SRP + AM (P > .05). PPD reduction was 1.96 ± 0.82 for SRP and 2.45 ± 0.77 mm for SRP + AM (P < .05). In the SRP group, IL-10 showed a predictive value for clinical response. The higher the IL-10 concentration at baseline, the higher the reduction in PPD at 6 months (P = .01, r = .68). However, when antimicrobials were administered, no significant influence was detected (P > .05). It can be concluded that the IL-10 levels in GFC act as a predictor of clinical response to GAgP. Moreover, the intake of antimicrobials appears to overlap the influence of the inflammatory response on clinical response to treatment. Clinical trial registration number: NCT03933501.

Assessment of microRNA-146a in generalized aggressive periodontitis and its association with disease severity.

BACKGROUND AND OBJECTIVE: MicroRNA-146a (miR-146a) is a small noncoding RNA that plays a critical role in the negative regulation of the innate immune response, and the dysregulation of miR-146a has been associated with several inflammatory disorders. In generalized aggressive periodontitis (GAgP) the degree of clinical inflammation appears to be similar to that of chronic periodontitis, and, in this situation, age of onset and family history are important additional criteria for diagnosis. This study was performed to evaluate the level of miR-146a expressed in gingival tissues of patients with GAgP and its association with disease severity. MATERIAL AND METHODS: Gingival samples from 18 patients with GAgP and 10 healthy subjects were collected and the level of miR-146a and its targets, including necrosis factor-alpha, interleukin-1beta, and interleukin-6, were assessed using real-time PCR. Clinical parameters, including probing depth and clinical attachment loss, were measured and their correlations with the level of miR-146a were determined. RESULTS: Our results demonstrated an elevation in the level of miR-146a expressed in patients with GAgP compared with healthy controls (P < .001), which was directly associated with disease severity (P < .05). Overexpression of miR-146a was accompanied by a reduction in the levels of pro-inflammatory cytokines. CONCLUSIONS: Our findings suggest that there is an association between miR-146a and GAgP and imply that miR-146a may serve as an indicator of periodontal disease severity. However, further studies and additional information are required to confirm this relationship and the precise role of miR-146a in the development and/or progression of periodontitis.

Analysis of metabolic profiles of generalized aggressive periodontitis.

BACKGROUND AND OBJECTIVE: The specific pathogenesis of generalized aggressive periodontitis (GAgP) has not yet been clarified, and few studies have focused on the association between GAgP and metabolomics. To elucidate the roles of metabolic profiles in the status of GAgP, this study aimed to identify the differential metabolic profiles between patients with GAgP and healthy controls using an untargeted metabolomic profiling method. MATERIAL AND METHODS: Serum and gingival crevicular fluid samples were collected from healthy controls (n = 20) and patients with GAgP (n = 20) in this cross-sectional study. The relative levels of biomarkers in the samples were measured by gas chromatography-mass spectrometry. Principal components analysis and orthogonal partial least-squares discriminant analysis were used for statistical analysis. Metabolites were analysed qualitatively using the FiehnLib and NIST databases. Full-mouth probing depth and clinical attachment loss were recorded as indexes of periodontal disease. RESULTS: A total of 349 metabolites were qualitatively detected in the gingival crevicular fluid samples, and 200 metabolites were detected in the serum samples. Compared with healthy controls, patients with GAgP showed significant increases in serum urea and allo-inositol levels. In contrast, glutathione, 2,5-dihydroxybenzaldehyde, adipic acid and 2-deoxyguanosine levels were decreased in patients with GAgP. In the gingival crevicular fluid samples, noradrenaline, uridine, α-tocopherol, dehydroascorbic acid, xanthine, galactose, glucose-1-phosphate and ribulose-5-phosphate levels were increased in patients with GAgP, while thymidine, glutathione and ribose-5-phosphate levels were decreased. CONCLUSION: The metabolomics analysis by gas chromatography-mass spectrometry is an effective and minimally non-invasive way to differentiate the metabolites characteristic of patients with GAgP. Both serum and gingival crevicular fluid metabolomics are significantly different between patients with GAgP and healthy controls. These metabolic profiles have great potential in detecting GAgP and helping to understand its underlying mechanisms.

Moderate- to long-term therapeutic outcomes of treated aggressive periodontitis patients without regular supportive care.

