Juvenile Periodontitis Research Articles

A Comparison between Scaling and Root Planning (SRP), Antibiotic and Diode Laser Application in Treatment of Localized Juvenile Periodontitis (Microscopical Study)

The present study aimed to study different ways for treatment of Localized Juvenile periodontitis, cultural and microscopic results of specimens from base line, appeared the following bacterial strains: Bacteroides gracilis ,Fusobacterium nuclautum, Porphyromonas intermedia, Actinomyces, peptostreptococcus species, eikenella corrodens, streptococcus intermedius, Streptococcus salivaris. Which distribution in 50% gram positive and 50% gram negative. Cultural and microscopical result after ten days of the experimental design appeared significant difference P≥ 0.05, at the SRP group results of microscopic and culturing show Peptostreptoccal species, Prevotella intermedia, Fusobacterium nuclautum, Streptococcus Saliveris. While at the SRP and antibiotic treated group (Doxycyclin 100 mg) the pattern of microbial study appeared the following bacteria: Fusobacterium nucleotum, Peptostreptococcus, Streptococcus salivaris. At the other hand the results of third group SRP and diode Laser appeared no growth of microorganism at all site subjected to Laser 0.8 w, 940 nm for 20 sec after ten days of study.

Treatment of Periodontitis Affecting Human Primary Teeth-A Systematic Review.

The aim of this systematic review is to report the treatment options (Intervention) and outcomes (O) for primary teeth affected by periodontitis (Population) and if the treatment of primary teeth can prevent the spread of periodontitis to permanent teeth (Outcomes). The following databases were searched for papers published before December 2022: PubMed, Embase, Web of Science, and Ebscohost. Studies on children affected by periodontitis involving the primary teeth were included and those on children who presented with periodontitis as a manifestation of systemic disease were excluded. Narrative synthesis and methodological quality assessments were performed for the included studies. Three interventional studies (without a control group) that evaluated treatments involving scaling and root planing (SRP with antibiotics) and extraction were included (total n = 60 patients). Additionally, twelve case reports/case series articles (n = 19 patients) were identified. The diagnoses ranged from aggressive periodontitis to juvenile periodontitis and pre-pubertal periodontitis. Based on a limited number of published studies, it was found that the early treatment of periodontitis affecting the primary teeth using SRP and systemic antibiotics resulted in favorable improvements in PD and CAL. Limited evidence suggests that SRP and the extraction of the primary teeth involved have the potential to prevent periodontitis affecting permanent teeth. Future trials are required to standardize the treatment protocols and to confirm these findings.

Herpesvirus-Bacteria pathogenic interaction in juvenile (aggressive) periodontitis. A novel etiologic concept of the disease.

Localized juvenile (aggressive) periodontitis starts at puberty in otherwise healthy individuals and involves the proximal surfaces of permanent incisors and first molars. The disease destroys a sizeable amount of periodontal bone within a few months despite minimal dental plaque and gingival tissue inflammation. Cytomegalovirus and Epstein-Barr virus, as well as the two main periodontopathic bacteria Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, are linked to juvenile periodontitis. Juvenile periodontitis-affected teeth show cementum hypoplasia. We hypothesize that an active herpesvirus infection, at the time of root formation, hampers cementum formation and, at puberty, herpesvirus reactivation triggers an upgrowth of bacterial pathogens which produce rapid periodontal destruction on teeth with a defective periodontium. A pathogenic interaction between active herpesviruses and bacterial pathogens can potentially explain the etiology and incisor-first molar destructive pattern of juvenile periodontitis. Effective treatment of juvenile periodontitis may target the herpesvirus-bacteria co-infection.

