Analysis of Biomarkers and Marginal Bone Loss in Platform-Switched and Nonplatform-Switched Implants: A Randomized Clinical Trial.

Objectives: To compare the peri-implant crevicular fluid (PICF) biomarker levels, peri-implant status, and marginal bone level (MBL) differences of implants restored with randomly assigned nonplatform-switched (NPS) or platform-switched (PS) abutments. Methods: Ninety-four implants in 27 subjects were included in this study. Receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG), interleukin-1ß (IL-1ß), monocyte chemotactic protein-1 (MCP-1) levels in PICF, peri-implant health, and the change in the MBL were evaluated at the time of restoration (T 1) and after 12 months (T 2). Results: The IL-1ß levels decreased and the RANKL, OPG, and MCP-1 levels increased from T 1 to T 2 (P < 0.05) in both groups. RANKL/OPG ratio at T 1, MCP-1 levels at T 2, and the MCP-1 change from T 1 to T 2 were lower in the PS group than in the NPS group (P < 0.05). MBL change was lower (0.51 ± 0.31 mm) in the PS group than that (0.75 ± 0.29 mm) in the NPS group at T 2 (P < 0.001). Peri-implant health status between the study groups was negligible. Conclusion: PS was superior to NPS regarding the preservation of MBL. Higher MCP-1 levels, altered RANKL/OPG ratio, and lower OPG levels in the NPS group could be associated with subclinical peri-implant bone remodeling.

Evaluation of Surface Change and Roughness in Implants Lost Due to Peri-Implantitis Using Erbium Laser and Various Methods: An In Vitro Study.

The aim of our study was to obtain similar surface properties and elemental composition to virgin implants after debridement of contaminated titanium implant surfaces covered with debris. Erbium-doped:yttrium, aluminum, and garnet (Er:YAG) laser, erbium, chromium-doped:yttrium, scandium, gallium, and garnet (Er,Cr:YSGG) laser, curette, and ultrasonic device were applied to contaminated implant surfaces. Scanning electron microscopy (SEM) images were taken, the elemental profile of the surfaces was evaluated with energy dispersive X-ray spectroscopy (EDX), and the surface roughness was analyzed with profilometry. Twenty-eight failed implants and two virgin implants as control were included in the study. The groups were designed accordingly; titanium curette group, ultrasonic scaler with polyetheretherketone (PEEK) tip, Er: YAG very short pulse laser group (100 µs, 120 mJ/pulse 10 Hz), Er: YAG short-pulse laser group (300 µs, 120 mJ/pulse, 10 Hz), Er: YAG long-pulse laser group (600 µs, 120 mJ/pulse, 10 Hz), Er, Cr: YSGG1 laser group (1 W 10 Hz), Er, Cr: YSGG2 laser group (1.5 W, 30 Hz). In each group, four failed implants were debrided for 120 s. When SEM images and EDX findings and profilometry results were evaluated together, Er: YAG long pulse and ultrasonic groups were found to be the most effective for debridement. Furthermore, the two interventions have shown the closest topography of the sandblasted, large grit, acid-etched implant surface (SLA) as seen on virgin implants.

Immunohistochemical analysis of the gingiva with periodontitis of type I plasminogen deficiency compared to gingiva with gingivitis and periodontitis and healthy gingiva.

OBJECTIVE: Type I plasminogen deficiency (Plgdef) is an uncommon chronic inflammation of mucous membranes. Gingival enlargements usually proceed with progressive periodontal destruction and tooth-loss. Plasmin(ogen)-independent enzymatic mechanisms for fibrin clearance have already been discussed in the literature. Our primary objective was to verify, immunohistochemically, the occurrence of different enzymatic factors involved in tissue breakdown of inflamed compared to healthy gingiva. Secondly, we tried to find out, if these patients have a similar microbiological profile to the patients with known gingivitis and periodontitis. MATERIALS AND METHODS: Immunohistochemical analysis of enzymes elastase, plasminogen (plg), cathepsin G, matrix-metalloproteinase (MMP)-3 and MMP-7 and of glycoprotein fibrinogen were performed with gingival tissues from 3 healthy controls, 8 patients with Plgdef and 3 patients with gingivitis and periodontitis. Furthermore, plaque from 5 patients with plasminogen deficiency were also obtained to determine the microbiological profile. RESULTS: Significantly high numbers of elastase positive leukocytes were detected in all samples. Staining for MMP-3 and MMP-7 was seen in samples with gingivitis and periodontitis with a stronger staining in samples with periodontitis by Plgdef. Fibrinogen was detectable in all samples. Staining for plg was stronger in samples with periodontitis than in other samples. Staining for cathepsin G was weak in gingivitis and periodontitis. Subgingival microbial flora showed elevated colony forming units of Prevotella intermedia/nigrescens, Fusobacterium spp., Eikenella corrodens, Porphyromonas gingivalis and viridans streptococci. CONCLUSION: Strong staining of elastase, MMP-3 and MMP-7 and weak staining of plg in Plgdef samples supports the plasmin(ogen) - independent fibrin clearance. Similar subgingival microbiological flora was observed in periodontitis with Plgdef as in other periodontal diseases. Further investigations should determine the exact pathomechanism and focus on effective treatment methods of this entity.

