Effects of gingival retraction materials on gingival blood flow

PURPOSE: The effects of 2 chemical retraction agents on gingival blood flow and systemic blood pressure in subjects with healthy gingiva were investigated. MATERIALS AND METHODS: Thirty volunteer dental students were selected for the study and randomly divided into 2 groups. Aluminium chloride-impregnated cord (right side) and nonimpregnated cord (left side) were placed in the gingival sulcus of group 1. Epinephrine-impregnated cord (right side) and nonimpregnated cord (left side) were placed in group 2. Blood flow in the retracted marginal gingiva was measured by laser Doppler flowmetry, and the systemic blood pressures of subjects were recorded before and after the retraction procedure. RESULTS: A statistically significant decrease in blood flow was observed in group 2, but there was no significant change in gingival blood flow in group 1. A decrease in diastolic blood pressure of the subjects in group 2 was also observed. However, there was no significant change in blood pressure of the subjects in group 1. CONCLUSION: Gingival retraction affects gingival blood flow temporarily. Epinephrine-impregnated cords can be used safely in patients who have healthy gingiva, if patient stress and gingival trauma are avoided during cord placement.     

Amlodipine-induced gingival hyperplasia

Drug-induced gingival hyperplasia is a serious concern both for the patient and the clinician. A 45 year-old Caucasian male patient with hypertension, who received amlodipine (10 mg/day, single dose orally) for two months, sought medical attention because of the new-onset gingival enlargement. On clinical examination a generalized and firm overgrowth of the gingival throughout the maxilla and the mandible were evident. The lack of gingival inflammation and purulent discharge were other features of the clinical scenario. Histological assessment of the biopsy specimen revealed the hyperplasia of connective tissue, epithelial acanthosis, and elongated rete ridges along with few inflammatory cells. The histological and the clinical evidences were consistent with amlodipine-induced gingival hyperplasia. We believe that the present report indicates the most rapidly developed case of amlodipine-induced gingival hyperplasia reported to date. The related literature is reviewed and the underlying pathogenic mechanisms of this rare side-effect are discussed here.     

Cytotoxic effects of gingival retraction cords on human gingival fibroblasts in vitro

The objective of this study was to determine the cytocompatibility of three different extracts of gingival retraction cords and to compare the cytotoxic effect of these materials on human gingival fibroblasts. Gingival retraction cords impregnated with aluminium sulphate (Gingi-Aid), dl-adrenaline HCl (Gingi-Pak) and non-drug-impregnated cord (Gingi-Plain) were eluted with culture medium for 10 min and 24 h. Cytotoxicity was judged using a tetrazolium bromide reduction assay. Our data demonstrated that gingival retraction cords applied alone almost completely inhibited cell viability (P < 0.05). In addition, the results also showed that the eluates from aluminium sulphate-impregnated cord, dl-adrenaline HCl-impregnated cord and non-drug-impregnated cord were cytotoxic to primary human gingival fibroblast cultures (P < 0.05). The cell viability of incubation of gingival fibroblasts containing 10-min eluates of aluminium sulphate, dl-adrenaline HCl and non-drug-impregnated cord was 61, 21 and 70%, respectively. The cell viability of incubation of gingival fibroblasts containing 24 h eluates of aluminium sulphate, dl-adrenaline HCl and non-drug-impregnated cord was 68, 58 and 72%, respectively. It was found that dl-adrenaline HCl-impregnated gingival retraction cord was the most toxic gingival retraction cord among the materials tested in all cultures (P < 0.05). The cytotoxicity decreased in an order of dl-adrenaline HCl-impregnated cord > aluminium sulphate-impregnated cord > non-drug-impregnated cord. The extent or degree of the cytotoxicity depended on the materials tested. Gingival retraction cords have significant potential for gingival toxicity. Careful management of gingiva retraction cords would lower the risk of potential gingival tissue damage during clinical application procedure and thus increase the success of prosthodontic procedures.     

环孢素诱导牙龈上皮细胞增生的机制

药物性牙龈增生(DGO)是由于服用免疫抑制剂、钙通道阻滞剂、抗癫痫药物等而引发的牙龈病变.传统意义上将DGO定义为服用某些药物引起的牙龈纤维增生和体积增大.近来发现,牙龈上皮细胞增厚也是引起DGO的重要原因之一.下文就环孢素抑制牙龈上皮程序性细胞死亡和促进牙龈上皮细胞增殖等机制作一.     