Епідеміологія і етіопатогенетичні фактори розвитку агресивних форм пародонтиту

The purpose of the work was to study the etiology and main etiopathological factors of the development of aggressive forms of periodontitis based on the analysis of additional pathogenetic aspects of mineral metabolism disorders according to modern literature. Materials and methods. The bibliosemantic method was used to clarify the state of the problem, study the analysis of the results of previous scientific research based on literature sources and electronic resources. Results. Periodontitis is the most widespread disease among all periodontal pathologies (chronic generalized periodontitis occurs in 90% of cases). Until recently, aggressive forms of periodontitis were not given due attention, since according to epidemiological studies by S. Renvert and M. Wikstom (1996), in the general structure of periodontal diseases, aggressive forms of periodontitis occur with a frequency of 5–10%. To understand the mechanisms of the development of aggressive forms of periodontitis, attention is paid to their development in children and adolescents. Clinical and radiological examinations of children and adolescents showed different frequency of aggressive forms of periodontitis (localized juvenile periodontitis and generalized juvenile periodontitis): in the USA – 2.27%, in Denmark – 0.1%, in Finland – 0.1%, in Nigeria – 0.8%, in Brazil – 0.3%, in England – 0.17%, in Chile – 0.32%. Studies have shown that aggressive forms of periodontitis are equally common in children and adolescents, regardless of gender. At the same time, localized juvenile periodontitis is 3 times more common in boys, not the same for girls. A new and rather promising vector of periodontology is the study of the role of juvenile changes in the bone skeleton on the development and course of periodontal diseases. The development of mineral metabolism disorders in aggressive forms of periodontitis in different age groups requires further study, while the data obtained by molecular geneticists become relevant for understanding the possible ways of research. Considering the fact that the jaw bones are a component of the skeleton, the strength of which can be affected by various exogenous and endogenous factors, in particular genetic ones, the main direction of searching for candidate sensitivity genes is conducted among the markers of bone metabolism disorders. Of many candidate genes that determine bone mineral density, the most well-known is the vitamin D receptor gene. Conclusion. The analysis of the available literature showed that the study of the role of mineral and bone metabolism disorders in the emergence and development of aggressive forms of periodontitis has a wide scientific perspective, and obtaining new data on the state of systemic regulatory factors and their effects on the local mechanisms of periodontal tissue damage will allow not only to improve the diagnosis of various forms, but also to increase the effectiveness of the treatment of this pathology

Dental Paleobiology in a Juvenile Neanderthal (Combe-Grenal, Southwestern France).

Simple SummaryNumerous prehistoric sites in Europe and the Near East provided bones and dental remains of the populations of the past. One of them is the Combe-Grenal Cave (SW France), where fossils of children and adults represent the Neanderthals who lived there more than 60 ky ago, during a harsh period of the last glaciation. In this paper, we analyze a sample of the tartar of a juvenile individual. The numerous bacteria forming the plaque are compared to those of one adult from Israel, Kebara 2, revealing the differences between the most common bacteria in a young and an older individual, probably because of their immunological systems, and the different living conditions of the human groups they represented.Combe-Grenal site (Southwest France) was excavated by F. Bordes between 1953 and 1965. He found several human remains in Mousterian levels 60, 39, 35 and especially 25, corresponding to MIS 4 (~75–70/60 ky BP) and with Quina Mousterian lithics. One of the fossils found in level 25 is Combe-Grenal IV, consisting of a fragment of the left corpus of a juvenile mandible. This fragment displays initial juvenile periodontitis, and the two preserved teeth (LLP4 and LLM1) show moderate attrition and dental calculus. The SEM tartar analysis demonstrates the presence of cocci and filamentous types of bacteria, the former being more prevalent. This result is quite different from those obtained for the two adult Neanderthals Kebara 2 and Subalyuk 1, where more filamentous bacteria appear, especially in the Subalyuk 1 sample from Central Europe. These findings agree with the available biomedical data on periodontitis and tartar development in extant individuals, despite the different environmental conditions and diets documented by numerous archeological, taphonomical and geological data available on Neanderthals and present-day populations. New metagenomic analyses are extending this information, and despite the inherent difficulties, they will open important perspectives in studying this ancient human pathology.