BACKGROUND AND OBJECTIVE: Risk for deterioration in treated aggressive periodontitis (AgP) individuals remained unclear. This retrospective cohort study investigated 7-26 years of periodontal outcomes and oral health-related quality of life (OHRQoL) of young adults with advanced periodontitis. MATERIAL AND METHODS: Eighty-nine previously treated patients with AgP were re-examined. Clinical and radiographic parameters before treatment discontinuation and at re-examination were compared. OHRQoL at re-call was assessed with the short-form Oral Health Impact Profile (OHIP-14S). RESULTS: None of the subjects adhered to suggested periodontal therapy and maintenance after discharge. Mean percentage of sites with probing pocket depth (PPD) ≥6 mm at re-examination was 4.5 ± 5.9%. A total of 182 teeth had been lost over time. Tooth loss rate was 0.14/patient/year. From 68 subjects with documented favorable treatment outcomes, higher percentage of sites with PPD ≥6 mm at re-examination and higher radiographic proximal bone loss was associated with current smoking status. Patients with AgP with <20 teeth at re-call had worse OHRQoL than those with ≥20 teeth. Patients with higher full-mouth mean PPD also reported poorer OHRQoL. CONCLUSION: Treatment in patients with AgP who smoke and neglect proper supportive care, risk periodontal disease progression. Substantial tooth loss and higher full-mouth mean PPD led to poorer OHRQoL in this cohort.

Definition of aggressive periodontitis in periodontal research. A systematic review.

Since its introduction in 1999, the term aggressive periodontitis (AgP) has been the topic of many investigations. Articles supporting the International Workshop for a Classification of Periodontal Diseases list several disease features, but do not offer operational criteria for identifying cases. Consequently, considerable variation in the understanding of AgP can be anticipated. AIM: To systematically assess the definitions of AgP reported in original periodontal research. METHODS: A systematic review of original research on AgP published in English. RESULTS: The electronic search yielded 833 abstracts. Of these, 472 publications fulfilled the inclusion criteria and were appraised. In 26.5% of the publications, no information on AgP operationalization is presented, but reference is made to another article. In 12.7% of the publications, no information is provided as to how the cases were defined. Many combinations of criteria for case definition were found. CONCLUSIONS: This study revealed significant heterogeneity in the understanding and use of the term AgP in original research and poor documentation of the identification of cases. The direction and magnitude of the influence of misclassification and selection bias are unknown, but ought to be considered by the critical reader, professionals and patients using this term.

What exactly distinguishes aggressive from chronic periodontitis: is it mainly a difference in the degree of bacterial invasiveness?

At the International Workshop for Classification of Periodontal Diseases and Conditions in 1999, the classification of aggressive and chronic periodontitis that is presently used was introduced. A literature review of papers published in 2015 and having aggressive periodontitis in the title revealed that most studies use this terminology but it is questionable whether all established criteria were really applied correctly. Review of the literature showed no qualitative differences between aggressive and chronic periodontitis regarding bacterial and viral aspects. It is also unlikely that that there are major immunologic differences between aggressive and chronic periodontitis. Neutrophil function can be compromised in both conditions but may be more genetically related in aggressive periodontitis and be associated more with lifestyle factors in chronic periodontitis. In general, genetics plays a more important role in aggressive periodontitis than in chronic periodontitis. It is likely that periodontitis progresses by recurrent acute episodes during which invasion of bacteria into the connective tissue may occur. Two cases are presented for which invasive periodontitis is treated with systemic antibiotics, showing remarkable periodontal healing in terms of probing attachment gain, as well as radiographic bone gain. Periodontitis in an active state with bacterial invasion is probably accompanied with a significant increase in subgingival temperature. It is hypothesized that elevated subgingival temperature may help to distinguish between bacterial and nonbacterial invasive periodontitis. Scaling and root planing during a burst of disease activity may result in removal of connective tissue fiber attachment and down-growth of epithelium, thereby preventing the reattachment of connective tissue. Because the burst of disease is accompanied by an increase of temperature, assessment of the temperature may help in deciding whether or not to prescribe systemic antibiotics. When the use of systemic antibiotics is indicated, the antibiotic therapy may help to maintain the connective tissue attachment at the most possible coronal level. The above implies that the ability to diagnose bacterial invasive periodontitis is quite important, and future research is needed to determine if assessment of subgingival temperature may help in diagnosing invasive periodontitis. In addition, it is suggested that future classification systems of periodontitis include the item of bacterial invasive periodontitis.

