Comparison of peri‐implant clinical and radiographic inflammatory parameters among cigarette and waterpipe (narghile) smokers and never‐smokers

1 Background

The authors hypothesized that peri‐implant clinical and radiographic inflammatory parameters are worse in waterpipe smokers (WS) and cigarette smokers (CS) compared with never‐smokers (NS). The aim of the present retrospective study is to compare peri‐implant clinical and radiographic inflammatory parameters among WS, CS, and NS.

2 Methods

Forty‐four CS (group 1), 41 WS (group 2), and 43 NS (group 3) were included. Demographic data were collected using a questionnaire. Peri‐implant plaque index (PI), bleeding on probing (BOP), and probing depth (PD) were measured, and crestal bone loss (CBL) was assessed on standardized digital radiographs. Sample size was estimated, and statistical analyses were performed using Kruskal–Wallis and Wilcoxon rank‐sum tests. For multiple comparisons, Bonferroni post hoc test was performed. P values < 0.05 were considered statistically significant.

3 Results

Peri‐implant PI and PD were higher in groups 1 (P < 0.05) and 2 (P < 0.05) compared with group 3. Peri‐implant BOP was significantly higher in group 3 compared with individuals in groups 1 (P < 0.01) and 2 (P < 0.01). Peri‐implant total marginal bone loss was significantly higher in groups 1 (P < 0.05) and 2 (P < 0.05) compared with group 3. There were differences in PI, BOP, PD, and CBL among participants in groups 1 and 2.

4 Conclusions

Peri‐implant soft tissue inflammatory parameters and CBL are worse in CS and WS compared with NS. There is no difference in these parameters between CS and WS.     

Management of peri‐implant mucositis and peri‐implantitis

Peri‐implant diseases are defined as inflammatory lesions of the surrounding peri‐implant tissues and include peri‐implant mucositis (an inflammatory lesion limited to the surrounding mucosa of an implant) and peri‐implantitis (an inflammatory lesion of the mucosa that affects the supporting bone with resulting loss of osseointegration). This review aims to describe the different approaches to manage both entities and to provide a critical evaluation of the evidence available on their efficacy. Therapy of peri‐implant mucositis and nonsurgical therapy of peri‐implantitis usually involve mechanical debridement of the implant surface using curettes, ultrasonic devices, air‐abrasive devices or lasers, with or without the adjunctive use of local antibiotics or antiseptics. The efficacy of these therapies has been demonstrated for mucositis: controlled clinical trials show an improvement in clinical parameters, especially in bleeding on probing. For peri‐implantitis, the results are limited, especially in terms of probing pocket‐depth reduction. Surgical therapy of peri‐implantitis is indicated when nonsurgical therapy fails to control the inflammatory changes. Selection of the surgical technique should be based on the characteristics of the peri‐implant lesion. In the presence of deep circumferential and intrabony defects, surgical interventions should aim to provide thorough debridement, implant‐surface decontamination and defect reconstruction. In the presence of defects without clear bony walls or with a predominant suprabony component, the aim of the surgical intervention should be the thorough debridement and the repositioning of the marginal mucosa to enable the patient to perform effective oral‐hygiene practices, although this aim may compromise the esthetic result of the implant‐supported restoration.     

Animal models for peri‐implant mucositis and peri‐implantitis

The treatment of infectious diseases affecting osseointegrated implants in function has become a demanding issue in implant dentistry. Since the early 1990s, preclinical data from animal studies have provided important insights into the etiology, pathogenesis and therapy of peri‐implant diseases. Established lesions in animals have shown many features in common with those found in human biopsy material. The current review focuses on animal studies, employing different models to induce peri‐implant mucositis and peri‐implantitis.     

Clinical approaches to treat peri‐implant mucositis and peri‐implantitis

Therapies proposed for the treatment of peri‐implant diseases are primarily based on the evidence available from treating periodontitis. The primary objective is elimination of the biofilm from the implant surface, and nonsurgical therapy is a commonly used treatment. A number of adjunctive therapies have been introduced to overcome accessibility problems or difficulties with decontamination of implant surfaces as a result of specific surface characteristics. It is now accepted that following successful decontamination, clinicians can attempt to regenerate the bone that was lost as a result of infection. The ultimate goal is re‐osseointegration, and a number of regenerative techniques have been introduced. By reviewing the existing evidence, it seems that peri‐implant mucositis is reversible when appropriately treated. Additionally, a combined therapy (mechanical therapy with local antimicrobials as adjuncts) can serve as an alternative to surgical intervention when treating peri‐implantits in cases not suitable for surgery. Surgical therapy is an effective method for treating peri‐implantitis, and various degrees of success of the use of regenerative procedures have been reported, regardless of whether or not radiographic evidence of defect fill has been achieved. Finally, no matter which therapy is employed, a prerequisite for the long‐term stability of treatment results obtained is the ability of the patient to maintain good oral hygiene.     