Smoking cessation increases gingival blood flow and gingival crevicular fluid

OBJECTIVES: The purpose of the present study was to determine the effect of smoking cessation on gingival blood flow (GBF) and gingival crevicular fluid (GCF). MATERIAL AND METHODS: Sixteen male smokers (aged 22-39 (25.3+/-4.0) years), with no clinical signs of periodontal and systemic diseases, were recruited. The experiment was performed before (baseline) and at 1, 3 and 5 days, and at 1, 2, 4 and 8 weeks after smoking cessation. The status of smoking and smoking cessation was verified by exhaled carbon monoxide (CO) concentration, and by serum nicotine and cotinine concentrations. A laser Doppler flowmeter was used to record relative blood flow continuously, on three gingival sites of the left maxillary central incisor (mid-labial aspect of the gingival margin and bilateral interdental papillae). The GCF was collected at the mesio- and disto-labial aspects of the left maxillary central incisor and the volume was calculated by the Periotron 6000(R) system. The same measurements except for the GBF were performed on 11 non-smoking controls (four females and seven males), aged 23-27 (24.4+/-1.2) years. RESULTS: Eleven of 16 smokers successfully completed smoking cessation for 8 weeks. At 1 day after smoking cessation, there was a significantly lower CO concentration than at baseline (p<0.01). Also, nicotine and cotinine concentrations markedly decreased at the second measurement. The GBF rate of smokers was significantly higher at 3 days after smoking cessation compared to the baseline (p<0.01). While the GCF volume was significantly increased at 5 days after smoking cessation compared to the baseline (p<0.01), it was significantly lower than that of non-smokers until 2 weeks after smoking cessation (p<0.01). CONCLUSION: The results show that the gingival microcirculation recovers to normal in the early stages of smoking cessation, which could activate the gingival tissues metabolism/remodeling, and contribute to periodontal health.     

Nifedipine-induced gingival overgrowth in the presence or absence of gingival inflammation in rats

One adverse effect of nifedipine, a long-acting vasodilator, is gingival overgrowth. Preexisting gingival inflammation and/or dental plaque has been suggested to be responsible for the progression of this side effect, but the precise mechanism is uncertain because of a lack of suitable animal models. A study was therefore done to establish an experimental model of gingival overgrowth in rats and to investigate the possible involvement of gingival inflammation and/or dental plaque in its development. Specific pathogen-free Fischer rats (male, 14 days old) were used . Gingival inflammation and dental plaque accumulation were induced by infection with Streptococccus mutans MT8148R. The nifedipine-treated rats (experimental group) were fed a caries-inducing diet contai ning nifedipine either with or without infection, while the nifedipine-untreated rats (control group) were fed the same diet, similarly with or with out the infection. Marked gingival overgrowth was induced in the mandibular molar region of nifedipine-treated rats regardless of S. mutans infection, although the infection resulted in a further increase in the degree of gingival overgrowth. Histological examination of the gingival overgrowth revealed the presence of redundant subepithelial connective tissue in the treated rats, and inflammatory cell infiltration was apparent only in the tissue of the S. mutans-infected rats regardless of the nifedipine administration. These findings suggest that nifedipine induces gingival overgrowth in rats either in the presence or absence of gingival inflammatio n and/or dental plaque, although these factors can augment the effect of the drug. Our experimental system seems to be a useful model for studying the mechanism of this side effect.     

Plasma and gingival crevicular fluid phenytoin concentrations as risk factors for gingival overgrowth

BACKGROUND: Gingival enlargement is one of the side effects associated with the administration of phenytoin. The mechanism by which phenytoin induces gingival enlargement is not well understood. This study was conducted to investigate the relationship between plasma and gingival crevicular fluid (GCF) phenytoin concentrations and the degree of gingival overgrowth in patients with similar gingival and plaque indices and also to determine the risk factors for gingival enlargement. METHODS: Eighteen patients taking phenytoin in regular doses > or =6 months prior to the investigation participated in the study. Gingival enlargement was evaluated with two indices to score vertical and horizontal overgrowth. The gingival index (GI), plaque index (PI), gingival bleeding time index (GBTI), probing depth (PD), and clinical attachment level (CAL) were also evaluated. GCF and plasma phenytoin concentrations were determined by using high-performance liquid chromatography (HPLC). RESULTS: There was no significant difference between responders and non-responders for PD, CAL, PI, GI, and GBTI. Phenytoin was detected in all of the GCF and plasma samples using the HPLC analysis method. The mean concentration of phenytoin in GCF was significantly greater than the concentration of phenytoin in plasma. No significant difference was observed for the concentration of GCF phenytoin between responders and non-responders. However, the concentration of plasma phenytoin was significantly higher in responders than non-responders. CONCLUSION: This study showed that plasma phenytoin level appeared to be a risk factor for phenytoin-induced gingival overgrowth.     