Exome Sequencing of 5 Families with Severe Early-Onset Periodontitis

Periodontitis is characterized by alveolar bone loss leading to tooth loss. A small proportion of patients develop severe periodontitis at the juvenile or adolescent age without exposure to the main risk factors of the disease. It is considered that these cases carry rare variants with large causal effects, but the specific variants are largely unknown. In this study, we performed exome sequencing of 5 families with children who developed stage IV, grade C, periodontitis between 3 and 18 y of age. In 1 family, we found compound heterozygous variants in the gene CTSC (p.R272H, p.G139R), 1 of which was previously identified in a family with prepubertal periodontitis. Subsequent targeted resequencing of the CTSC gene in 24 patients <25 y of age (stage IV, grade C) identified the known mutation p.I453V (odds ratio = 4.06, 95% CI = 1.6 to 10.3, P = 0.001), which was previously reported to increase the risk for adolescent periodontitis. An affected sibling of another family carried a homozygous deleterious mutation in the gene TUT7 (p.R560Q, CADD score >30 [Combined Annotation Dependent Depletion]), which is implicated in regulation of interleukin 6 expression. Two other affected siblings shared heterozygous deleterious mutations in the interacting genes PADI1 and FLG (both CADD = 36), which contribute to the integrity of the environment–tissue barrier interface. Additionally, we found predicted deleterious mutations in the periodontitis risk genes ABCA1, GLT6D1, and SIGLEC5. We conclude that the CTSC variants p.R272H and p.I453V have different expressivity and diagnostic relevance for prepubertal and adolescent periodontitis, respectively. We propose additional causal variants for early-onset periodontitis, which also locate within genes that carry known susceptibility variants for common forms. However, the genetic architecture of juvenile periodontitis is complex and differs among the affected siblings of the sequenced families.

Optical profile: A key determinant of antibacterial efficacy of photodynamic therapy in dentistry

BackgroundPeriodontal disease effects 20–50% of the population worldwide, posing a global health challenge. It has been reported to be more prevalent among adults. Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) is an important organism associated with localized juvenile periodontitis. Photodynamic therapy (PDT) has been widely utilized for the treatment of periodontal disease; however, the effect of laser (light) profile on the antibacterial efficacy of PDT remains to be established. The quantitative measurement of laser profile is required to confirm the in vitro efficacy of PDT. AimIn the present study, a low cost PDT system comprising of six copper tube waveguides (CTW) was developed to provide more uniform irradiation of the culture plate. MethodsThe antibacterial effect of PDT, in combination with 200 μg/mL methylene blue (MB) as photosensitizer and 60 sec of irradiation, was studied on A. actinomycetemcomitans and Streptococcus mutans (S. mutans). In the present case, 660 nm laser guided with unpolished CTW, polished CTW, and optical fiber waveguide (OFW) provided radiant exposure of 0.86, 1.38, and 1.36 J/cm2, respectively, for a 24‐well culture plate. ResultsThe designed PDT system provided antimicrobial efficacy of 98% and 91% for A. actinomycetemcomitans and S. mutans, respectively, which was significantly higher as compared to OFW guided PDT. ConclusionThe results of the study highlighted the importance of laser profile as a key parameter that determines the survival rate of bacteria at the edge of the culture plate. Thus, the dose of PDT at the margin of optical profile is important for antibacterial activity for in vitro evaluation.

Complications of Teeth Affected by Molar-Incisor Malformation and Pathogenesis According to Microbiome Analysis

A molar-incisor malformation (MIM) is a recently reported dental anomaly that causes premature loss of the first molar with severe dentoalveolar infection. However, there has been no research on the pathogenesis yet. The aim of this study was to report the clinical process of MIMs and investigate the pathogenesis by conducting a microbiome analysis. An eight-year-old girl was diagnosed with MIM and after two years, four permanent first molars were sequentially extracted due to severe dentoalveolar infection. We recorded the patient`s clinical progress and collected oral microbiome samples from the extracted teeth with MIM and sound teeth as controls. The sites of microbiome sampling were represented by five habitats in two groups. Group (1) was the perio group: ① supragingival plaque, ② subgingival plaque, and ③ a pical abscess; and group (2) was the endo group: ④ coronal pulp chamber and ⑤ root canal. The perio group was composed predominantly of genera Streptococcus, Veilonella, and Leptotrichia. Spirochetes appeared in one sample from a severe periodontal abscess. Aggregatibacter actinomyces were not identified. In the endo groups, pulp necrosis was observed in all MIM and the genera Peptostreptococcus and Parvimonas predominated. In conclusion, MIM teeth caused localized tooth-related periodontitis with pulp necrosis rather than localized juvenile periodontitis, resulting in a poor prognosis, and timely extraction is highly recommended.