Cytokine profile in gingival crevicular fluid and plasma of patients with aggressive periodontitis.

OBJECTIVE: This study aimed to determine the content of cytokines in gingival crevicular fluid (GCF) as well as in plasma of Sudanese patients with aggressive periodontitis (AgP) and healthy controls (HC). MATERIALS AND METHODS: Nineteen AgP patients and 19 HC were included. The mean probing pocket depth and clinical attachment level of the GCF sampled sites in patients were both ≥5 mm. The GCF and plasma levels of 27 cytokines were determined using 27-multiplex fluorescent bead-based immunoassays. Ratios were calculated among cytokines of the T-helper cell subsets Th1 and Th2. Descriptive statistics, the Mann-Whitney U-test and Spearman's rho rank correlation coefficient analysis were used. RESULTS: Interferon-γ was the only cytokine found in significantly lower levels in GCF of patients compared with HC. Levels of interleukin (IL)-10, IL-13, IL-1Ra, monocyte chemoattractant protein-1 (MCP-1), regulated on activation normal T-cell expressed and secreted (RANTES), granulocyte-colony-stimulating factor (G-CSF), and granulocyte-macrophage-CSF (GM-CSF) were significantly lower in plasma of AgP compared with HC. The ratios of Th1:Th2 in GCF and Treg:Th17 in plasma were significantly lower in AgP. CONCLUSIONS: The lower levels of cytokines detected systemically in plasma of AgP patients may have an impact on the immune response. The lower ratio of Th1:Th2 cytokines in GCF samples of AgP patients suggests a role for Th2 at the local site of disease.

Disease Staging Index for Aggressive Periodontitis.

Major advances in the knowledge about the aetiopathogenesis of aggressive periodontitis (AgP) have been achieved. An ever increasing number of scientific articles related to AgP are published every year contributing significantly to the knowledge of this unique and complex disease. AgP has been classified into localised and generalised forms based on their extent and disease progression with distinct clinical and radiological features. A classification of AgP based on severity (mild, moderate and severe) exists; however, it is not easily applicable. Therefore, studies on AgP do not categorise the disease based on severity. A disease staging index for AgP is proposed based on clinical and radiological features, as well as risk factors. Based on the presence or absence of risk factors confirmed by longitudinal studies, cases of AgP can be divided into low risk, medium risk and high risk profiles for disease progression. Clinicians can devise a broad treatment plan for their AgP cases based on this staging. More frequent recall intervals are proposed for patients at medium and high risk for disease progression. Ten cases of AgP with 10-year follow-up were used to validate the staging index by retrospectively assigning prognosis and associating it with tooth loss. The use of this staging by researchers would increase external validity of research on AgP. Long-term analysis of AgP cases are needed to validate this staging index longitudinally.

Diagnosis and Management of Chronic and Aggressive Periodontitis Part 1: Periodontal Assessment and Diagnosis.

common diseases that affect the oral cavity. The differential diagnosis between chronic and aggressive periodontitis can be complex for some clinicians and the correct diagnosis is a key element in disease management. The three-part series will review periodontal clinical assessment and diagnosis, periodontal management and finally will discuss two clinical cases. This paper will focus on periodontal disease pathogenesis, periodontal clinical assessment and diagnosis. Clinical relevance: This paper aims to provide the general dental practitioner with an understanding of periodontal disease pathogenesis and to highlight elements in the clinical assessment which will help to establish the diagnosis

A novel large deletion combined with a nonsense mutation in a Chinese child with Papillon-Lefèvre syndrome.

BACKGROUND AND OBJECTIVE: Papillon-Lefèvre Syndrome (PLS) is a rare autosomal recessive hereditary disease (MIM245000). The syndrome is characterized by palmoplantar keratoderma and early onset periodontitis, caused by CTSC gene mutation. The mutation in CTSC previously reported is mainly point mutations. Large deletion in the CTSC gene has not yet been reported. MATERIAL AND METHODS: We collected 5 mL peripheral blood from a patient with PLS and her family members and used the direct sequencing method to perform CTSC bidirectional sequencing. We also used FISH to analyze the approximate locations of the ends of the missing fragment and then determined the fragment sequence through direct sequencing. RESULTS: The result demonstrated that the patient have a 110 kb deletion (Chr11: 88032292: 88142997(NC_000011)) combined with a nonsense mutation (Gln182Ter) in this gene. CONCLUSION: Our study reveals a compound mutation consisting of a large deletion and a nonsense mutation, which provides a new insight in the mutation type of CTSC gene.