Retrospective investigation of gingival invaginations

BACKGROUND AND OBJECTIVE: Gingival invaginations are a frequent finding during tooth extraction and following orthodontic space closure. Based on the interdental localization and sometimes pronounced depth, it has been suggested that a gingival invagination may impede oral hygiene. In Part I of this series, the time until active tooth movement and the localization of extraction were identified as potential risk factors for the development of gingival invagination. The aims of the present study were the analysis of the microbial spectrum of a gingival invagination in comparison with pool samples of the sulcus of Ramfjord teeth, on the one hand, and the importance of genetic variations of the pro-inflammatory mediator interleukin-1 (IL-1) and its receptor antagonist (IL-1-RN), on the other hand. In addition, a possible role of smoking as a risk factor was evaluated. SUBJECTS AND METHODS: A total of 30 patients with (n=16) and without (n=14) gingival invagination were examined for the presence of eleven periodontal pathogen bacterial species with a commercially available test (micro-IDent?Plus, Hain Lifescience, Nehren, Germany). The genetic evaluation was performed with the GenoType? IL-1 test (Hain Lifescience). RESULTS: The results of the microbiological analysis of gingival invaginations showed that the bacterial flora might differ or even be higher than the pool sample from sulcus regions. The genetic evaluation demonstrated that in the group without gingival invagination only 14% showed an IL-1 polymorphism, whereas this value was twice as high (35%) in the group with gingival invagination. In addition, a combination of both polymorphisms IL-1 and IL-1-RN was only found in patients with gingival invagination (25%). Interestingly, smoking patients showed a significant increase of the severity of the gingival invagination. CONCLUSION: This retrospective study demonstrated that gingival invagination might be accompanied with an altered microbiological bacterial spectrum and a genetic IL-1 polymorphism. In addition, smoking was identified as another potential risk factor for the severity of gingival invaginations.     

三种排龈方法对龈沟液含量及成分的影响

目的：通过对3种临床常用排龈方法排龈后龈沟液及其成分的研究,筛选对牙周组织损伤最小的排龈方法,为临床工作提供实验依据。方法：对10名受试者随机化分组,每名受试者口内3个第二前磨牙分别采用Ultrapak不含药排龈线、Ultrapak盐酸肾上腺素排龈线、Expasyl排龈膏进行排龈,于排龈前、排龈后30min、1d、3d、7d、14d、28d提取受试牙位龈沟液,称重并检测其中天冬氨酸转氨酶（AST）和碱性磷酸酶（ALP）活性水平。结果：以时间作为整体因素考虑,3种排龈方法没有统计学差异。龈沟液量的变化：不含药排龈线在排龈后1d、3d龈沟液的量明显高于排龈前,含药排龈线在排龈后30min、1d、3d、7d明显高于排龈前,两组差异均有统计学意义（P〈0.05）;排龈膏在排龈后1d、3d、7d龈沟液的量明显高于排龈前,差异具有统计学意义（P〈0.01）。AST含量变化：不含药排龈线和含药排龈线组在排龈后1d、3d、7d明显高于排龈前,差异具有统计学意义（P〈0.05）,排龈膏组仅在3d时与排龈前有统计学差异（P〈0.05）。ALP含量的变化：含药排龈线仅在排龈后3d时与排龈前有统计学差异（P〈0.05）,而不含药排龈线和排龈膏在各个时相均与排龈前无统计学差异。结论：三种排龈方法对牙周组织都存在一定损伤,排龈线对牙周组织造成的急性损伤最重但恢复较快,排龈膏损伤较小但恢复也较慢。     

Pathogenesis of cyclosporine induced gingival overgrowth

Several studies, during the last 20 years, tried to explain the pathogenetic mechanisms of the cyclosporine (CS) induced gingival overgrowth (and in general, of the drugs induced gingival overgrowth), but they are still poorly understood. The relationship between the drug and the different pharmacokinetic variables (dosage, duration of therapy, plasmatic and salivary Cs concentration) is still on discussion. It is accepted that a threshold concentration is necessary, in the gingival tissues, to begin or to enhance the morphostructural changes of the gums, but the total Cs weight, from the beginning of the therapy to the time of clinical examinations, has to be evaluated. The pharmacokinetic variables are associated with many other factors (first of all the oral hygiene score) that are probably connected with the developing of the gingival lesions. Gingival inflammation could be very important in the pathogenesis of gingival overgrowth. It has been shown by several cross-sectional studies a strong association between plaque and gingival lesions, but it is not yet clear if plaque accumulation is a causal factor or a consequence of the morphological gums changes. It would seem that the morphological alterations, in drug-induced gingival overgrowth, could be started by the plaque induced inflammation, and this would lead to an hyperemic and edematous gingival tissue. Oral hygiene (professional and at home) is more difficult and represents an irritation factor that makes the pathological cycle to go on. Other factors, probably connected with the cyclosporine induced gingival overgrowth, are represented by age, gender, genetic predisposition, alterations of gingival connective homeostasis and metabolism, inflammatory alterations, interactions with the growth factors and protective or synergic effects of other drugs.     

