Background
To develop preventive strategies addressing peri‐implant diseases, a thorough understanding of the epidemiology is required.
Aim
The aim was to systematically assess the scientific ...literature in order to evaluate the prevalence, extent and severity of peri‐implant diseases.
Material & Methods
Data were extracted from identified studies. Meta‐analyses for prevalence of peri‐implant mucositis and peri‐implantitis were performed. The effect of function time and disease definition on the prevalence of peri‐implantitis was evaluated by meta‐regression analyses. Data on extent and severity of peri‐implant diseases were estimated if not directly reported.
Results
Fifteen articles describing 11 studies were included. Case definitions for mucositis and peri‐implantitis varied. The prevalence of peri‐implant mucositis and peri‐implantitis ranged from 19 to 65% and from 1 to 47%, respectively. Meta‐analyses estimated weighted mean prevalences of peri‐implant mucositis and peri‐implantitis of 43% (CI: 32–54%) and 22% (CI: 14–30%), respectively. The meta‐regression showed a positive relationship between prevalence of peri‐implantitis and function time and a negative relationship between prevalence of peri‐implantitis and threshold for bone loss. Extent and severity of peri‐implant diseases were rarely reported.
Conclusion
Future studies on the epidemiology of peri‐implant diseases should consider (i) applying consistent case definitions and (ii) assessing random patient samples of adequate size and function time.
Peri‐implantitis Schwarz, Frank; Derks, Jan; Monje, Alberto ...
Journal of clinical periodontology,
June 2018, Letnik:
45, Številka:
S20
Journal Article
Recenzirano
Odprti dostop
Objectives
This narrative review provides an evidence‐based overview on peri‐implantitis for the 2017 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions.
...Methods
A literature review was conducted addressing the following topics: 1) definition of peri‐implantitis; 2) conversion from peri‐implant mucositis to peri‐implantitis, 3) onset and pattern of disease progression, 4) characteristics of peri‐implantitis, 5) risk factors/indicators for peri‐implantitis, and 6) progressive crestal bone loss in the absence of soft tissue inflammation.
Conclusions
1)Peri‐implantitis is a pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri‐implant connective tissue and progressive loss of supporting bone.
2)The histopathologic and clinical conditions leading to the conversion from peri‐implant mucositis to peri‐implantitis are not completely understood.
3)The onset of peri‐implantitis may occur early during follow‐up and the disease progresses in a non‐linear and accelerating pattern.
4a)Peri‐implantitis sites exhibit clinical signs of inflammation and increased probing depths compared to baseline measurements.
4b)At the histologic level, compared to periodontitis sites, peri‐implantitis sites often have larger inflammatory lesions.
4c)Surgical entry at peri‐implantitis sites often reveals a circumferential pattern of bone loss.
5a)There is strong evidence that there is an increased risk of developing peri‐implantitis in patients who have a history of chronic periodontitis, poor plaque control skills, and no regular maintenance care after implant therapy. Data identifying “smoking” and “diabetes” as potential risk factors/indicators for peri‐implantitis are inconclusive.
5b)There is some limited evidence linking peri‐implantitis to other factors such as: post‐restorative presence of submucosal cement, lack of peri‐implant keratinized mucosa and positioning of implants that make it difficult to perform oral hygiene and maintenance.
6)Evidence suggests that progressive crestal bone loss around implants in the absence of clinical signs of soft tissue inflammation is a rare event.
Peri‐implantitis Schwarz, Frank; Derks, Jan; Monje, Alberto ...
Journal of periodontology (1970),
June 2018, Letnik:
89, Številka:
S1
Journal Article
Recenzirano
Odprti dostop
Objectives
This narrative review provides an evidence‐based overview on peri‐implantitis for the 2017 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions.
...Methods
A literature review was conducted addressing the following topics: 1) definition of peri‐implantitis; 2) conversion from peri‐implant mucositis to peri‐implantitis, 3) onset and pattern of disease progression, 4) characteristics of peri‐implantitis, 5) risk factors/indicators for peri‐implantitis, and 6) progressive crestal bone loss in the absence of soft tissue inflammation.