Potential role of diacylglycerol kinases in immune-mediated diseases.

The mechanism promoting exacerbated immune responses in allergy and autoimmunity as well as those blunting the immune control of cancer cells are of primary interest in medicine. Diacylglycerol kinases (DGKs) are key modulators of signal transduction, which blunt diacylglycerol (DAG) signals and produce phosphatidic acid (PA). By modulating lipid second messengers, DGK modulate the activity of downstream signaling proteins, vesicle trafficking and membrane shape. The biological role of the DGK α and ζ isoforms in immune cells differentiation and effector function was subjected to in deep investigations. DGK α and ζ resulted in negatively regulating synergistic way basal and receptor induced DAG signals in T cells as well as leukocytes. In this way, they contributed to keep under control the immune response but also downmodulate immune response against tumors. Alteration in DGKα activity is also implicated in the pathogenesis of genetic perturbations of the immune function such as the X-linked lymphoproliferative disease 1 and localized juvenile periodontitis. These findings suggested a participation of DGK to the pathogenetic mechanisms underlying several immune-mediated diseases and prompted several researches aiming to target DGK with pharmacologic and molecular strategies. Those findings are discussed inhere together with experimental applications in tumors as well as in other immune-mediated diseases such as asthma.

Aggregatibacter, A Low Abundance Pathobiont That Influences Biogeography, Microbial Dysbiosis, and Host Defense Capabilities in Periodontitis: The History of A Bug, And Localization of Disease.

Aggregatibacter actinomycetemcomitans, the focus of this review, was initially proposed as a microbe directly related to a phenotypically distinct form of periodontitis called localized juvenile periodontitis. At the time, it seemed as if specific microbes were implicated as the cause of distinct forms of disease. Over the years, much has changed. The sense that specific microbes relate to distinct forms of disease has been challenged, as has the sense that distinct forms of periodontitis exist. This review consists of two components. The first part is presented as a detective story where we attempt to determine what role, if any, Aggregatibacter plays as a participant in disease. The second part describes landscape ecology in the context of how the host environment shapes the framework of local microbial dysbiosis. We then conjecture as to how the local host response may limit the damage caused by pathobionts. We propose that the host may overcome the constant barrage of a dysbiotic microbiota by confining it to a local tooth site. We conclude speculating that the host response can confine local damage by restricting bacteremic translocation of members of the oral microbiota to distant organs thus constraining morbidity and mortality of the host.

Periodontitis: a host mediated disruption of microbial homeostasis.

In a prolific scientific career, Dr. Robert J. Genco dedicated himself to enriching our understanding of the pathogenesis of periodontitis. During a period of time in the 1970s and 1980s, when periodontitis was considered a classic infectious disease, Bob had the foresight to investigate and characterize the immune/inflammatory response in periodontitis, particularly Juvenile Periodontitis. His leadership in this area brought to the fore our appreciation of host-microbiome interactions that many years later (2008) culminated in the realization that periodontitis is a fundamental inflammatory disease. In this review, the question of how the host regulates the inflammatory response will be addressed in the context of how more recently-discovered pathways of resolution of inflammation play a role in disease pathogenesis. The host inflammatory response to commensal organisms creates excess inflammation in susceptible individuals and likely drives the dysbiosis of the oral microbiome observed in people with Periodontitis. In periodontal health, the oral microbiome is in balance with the host response. It is the loss of this symbiotic relationship with excess inflammation and microbiome dysbiosis that characterizes progressive disease. In recent years, the role of mediators of resolution of inflammation in the loss of balance and their potential use as therapeutics to restore homeostasis has extended our knowledge of how the host drives immune responses to affect oral dysbiosis. Dr. Genco provided the foundation for our ever-emerging understanding host-microbial interactions. The discovery of inflammation resolution pathways has furthered our knowledge in periodontal homeostasis. More studies are needed to understand how the host regulates the microbiome to fulfill the ultimate goal of more efficient therapeutics for periodontitis and related inflammatory diseases.

Herpesvirus-bacteria synergistic interaction in periodontitis.