Altered functional activity patterns of fibroblasts related to periodontitis by systemic plasminogen deficiency (ligneous periodontitis).

We report one case of ligneous periodontitis, which is a clinical sign of hypoplasmino-genemia. It appears as massive, painless ulcerated gingival enlargements and alveolar bone destruction in the affected area. The course of the disease is progressive and typically ends with early loss of teeth. At present, no efficient treatment option seems to be available. To investigate the cause of the rapid bone destruction in this disease, gingival tissue specimens were taken from one patient and a healthy control patient to compare the function of fibroblastic cells. Our results showed that diseased fibroblasts (1) reorganized collagen lattices more rapidly than normal cells, (2) demonstrated a greater overall production of pro and active matrix metalloproteinase-2 (MMP-2) and increased activation of this protease, and (3) showed a more active phenotype than healthy fibroblastic cells. From these preliminary results, there seems to be increased MMP-2 production and activation, which might be one compensatory (but insufficient) mechanism for the decreased (plasmin-dependent) pericellular fibrinolysis in plasminogen-deficient patients. Further studies on this subject should evaluate the exact pathomechanism of plasminogen on this enzymatic bone and connective tissue destruction.

Identification of three novel plasminogen (PLG) gene mutations in a series of 23 patients with low PLG activity.

Inherited severe hypoplasminogenaemia is a multisystemic disorder leading to deficient extravascular fibrinolysis. As a clinical consequence wound healing capacity of mucous membranes is markedly impaired leading to ligneous conjunctivitis and several other manifestations. Here we report the molecular genetic and clinical findings on 23 new cases with severe hypoplasminogenaemia. Homozygous or compound-heterozygous mutations in the plasminogen (PLG) gene were found in 16 of 23 patients (70%), three of which were novel mutations reported here for the first time (C166Y, Y264S, IVS10-7T/G). Compared to 79 previously published cases, clinical manifestations of the current group of patients showed higher percentages of ligneous periodontitis, congenital hydrocephalus, and involvement of the female genital tract. In contrast, involvement of the gastrointestinal or urogenital tract was not observed in any of the cases. Patients originated to a large extent (61%) from Turkey and the Middle East, and showed a comparably frequent occurrence of consanguinity of affected families and a greater female to male ratio than was derived from previous reports in the literature. Individual treatment of ligneous conjunctivitis included topical plasminogen or heparin eye drops, topical or systemic fresh frozen plasma, and surgical removal of ligneous pseudomembranes, mostly with modest or transient efficacy. In conclusion, the present study underscores the broad range of clinical manifestations in PLG-deficient patients with a trend to regional differences. Transmission of genetic and clinical data to the recently established Plasminogen Deficiency Registry should help to determine the prevalence of the disease and to develop more efficient treatment strategies.

An atypical form of necrotizing periodontitis.

BACKGROUND: Necrotizing ulcerative gingivitis/periodontitis are considered necrotizing periodontal diseases. This case report presents an atypical form of necrotizing periodontitis, which does not fit into this classification. METHODS: A 12-year-old child was referred to our clinic for gingival inflammation, extensive alveolar bone loss, and tooth mobility. Clinical and microbiologic examinations were carried out, and radiographs were taken. Clinical examination revealed soft and hard tissue destruction up to the mucogingival junction at the right maxillary premolar and mandibular incisors. Unusual infections or abnormalities in systemic functions were not detected through clinical and laboratory evaluations made at the Pediatrics Department, Istanbul University. Although an intensive established treatment protocol for necrotizing periodontitis was completed, management of long-standing health conditions could not be achieved because of recurrence of the disease, which caused us to repeat this treatment protocol at short intervals. RESULTS: Investigation led to a diagnosis of an atypical form of necrotizing periodontitis because the disease had a recurrent acute phase even under a standard treatment protocol. CONCLUSIONS: Our patient exhibits an unusual, necrotizing form of periodontal disease. The reason for the rapid rate of periodontal disease progression remains unclear.