Conclusions
1)Peri‐implantitis is a pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri‐implant connective tissue and progressive loss of supporting bone.
2)The histopathologic and clinical conditions leading to the conversion from peri‐implant mucositis to peri‐implantitis are not completely understood.
3)The onset of peri‐implantitis may occur early during follow‐up and the disease progresses in a non‐linear and accelerating pattern.
4a)Peri‐implantitis sites exhibit clinical signs of inflammation and increased probing depths compared to baseline measurements.
4b)At the histologic level, compared to periodontitis sites, peri‐implantitis sites often have larger inflammatory lesions.
4c)Surgical entry at peri‐implantitis sites often reveals a circumferential pattern of bone loss.
5a)There is strong evidence that there is an increased risk of developing peri‐implantitis in patients who have a history of chronic periodontitis, poor plaque control skills, and no regular maintenance care after implant therapy. Data identifying “smoking” and “diabetes” as potential risk factors/indicators for peri‐implantitis are inconclusive.
5b)There is some limited evidence linking peri‐implantitis to other factors such as: post‐restorative presence of submucosal cement, lack of peri‐implant keratinized mucosa and positioning of implants that make it difficult to perform oral hygiene and maintenance.
6)Evidence suggests that progressive crestal bone loss around implants in the absence of clinical signs of soft tissue inflammation is a rare event.
Background
While information on the prevalence of peri‐implantitis is available, data describing onset and progression of the disease are limited.
Material & Methods
A 9‐year follow‐up examination of ...596 randomly selected implant‐carrying individuals identified 62 patients with moderate/severe peri‐implantitis. Longitudinal assessments of peri‐implant marginal bone levels were used to construct a statistical model with bone loss as the dependent variable. A multilevel growth model estimated the pattern of bone loss for each implant/patient. Onset of peri‐implantitis was determined by evaluating the cumulative percentage of implants/patients presenting with estimated bone loss at each year following prosthesis delivery.
Results
The analysis showed a non‐linear, accelerating pattern of bone loss at the 105 affected implants. The onset of peri‐implantitis occurred early, and 52% and 66% of implants presented with bone loss of >0.5 mm at years 2 and 3 respectively. A total of 70% and 81% of subjects presented with ≥1 implants with bone loss of >0.5 mm at years 2 and 3 respectively.
Conclusions
It is suggested that peri‐implantitis progresses in a non‐linear, accelerating pattern and that, for the majority of cases, the onset occurs within 3 years of function.
Aim
To review the quality of reporting and the methodology of clinical research on the incidence, prevalence and risk factors of peri‐implant diseases.
Methods
A MEDLINE search was conducted for ...cross‐sectional, case‐control and prospective longitudinal studies reporting on peri‐implant diseases. To evaluate the quality of reporting of the selected studies the STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) checklist was utilized.
Results
The search provided 306 titles and s, out of which 40 were selected for full‐text analysis. Finally, 16 studies were included out of which five assessed prevalence and only two the incidence of peri‐implant diseases. 13 articles studied risk indicators for peri‐implant diseases. None of the scrutinized articles adhered fully to the STROBE criteria. The large majority of articles did not (i) clearly state the applied study design, (ii) describe any effort to address potential sources of bias, (iii) explain how missing data were addressed, (iv) perform any kind of sensitivity analysis, (v) indicate the number of participants with missing data for each variable of interest.
Conclusion
Collectively, the findings of this review indicate a need for improved reporting of epidemiological studies on peri‐implant diseases.
A classification for peri‐implant diseases and conditions was presented. Focused questions on the characteristics of peri‐implant health, peri‐implant mucositis, peri‐implantitis, and soft‐ and ...hard‐tissue deficiencies were addressed.
Peri‐implant health is characterized by the absence of erythema, bleeding on probing, swelling, and suppuration. It is not possible to define a range of probing depths compatible with health; Peri‐implant health can exist around implants with reduced bone support.