Effect of patient age awareness on diagnostic agreement of chronic or aggressive periodontitis between clinicians; a pilot study.

BACKGROUND: The aim of this pilot study was to test whether diagnostic agreement of aggressive and chronic periodontitis amongst Board Certified Periodontists, is influenced by knowledge of a patient's age. In 1999 at the International World Workshop age was removed as a diagnostic criteria for aggressive periodontitis. The impact of this change on the diagnostic reliability amongst clinicians has not yet been assessed. METHODS: Nine periodontal case reports were twice presented to sixteen board certified periodontists, once with age withheld and again with patient age provided. Participants were instructed to choose a diagnosis of Chronic Periodontitis or Aggressive Periodontitis. Diagnostic agreement was calculated using the Fleiss Kappa test. RESULTS: Including the patients' age in case report information increased diagnostic agreement (the kappa statistic) from 0.49 (moderate agreement) to 0.61 (substantial agreement). CONCLUSION: These results suggest that knowledge of a patients' age influenced clinical diagnosis, when distinguishing between aggressive periodontitis and chronic periodontitis, which may in turn impact treatment decision-making.

Periodontal Examination Profiles and Treatment Approaches of a Group of Turkish General Dentists.

PURPOSE: To investigate the periodontal examination profiles and treatment approaches of a group of Turkish general dentists. MATERIALS AND METHODS: 457 general dentists were called and 173 dentists agreed to participate in the study. The questionnaire comprised 10 questions including gender, years of experience, periodontal probing during examination, oral hygiene motivation methods (do you perform, yes/no; the oral hygiene motivation method; verbal expression or using visual materials), periodontal treatments (supragingival scaling, subgingival scaling and planing or surgery) and knowledge about diagnosis and treatment for aggressive and chronic periodontitis. The participants were grouped according to their years of clinical experience: group 1: 0 to 10 years of clinical practice (n = 58); group 2: 10 to 20 years (n = 68); group 3: >20 years (n = 47). RESULTS: The 'periodontal probing' performance percentages were 70.69%, 26.47% and 40.43% in groups 1, 2 and 3, respectively. The oral hygiene motivation rate was high in the first 10 years of clinical practice (60.3%). In addition, 72.4% of the dentists in group 1 used visual materials in addition to verbal expression during oral hygiene motivation. 72.25% of the general dentists performed supragingival scaling. The knowledge of diagnosis and treatment of chronic periodontitis was present in >90% of the dentists surveyed. In contrast, >50% of the general dentists were not knowledgeable in the diagnosis and treatment of aggressive periodontitis. CONCLUSION: Periodontal probing is a gold standard for periodontal diagnosis, but as the dentists' clinical experience increases, the frequency of its performance decreases. The percentage of the knowledge and treatment of chronic periodontitis is higher than that of aggressive periodontitis. Postgraduate education in periodontology is important to keep general dentists up to date on current periodontal practice and improve awareness of periodontal diseases.

Effects of azithromycin versus metronidazole-amoxicillin combination as an adjunct to nonsurgical periodontal therapy of generalized aggressive periodontitis.

OBJECTIVE: This study evaluated the short-term clinical benefits of two systemic antibiotic regimes added to the nonsurgical periodontal treatment of generalized aggressive periodontitis. MATERIALS AND METHODS: The patient records were reviewed and 45 patients were selected and divided into the following three groups: Scaling and root planning (SRP) only; SRP plus azithromycin (AZT group); and SRP plus metronidazole and amoxicillin (M+A group). The periodontal indexes were recorded at baseline and 3-month posttherapy. RESULTS: The periodontal parameters were improved in all groups 3-month posttherapy. The scores were decreased more in the AZT and M+A groups than the controls, but this difference did not reach significance. In addition, the decrease in the plaque index from baseline to 3-month in the AZT group was not significant. CONCLUSION: Nonsurgical therapy reduces the probing depth, clinical attachment level, and clinical inflammation findings. This healing tendency was observed in the AZT group despite the baseline plaque scores. Therefore, AZT might be active against the bacteria in dental biofilms.