The etiopathogenesis of severe periodontitis includes herpesvirus-bacteria coinfection. This article evaluates the pathogenicity of herpesviruses (cytomegalovirus and Epstein-Barr virus) and periodontopathic bacteria (Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis) and coinfection of these infectious agents in the initiation and progression of periodontitis. Cytomegalovirus and A.actinomycetemcomitans/P. gingivalis exercise synergistic pathogenicity in the development of localized ("aggressive") juvenile periodontitis. Cytomegalovirus and Epstein-Barr virus are associated with P. gingivalis in adult types of periodontitis. Periodontal herpesviruses that enter the general circulation may also contribute to disease development in various organ systems. A 2-way interaction is likely to occur between periodontal herpesviruses and periodontopathic bacteria, with herpesviruses promoting bacterial upgrowth, and bacterial factors reactivating latent herpesviruses. Bacterial-induced gingivitis may facilitate herpesvirus colonization of the periodontium, and herpesvirus infections may impede the antibacterial host defense and alter periodontal cells to predispose for bacterial adherence and invasion. Herpesvirus-bacteria synergistic interactions, are likely to comprise an important pathogenic determinant of aggressive periodontitis. However, mechanistic investigations into the molecular and cellular interaction between periodontal herpesviruses and bacteria are still scarce. Herpesvirus-bacteria coinfection studies may yield significant new discoveries of pathogenic determinants, and drug and vaccine targets to minimize or prevent periodontitis and periodontitis-related systemic diseases.

CHRONIC SUPPURATIVE OSTEOMYELITIS IN A PATIENT WITH AUTISM SPECTRUM DISORDER: CHALLENGES IN CLINICAL MANAGEMENT

The present study reports the challenges faced during the diagnosis and treatment of chronic suppurative osteomyelitis in a patient with autism spectrum disorder (ASD). A 23-year-old woman intern in a special care institution attended the special care dental clinic of the authors with an unusual periodontal lesion involving tooth 47. Tooth extraction was performed with curettage of the surrounding structures for histopathologic examination. Microscopic examination diagnosed an aggressive juvenile periodontitis leading to suppurative osteomyelitis. Based on the pathologic report, a tomographic examination was performed and revealed the extension of the bone destruction as well as bone sequestrum. The patient was referred for surgical approach under general anesthesia to remove all necrotic and infected bone. After 1 year of the diagnosis the patient still under treatment without complete resolution of the lesion.

DGKα in Neutrophil Biology and Its Implications for Respiratory Diseases.

Diacylglycerol kinases (DGKs) play a key role in phosphoinositide signaling by removing diacylglycerol and generating phosphatidic acid. Besides the well-documented role of DGKα and DGKζ as negative regulators of lymphocyte responses, a robust body of literature points to those enzymes, and specifically DGKα, as crucial regulators of leukocyte function. Upon neutrophil stimulation, DGKα activation is necessary for migration and a productive response. The role of DGKα in neutrophils is evidenced by its aberrant behavior in juvenile periodontitis patients, which express an inactive DGKα transcript. Together with in vitro experiments, this suggests that DGKs may represent potential therapeutic targets for disorders where inflammation, and neutrophils in particular, plays a major role. In this paper we focus on obstructive respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD), but also rare genetic diseases such as alpha-1-antitrypsin deficiency. Indeed, the biological role of DGKα is understudied outside the T lymphocyte field. The recent wave of research aiming to develop novel and specific inhibitors as well as KO mice will allow a better understanding of DGK’s role in neutrophilic inflammation. Better knowledge and pharmacologic tools may also allow DGK to move from the laboratory bench to clinical trials.

Preventing alveolar ridge resorption by rehabilitating with fenestrated and overdenture in aggressive periodontitis

Aggressive periodontitis, is characterized by severe loss of attachment and destruction of alveolar bone around one or more permanent teeth during the period of pubescence. It is currently believed that a combination of bacteriologic and immunologic factors are of major importance in the etiology of this disease. The objective of this study was to point out the importance of early patient presentation, correct diagnosis, and proper prosthodontic management of the disease condition by the dentist. Our case was an 18-year-old male and his clinical and radiographic findings were typical for generalized juvenile periodontitis. Treatment consisted of thorough training in techniques of plaque control, scaling and root planing and administration of tetracycline 250 mg every six hours for three weeks. Preservation of facial countours and replacement of missing teeth with overdenture and fenestrated denture. There was significant improvement of these clinical parameters six months after treatment, and replacement of the missing teeth improved their appearance as expected. The psychotherapy offered gave the patients positive psychological effects that further restored their ability to socialize in their environment, which added to their positive experience of life. Longer follow-ups will add more knowledge about the treatment modalities for rehabilitation of aggressive periodontitis patients.