The main clinical characteristic of peri‐implant mucositis is bleeding on gentle probing. Erythema, swelling, and/or suppuration may also be present. An increase in probing depth is often observed in the presence of peri‐implant mucositis due to swelling or decrease in probing resistance. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri‐implant mucositis.
Peri‐implantitis is a plaque‐associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri‐implant mucosa and subsequent progressive loss of supporting bone. Peri‐implantitis sites exhibit clinical signs of inflammation, bleeding on probing, and/or suppuration, increased probing depths and/or recession of the mucosal margin in addition to radiographic bone loss.
The evidence is equivocal regarding the effect of keratinized mucosa on the long‐term health of the peri‐implant tissue. It appears, however, that keratinized mucosa may have advantages regarding patient comfort and ease of plaque removal.
Case definitions in day‐to‐day clinical practice and in epidemiological or disease‐surveillance studies for peri‐implant health, peri‐implant mucositis, and peri‐implantitis were introduced. The proposed case definitions should be viewed within the context that there is no generic implant and that there are numerous implant designs with different surface characteristics, surgical and loading protocols. It is recommended that the clinician obtain baseline radiographic and probing measurements following the completion of the implant‐supported prosthesis.
A classification for peri‐implant diseases and conditions was presented. Focused questions on the characteristics of peri‐implant health, peri‐implant mucositis, peri‐implantitis, and soft‐ and ...hard‐tissue deficiencies were addressed.
Peri‐implant health is characterized by the absence of erythema, bleeding on probing, swelling, and suppuration. It is not possible to define a range of probing depths compatible with health; Peri‐implant health can exist around implants with reduced bone support.
The main clinical characteristic of peri‐implant mucositis is bleeding on gentle probing. Erythema, swelling, and/or suppuration may also be present. An increase in probing depth is often observed in the presence of peri‐implant mucositis due to swelling or decrease in probing resistance. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri‐implant mucositis.
Peri‐implantitis is a plaque‐associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri‐implant mucosa and subsequent progressive loss of supporting bone. Peri‐implantitis sites exhibit clinical signs of inflammation, bleeding on probing, and/or suppuration, increased probing depths and/or recession of the mucosal margin in addition to radiographic bone loss.
The evidence is equivocal regarding the effect of keratinized mucosa on the long‐term health of the peri‐implant tissue. It appears, however, that keratinized mucosa may have advantages regarding patient comfort and ease of plaque removal.
Case definitions in day‐to‐day clinical practice and in epidemiological or disease‐surveillance studies for peri‐implant health, peri‐implant mucositis, and peri‐implantitis were introduced. The proposed case definitions should be viewed within the context that there is no generic implant and that there are numerous implant designs with different surface characteristics, surgical and loading protocols. It is recommended that the clinician obtain baseline radiographic and probing measurements following the completion of the implant‐supported prosthesis.
Synthetic glucocorticoids are administered to pregnant women at risk for preterm delivery, to enhance fetal lung maturation. The benefit of this treatment is well established, however caution is ...necessary because of possible unwanted side effects on development of different organ systems, including the brain. Actions of glucocorticoids are mediated by corticosteroid receptors, which are highly expressed in the hippocampus, a brain structure involved in cognitive functions. Therefore, we analyzed the effects of a single antenatal dexamethasone treatment on the development of the mouse hippocampus. A clinically relevant dose of dexamethasone (0.4 mg/kg) was administered to pregnant mice at embryonic day 15.5 and the hippocampus was analyzed from embryonic day 16 until adulthood. We investigated the effects of dexamethasone treatment on anatomical changes, apoptosis and proliferation in the hippocampus, hippocampal volume and on total body weight. Our results show that dexamethasone treatment reduced body weight and hippocampal volume transiently during development, but these effects were no longer detected at adulthood. Dexamethasone treatment increased the number of apoptotic cells in the hippocampus until birth, but postnatally no effects of dexamethasone treatment on apoptosis were found. During the phase with increased apoptosis, dexamethasone treatment reduced the number of proliferating cells in the subgranular zone of the dentate gyrus. The number of proliferative cells was increased at postnatal day 5 and 10, but was decreased again at the adult stage. This latter long-term and negative effect of antenatal dexamethasone treatment on the number of proliferative cells in the hippocampus may have important implications for hippocampal network function.