[Complete dental care of patients suffering from localized aggressive periodontitis. Case report]. / Lokalizált agresszív parodontitisben szenvedo páciens komplett fogászati ellátása. Esetismertetés.

A 34 years old male patient was referred to our clinic for restorative dental treatment. During detailed consultation and dental examination a relatively rare form of periodontal disease had been diagnosed. Intraoral examination included recording of dental and periodontal status. Based on patient's dental history, measurements of probing pocket depths (PPD), clinical attachment level (CAL), and also the X-ray findings, Localized Aggressive Periodontitis (LAP) unknown by the patient was diagnosed. After patient's consent the comprehensive treatment plan covered the dental prevention, periodontal non-surgical and surgical therapy and rehabilitation. The treatment started with oral hygienic instruction, motivation then supra- and subgingival scaling and rootplaning. Later extraction and elective root canal treatment were performed, followed by open flap periodontal surgery combined with hemisection of two molars. After a full mouth conservative restorative therapy, function and esthetics were restored by fix dental prostheses. This case is a good example to underline the importance of periodontal examination during the dental screening and dental status recording for each patients showing up at dental clinics. Otherwise in many cases this asympthomatic disease can remain undetected.

Aggressive periodontitis: case definition and diagnostic criteria.

Aggressive periodontitis is a destructive disease characterized by the following: the involvement of multiple teeth with a distinctive pattern of periodontal tissue loss; a high rate of disease progression; an early age of onset; and the absence of systemic diseases. In some patients periodontal tissue loss may commence before puberty, whereas in most patients the age of onset is during or somewhat after the circumpubertal period. Besides infection with specific microorganisms, a host predisposition seems to play a key role in the pathogenesis of aggressive periodontitis, as evidenced by the familial aggregation of the disease. In this article we review the historical background of the diagnostic criteria of aggressive periodontitis, present a contemporary case definition and describe the clinical parameters of the disease. At present, the diagnosis of aggressive periodontitis is achieved using case history, clinical examination and radiographic evaluation. The data gathered using these methods are prone to relatively high measurement errors. Besides, this diagnostic approach measures past disease history and may not reliably measure existing disease activity or accurately predict future tissue loss. A diagnosis is often made years after the onset of the disease, partly because current assessment methods detect established disease more readily and reliably than they detect incipient or initial lesions where the tissue loss is minimal and usually below the detection threshold of present examination methods. Future advancements in understanding the pathogenesis of this disease may contribute to an earlier diagnosis. Insofar, future case definitions may involve the identification of key etiologic and risk factors, combined with high-precision methodologies that enable the early detection of initial lesions. This may significantly enhance the predictive value of these tests and detect cases of aggressive periodontitis before significant tissue loss develops.

Aggressive and acute periodontal diseases.

Inflammatory periodontal diseases are highly prevalent, although most of these diseases develop and progress slowly, often unnoticed by the affected individual. However, a subgroup of these diseases include aggressive and acute forms that have a relatively low prevalence but show a rapid-course, high rate of progression leading to severe destruction of the periodontal tissues, or cause systemic symptoms that often require urgent attention from healthcare providers. Aggressive periodontitis is an early-onset, destructive disease that shows a high rate of periodontal progression and distinctive clinical features. A contemporary case definition of this disease is presented. Population studies show that the disease is more prevalent in certain geographic regions and ethnic groups. Aggressive periodontitis is an infectious disease, and recent data show that in affected subjects the subgingival microbiota is composed of a mixed microbial infection, with a wide heterogeneity in the types and proportions of microorganisms recovered. Furthermore, there are significant differences in the microbiota of the disease among different geographic regions and ethnicities. There is also evidence that the Aggregatibacter actinomycetemycomitans-JP2 clone may play an important role in the development of the disease in certain populations. The host response plays an important role in the susceptibility to aggressive periodontitis, where the immune response may be complex and involve multiple mechanisms. Also, genetic factors seem to play an important role in the pathogenesis of this disease, but the mechanisms of increased susceptibility are complex and not yet fully understood. The available data suggest that aggressive periodontitis is caused by mutations either in a few major genes or in multiple small-effect genes, and there is also evidence of gene-gene and gene-environment interaction effects. Diagnostic methods for this disease, based on a specific microbiologic, immunologic or genetic profile, currently do not exist. Genetic markers have the potential to be implemented as screening tools to identify subjects at risk. This approach may significantly enhance treatment outcome through the early detection and treatment of affected subjects, as well as using future approaches based on gene therapy. At present, the treatment of this disease is directed toward elimination of the subgingival bacterial load and other local risk factors. Adjunctive use of appropriate systemic antibiotics is recommended and may contribute to a longer suppression of the microbial infection. Other aggressive forms of periodontal diseases occur in patients who are affected with certain systemic diseases, including the leukocyte adhesion deficiency syndrome, Papillon-Lefèvre syndrome, Chediak-Higashi syndrome and Down syndrome. Management of the periodontal component of these diseases is very challenging. Acute gingival and periodontal lesions include a group of disorders that range from nondestructive to destructive forms, and these lesions are usually associated with pain and are a common reason for emergency dental consultations. Some of these lesions may cause a rapid and severe destruction of the periodontal tissues and loss of teeth. Oral infections, particularly acute infections, can spread to extra-oral sites and cause serious medical complications, and even death. Hence, prompt diagnosis and treatment are paramount.