A Case of Feline Juvenile Periodontitis Treated with the Extraction of all the Premolars and Molars

A Case of Feline Juvenile Periodontitis Treated with the Extraction of all the Premolars and Molars

American Academy of Periodontology Task Force Report on the Update to the 1999 Classification of Periodontal Diseases and Conditions.

American Academy of Periodontology Task Force Report on the Update to the 1999 Classification of Periodontal Diseases and Conditions.

Periodontal Diseases and Dental Caries in Children with Type 1 Diabetes Mellitus.

Type 1 diabetes mellitus is a chronic metabolic disease of an autoimmune origin with early manifestation predominantly in the childhood. Its incidence has been rising in most European countries. Diabetes has been intensively studied by all branches of medicine. There were a number of studies investigating oral consequences of diabetes; however, unambiguous conclusions were drawn only for the relationship between diabetes and periodontal impairment. Many studies confirmed higher plaque levels and higher incidence of chronic gingivitis both in adults and in children with diabetes. Juvenile periodontitis is rare both in healthy subjects and in those with type 1 diabetes. Yet certain findings from well-conducted studies, for example, differences in oral microflora or the impact of metabolic control of diabetes on periodontal health, indicate a higher risk of periodontitis in children with type 1 diabetes. As for the association of diabetes and dental caries, the results of the studies are inconsistent. However, it was found that some risk factors for dental caries are either more or less prevalent in the diabetic population. Despite an extensive research in this area we have to acknowledge that many questions have remained unanswered. There is a need for continued, thorough research in this area.

Aggregatibacter actinomycetemcomitans - a tooth killer?

Strong evidence is available on Aggregatibacter actinomycetemcomitans (A.a) on its role as the causative agent of localised juvenile periodontitis (LJP), a disease characterised by rapid destruction of the tooth-supporting tissues. This organism possesses a large number of virulence factors with a wide range of activities which enable it to colonise the oral cavity, invade periodontal tissues, evade host defences, initiate connective tissue destruction and interfere with tissue repair. Adhesion to epithelial and tooth surfaces is dependent on the presence of surface proteins and structures such as microvesicles and fimbriae. Invasion has been demonstrated in vivo and in vitro. The organism has a number of means of evading host defences which include: (i) production of leukotoxin; (ii) producing immunosuppressive factors; (iv) secreting proteases capable of cleaving IgG; and (v) producing Fc-binding.

Avidity of antibody responses to Actinobacillus actinomycetemcomitans in periodontitis.

We designed a study to examine the serum IgG antibody avidity characteristics in: (i) normal subjects (N); (ii) Actinobacillus actinomycetemcomitans-infected adult periodontitis (AP Aa+); (iii) A. actinomycetemcomitans-infected localized juvenile periodontitis (LJP Aa+); and (iv) AP subjects (AP) with various antibody patterns and disease presentation. Although there were significant elevations in antibody levels for AP Aa+ and LJP Aa+ patients compared with AP and normal patients (P < 0.0001), there were no significant differences in the avidity indices (AI). Correlations of antibody levels to avidity revealed that functional activity of the antibody as measured by avidity was independent of antibody levels. Increasing antibody levels correlated with an increase in the number of infected sites, yet there was a trend for A1 to decrease with increased infection. Avidity indices for all patient groups did not appear to show a strong biologic relationship to plaque; however, in AP Aa+ and LJP Aa+ patients there was a generally positive relationship between avidity and bleeding on probing or pocket depth. In AP Aa+ and LJP Aa+ patients, and in AP patients there was a positive relationship of avidity through a threshold of approximately 8 active disease sites. This study hypothesized that antibody avidity to A. actinomycetemcomitans could help to explain the relationship between the active host response and chronic infection with this pathogen. The results provide evidence that both antibody levels and avidity may contribute to the variation in host resistance to infection and disease associated with A. actinomycetemcomitans.