The evaluation of peri‐implant sulcus fluid osteocalcin,osteopontin, and osteonectin levels in peri‐implant diseases

1 Background

Peri‐implant mucositis is an inflammation of the soft tissues surrounding an implant. Peri‐implantitis refers to a process characterized by peri‐implant bone loss along with an inflammation of the soft tissues. Osteocalcin, osteopontin, and osteonectin proteins are related to bone remodeling. The aim of the present study was to investigate peri‐implant sulcus fluid (PISF) osteocalcin, osteopontin, and osteonectin levels in peri‐implant mucositis and peri‐implantitis.

2 Methods

Fifty‐two implants with peri‐implantitis, 46 implants with peri‐implant mucositis, and 47 control implants were included in the study. Clinical parameters including probing depth, modified sulcus bleeding index and modified plaque index were recorded. PISF osteocalcin, osteopontin, and osteonectin levels were analyzed by ELISA kits.

3 Results

There were no significant differences in PISF osteocalcin, osteopontin, and osteonectin total amounts between healthy controls, peri‐implant mucositis and peri‐implantitis groups (P > 0.05). Probing depths were not correlated with PISF osteocalcin, osteopontin, and osteonectin levels in the study groups (P > 0.05).

4 Conclusions

Soft tissue inflammation around dental implants does not cause a change in osteocalcin, osteopontin, and osteonectin levels in PISF. Also, peri‐implantitis does not seem to give rise to an increase in PISF levels of osteocalcin, osteopontin, and osteonectin.     

Clinical and radiographic peri‐implant parameters and proinflammatory cytokine levels among cigarette smokers,smokeless tobacco users,and nontobacco users

Background

It is postulated that clinical and radiographic peri‐implant parameters are worse and levels of interleukin (IL)‐1β and matrix metalloproteinase (MMP)‐9 in the peri‐implant sulcular fluid (PISF) are higher in cigarette‐smokers (CS) and smokeless‐tobacco users (STU) compared with nontobacco user (NTU).

Purpose

The present study aimed to compare clinical and radiographic peri‐implant inflammatory parameters and levels of IL‐1β and MMP‐9 levels among CS, STU, and NTU.

Materials and Methods

Forty‐five CS (Group‐1), 42 STU (Group‐2), and 44 NTU (Group‐3) were included. Demographic data was collected using a structured baseline questionnaire. Peri‐implant plaque index (PI), bleeding on probing (BOP), and probing depth (PD) were recorded and crestal bone loss (CBL) were assessed using standardized digital radiographs. PISF volume and levels of IL‐1β and MMP‐9 in PISF were quantified using enzyme‐linked immunosorbent assay. Clinical peri‐implant parameters and PISF IL‐1β and MMP‐9 concentrations were analyzed with Kruskal‐Wallis test. Bonferroni post hoc adjustment test was used for multiple comparisons. P‐value was set at .05.

Results

Peri‐implant PI and PD were significantly worse in group‐1 and group‐2 patients as compared to group‐3 individuals (P < .05). Peri‐implant CBL was also significantly higher in group‐1 and group‐2 compared with group‐3 (P < .05). Peri‐implant BOP was significantly higher in group‐2 and group‐3 as compared to group‐1 individuals (P < .05). The PISF volume (P < .05) collected and levels of IL‐1β and MMP‐9 were statistically significantly elevated among individuals in group‐1 and group‐2 compared with group‐3 (P < .01). There was no significant difference in PI, PD, CBL, and PISF levels of IL‐1β and MMP‐9 among participants in groups 1 and 2.

Conclusion

Clinical and radiographic peri‐implant parameters were compromised among CS and STU as compared to NTU. Increased expression of local proinflammatory cytokines may explain greater susceptibility of CS and STU to peri‐implant breakdown.     

Comparison of peri‐implant clinical and radiographic status around short (6 mm in length) dental implants placed in cigarette‐smokers and never‐smokers: Six‐year follow‐up results

Background

It is hypothesized that peri‐implant clinical and radiographic inflammatory parameters (probing depth [PD], bleeding on probing [BOP] and plaque index [PI]; and radiographic (crestal bone loss [CBL]) are worse among cigarette‐smokers (CS) compared with never‐smokers (NS) with short implants.

Purpose

The present 6‐year follow‐up retrospective study compared the peri‐implant clinical and radiographic parameters in CS and NS with short dental implants (6 mm in length).

Materials and methods

Fifty‐six male individuals were included. These individuals divided into 2 groups as follows: (a) Group‐1: 29 self‐reported systemically healthy CS with 48 short‐implants; and (b) Group‐2: 27 self‐reported systemically healthy NS with 43 short implants. Peri‐implant PD, PI, BOP, and CBL were measured. Group comparisons were done using the Kruskal‐Wallis test and sample size was estimated. Level of significance was set at P values < .05.

Results

In groups 1 and 2, the follow‐up durations were 6.2 ± 0.1 years and 6.1 ± 0.3 years, respectively. A cigarette smoking history of 8.9 ± 3.6 pack years was reported by individuals in Group‐1. At follow‐up, scores of peri‐implant PD, BOP, PI, and mesial and distal CBL were comparable around short implants in both groups.

Conclusion

Under strict oral hygiene maintenance protocols, short dental implants can remain functionally stable in CS in a manner similar to NS.