Hypoplasminogenemia with ligneous periodontitis: a failed local therapeutic approach.

BACKGROUND: Hypoplasminogenemia is a rare condition that is associated with ligneous conjunctivitis, a form of chronic conjunctivitis characterized by firm, fibrin-rich, pseudomembranous lesions on the tarsal conjunctivae and oral lesions. Pseudomembranes may develop on the gingivae, and there may be periodontal involvement. METHODS: Several therapeutic approaches have been developed to treat such patients, but they have had limited effect. We used gingivectomies, topical heparin, and corticosteroids to treat periodontal lesions in an 18-year-old girl. RESULTS: This approach had no benefit. CONCLUSION: The question remains about how best to manage patients with hypoplasminogenemia.

Molecular and clinical spectrum of type I plasminogen deficiency: A series of 50 patients.

Severe type I plasminogen (PLG) deficiency has been causally linked to a rare chronic inflammatory disease of the mucous membranes that may be life threatening. Here we report clinical manifestations, PLG plasma levels, and molecular genetic status of the PLG gene of 50 patients. The most common clinical manifestations among these patients were ligneous conjunctivitis (80%) and ligneous gingivitis (34%), followed by less common manifestations such as ligneous vaginitis (8%), and involvement of the respiratory tract (16%), the ears (14%), or the gastrointestinal tract (2%). Four patients showed congenital occlusive hydrocephalus, 2 with Dandy-Walker malformation of cerebellum. Venous thrombosis was not observed. In all patients, plasma PLG levels were markedly reduced. In 38 patients, distinct mutations in the PLG gene were identified. The most common genetic alteration was a K19E mutation found in 34% of patients. Transient in vitro expression of PLG mutants R134K, delK212, R216H, P285T, P285A, T319_N320insN, and R776H in transfected COS-7 cells revealed significantly impaired secretion and increased degradation of PLG. These results demonstrate impaired secretion of mutant PLG proteins as a common molecular pathomechanism in type I PLG deficiency.

Endothelial dysfunction in patients with chronic periodontitis and its improvement after initial periodontal therapy.

BACKGROUND: Recent epidemiological data suggested that there is a relationship between periodontal health and atherosclerotic coronary heart disease. Although hypothetical models were proposed, the exact mechanism of this association has not been clarified. The aim of this study is to investigate whether there is an endothelial dysfunction in patients with chronic periodontitis and, if present, whether recovery is possible with therapy. METHODS: The study groups consisted of 28 patients (mean age: 45.5 +/- 8.6 years) with chronic periodontitis and without any atherosclerotic vascular disease, and 26 healthy controls (mean age: 43.7 +/- 6.8 years). Cardiovascular risk factors were investigated in both groups. Brachial artery responses to reactive hyperemia (endothelium-dependent dilatation [EDD]) and sublingual nitroglycerin (endothelium-independent dilatation [EID]) were measured using high-resolution vascular ultrasound in both groups. Measurements were taken before and after initial periodontal therapy in the periodontal patients. RESULTS: There was no significant difference between the groups with regard to cardiovascular risk factors. In the baseline measurements, EDD and EID were significantly impaired in patients with chronic periodontitis when compared with the controls (8.4% +/- 4.0% versus 19.4% +/- 8.1%, P<0.0001; 13.3% +/- 6.3% versus 29.5% +/- 10.0%, P<0.0001 for EDD and EID, respectively). After non-surgical periodontal therapy, EDD and EID improved significantly (from 8.4% +/- 4.0% to 17.7% +/- 5.7%, P<0.0001; and from 13.3% +/- 6.3% to 24.9% +/- 7.3%, P<0.0001 for FMD and EID, respectively). The EDD and EID changes in the controls were insignificant. CONCLUSION: This study showed that endothelial functions were impaired in patients with chronic periodontitis and that they improve following initial periodontal therapy.