Aggressive periodontitis in a Nigerian teaching hospital.

AIM: These case series were aimed at highlighting late presentations of aggressive periodontitis (AP) in a teaching hospital as well as proffering possible reasons for such presentations which would serve as part of the solution to prevent such presentations in the future. BACKGROUND: Aggressive periodontitis is a severe form of destructive periodontitis traditionally believed to present around puberty. However, many cases seen in a teaching hospital presented much later for yet-to-be explained reasons. CASE DESCRIPTION: Seven patients referred to the specialist periodontal clinic of a Nigerian teaching hospital presented with clinical features consistent with AP. Most of the patients were over twenty and some over thirty years of age. CONCLUSION: Aggressive periodontitis patients seen in our center were often outside the traditional age brackets. The range of treatment options available to the patients were under-utilized due to serious financial constraints. CLINICAL SIGNIFICANCE: Aggressive periodontitis comes with serious psychological challenges and severe morbidity. Prompt diagnosis and effective management hold the key to success It is important to investigate why many of the cases seen in our center presented that late. Could be due to ignorance and poverty or could be due to failure of dentists recognize these cases and consequent misdiagnosis? Further studies are needed to answer these questions.

Generalized aggressive periodontitis in prepubertal age: description and comparison of two cases.

Aggressive periodontitis is a rare form of periodontal disease and it can involve both the deciduous dentition and the permanent one. It causes a rapid loss of periodontal attachment. The paper aims to describe two cases of severe generalized prepubertal periodontitis: the first child doesn't suffer from neither systemic diseases nor alteration of functionality of polymorphonuclear and periodontal disease involved both his deciduous dentition and the first permanent molars. The second child had a deficiency of functionality of polymorphonuclear but periodontal disease involved only primary dentition thanks to his immediate improvement of home dental hygiene. This comparison shows the importance of early diagnosis and especially of optimal dental oral hygiene. Infant healthcare professionals, as pediatric dentists and pediatricians, should have the necessary knowledge for early and correct diagnosis and clinical management of disease.

Salivary type I collagen degradation end-products and related matrix metalloproteinases in periodontitis.

AIM: Type I collagen degradation end-products and related matrix metalloproteinases (MMPs) were examined aiming to detect potential markers of periodontitis in saliva, with high sensitivity and specificity. MATERIALS AND METHODS: The salivary concentrations of MMP-8, MMP-9 and MMP-13, tartrate-resistant acid phosphatase serum type 5b, C-terminal cross-linked telopeptide of type I collagen (CTx), N-terminal cross-linked telopeptide of type I collagen (NTx) and cross-linked carboxyterminal telopeptide of type I collagen were analysed in 230 subjects. Oral health examination included panoramic radiography. RESULTS: The concentrations of MMP-8, MMP-9 and MMP-13 in saliva were higher in subjects with generalized periodontitis than in controls. Of the tested salivary markers, MMP-8 was the only marker capable of differentiating subjects with severe alveolar bone loss from those with slight bone loss (p < 0.001). The association between the salivary MMP-8 levels and periodontitis remained significant after the adjustment with age, gender and smoking. In addition, significant correlations were found between the tested markers and periodontal parameters. CONCLUSION: Enzymes and end-products of type I collagen degradation have different associations with each other and with periodontal status that may reflect their roles in the cascade leading to alveolar bone loss. MMP-8 is a strong biomarker candidate for detecting alveolar bone destruction.