Aims
Over the past decades, the placement of dental implants has become a routine procedure in the oral rehabilitation of fully and partially edentulous patients. However, the number of ...patients/implants affected by peri‐implant diseases is increasing. As there are – in contrast to periodontitis – at present no established and predictable concepts for the treatment of peri‐implantitis, primary prevention is of key importance. The management of peri‐implant mucositis is considered as a preventive measure for the onset of peri‐implantitis. Therefore, the remit of this working group was to assess the prevalence of peri‐implant diseases, as well as risks for peri‐implant mucositis and to evaluate measures for the management of peri‐implant mucositis.
Methods
Discussions were informed by four systematic reviews on the current epidemiology of peri‐implant diseases, on potential risks contributing to the development of peri‐implant mucositis, and on the effect of patient and of professionally administered measures to manage peri‐implant mucositis. This consensus report is based on the outcomes of these systematic reviews and on the expert opinion of the participants.
Results
Key findings included: (i) meta‐analysis estimated a weighted mean prevalence for peri‐implant mucositis of 43% (CI: 32–54%) and for peri‐implantitis of 22% (CI: 14–30%); (ii) bleeding on probing is considered as key clinical measure to distinguish between peri‐implant health and disease; (iii) lack of regular supportive therapy in patients with peri‐implant mucositis was associated with increased risk for onset of peri‐implantitis; (iv) whereas plaque accumulation has been established as aetiological factor, smoking was identified as modifiable patient‐related and excess cement as local risk indicator for the development of peri‐implant mucositis; (v) patient‐administered mechanical plaque control (with manual or powered toothbrushes) has been shown to be an effective preventive measure; (vi) professional intervention comprising oral hygiene instructions and mechanical debridement revealed a reduction in clinical signs of inflammation; (vii) adjunctive measures (antiseptics, local and systemic antibiotics, air‐abrasive devices) were not found to improve the efficacy of professionally administered plaque removal in reducing clinical signs of inflammation.
Conclusions
Consensus was reached on recommendations for patients with dental implants and oral health care professionals with regard to the efficacy of measures to manage peri‐implant mucositis. It was particularly emphasized that implant placement and prosthetic reconstructions need to allow proper personal cleaning, diagnosis by probing and professional plaque removal.
Although postnatal corticosteroid (CS) therapy has well established beneficial effects on pulmonary function, it may also result in growth restriction during treatment. The course of early childhood ...growth is believed to predict cardiovascular and metabolic diseases in adulthood. Therefore, we determined the effects of postnatal dexamethasone (DEX) or hydrocortisone (HC) treatment on patterns of postnatal growth until approximately four years of age.
In an observational cohort study of children born prematurely (<32 weeks of gestation), we compared growth patterns for body weight, height, and head circumference from birth to age four years, of children who received DEX (boys: N = 30, girls: N = 14), HC (boys: N = 33, girls: N = 28) to a reference group that had not received postnatal CSs (boys: N = 52, girls: N = 53) using linear mixed-effects modeling.
Growth velocity curves of CS-treated neonates showed a shift to the right, representing a delay in time. They had decreased absolute growth velocities during and shortly after treatment, followed by an increase in growth velocity thereafter. A shift to the right was also seen for the age at which maximal growth velocity of weight/height was reached in boys and girls. Fractional growth rates of weight, height, and head circumference were generally reduced in the CS-treated groups during the first two months of age, with catch-up growth in the following months. In DEX-treated infants these changes were more pronounced than in HC-treated infants.
These data suggest that postnatal growth patterns of preterm born infants are affected by CS-treatment, more by DEX than by HC. Effects were observed mainly on growth velocities. This observation may have impact on health in later life for those individuals treated with CSs in the neonatal period. A definitive conclusion would require a randomized trial of these therapies.
PDF