Nitrendipine-induced gingival overgrowth in dogs

This study assessed the development of gingival overgrowth in dogs given nitrendipine, a new antihypertensive dihydropyridine. Nine male Beagle dogs with established plaque and gingivitis were used. Following a baseline examination, which involved assessment of plaque, gingivitis, and gingival enlargement, six dogs (test) received nitrendipine twice daily in a high dose, while 3 dogs (control) received placebo. Clinical scorings were repeated after 10 and 20 weeks. At termination of the study gingival biopsies were excised and examined morphometrically. Already at the 10-week examination definite changes in gingival size had occurred, and following 20 weeks of nitrendipine treatment the gingival enlargement had markedly increased. In none of the control dogs were there any signs of gingival size changes. The histopathological examination showed that the only principal changes in histopathological morphology were that areas of non-infiltrated connective tissue in test specimens showed an increase in vascularity and appeared more loose compared with the dense tissue in control specimens. The morphometric analysis demonstrated minor differences between test and control specimens in regard to all tissue fractions observed; however, such differences were numerically very small, and were not considered biologically significant. Thus, the results demonstrated that nitrendipine administered to Beagle dogs during a 20-week period causes marked overgrowth of gingival tissue of apparently normal composition. The fact that cases of gingival overgrowth have been reported among patients receiving other dihydropyridines suggest that the observed gingival overgrowth is an effect of this class of drugs.     

Pre-transplant gingival hyperplasia predicts severe cyclosporin-induced gingival overgrowth in renal transplant patients

Abstract. The relationship between the pre-transplant periodontal status and the development of post-transplant gingival overgrowth was investigated in a longitudinal study. The periodontal condition of 35 patients was examined on 2 occasions while they were on the transplant waiting list and then at 4–6, 10–12, 16 and 20 weeks post-transplant. At each visit the plaque index, the bleeding index and a pocket index (CPITN) were measured. Dental impressions were taken of the pre- and post-transplant gingival condition and used to make stone models which were used to score the gingival overgrowth index (GOI). The patients divided into 3 distinct groups having severe ( n = 13), mild ( n = 16) or no post-transplant gingival overgrowth ( n =6). Only 1 of the patients had taken cyclosporin prior to inclusion into the study. All the patients who developed severe overgrowth had evidence of gingival hyperplasia before the transplant. There was no difference in the serum cyclosporin levels between the three groups (χ²<2.28, p >0.319). Furthermore, there was no statistical difference for any of the periodontal indices. This study indicates that the hyperplastic gingival inflammatory response of some individuals appears to be potentiated by cyclosporin resulting in severe post-transplant overgrowth. In other patients the same reaction may allow the fibroblastic activity to occur to an extent where it produces a mild clinically apparent overgrowth.     

Dental plaque-induced gingival diseases

Gingival diseases are a diverse family of complex and distinct pathological entities found within the gingiva that are the result of a variety of etiologies. There are several clinical characteristics common to all gingival diseases and these features include clinical signs of inflammation, signs and symptoms that are confined to the gingiva, reversibility of the disease by removing the etiology, the presence of bacterial laden plaque to initiate and/or exacerbate the severity of the disease and a possible role as a precursor for attachment loss around teeth. Defining and classifying gingival diseases has not been an easy task. The tools and methods to identify gingival diseases have varied depending on the criteria used by epidemiologists, researchers, or the practicing clinician. The classification of gingival disease in this review relied upon experimental and/or epidemiological human studies that accurately and reliably assessed an underlying functional derangement that was localized to the gingiva and was reported in a peer-reviewed journal. The classification of gingival diseases that depends on dental plaque to initiate the disease process(es) has been categorized into two groups. The two categories of plaque-induced gingival diseases are those affected by local factors and those that are affected by local factors and modified by specific systemic factors found in the host. In this review, the clinical characteristics of gingival disease associated with plaque, endogenous hormone fluctuations, drugs, systemic diseases, and malnutrition were investigated.     

Immunohistochemical demonstration of the plasminogen activator system in human gingival tissues and gingival fibroblasts

The relative distribution of urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) was studied in cultured human gingival fibroblasts, healthy gingival tissues and inflamed gingival tissues by immunohistochemistry. In cultured gingival fibroblasts t-PA, u-PA and PAI-1 were expressed in cytoplasm; u-PA and PAI-1 were more intensely stained than t-PA; PAI-2 was not detectable in gingival fibroblasts. Following interleukin 1β (IL-1β) stimulation, the intensity of intracellular staining for t-PA was increased and a number of cells staining strongly for PAI-2 were seen; no difference in the intensity of immunostaining level was noted for the expression of u-PA and PAI-1 between IL-1β stimulated cells and unstimulated cells. In healthy gingival tissues, u-PA and PAI-1 displayed a wide distribution throughout all the connective tissue and epithelium; t-PA localized mainly in the connective tissue while PAI-2 showed little association with the connective tissue but did faintly stain in the epithelial layer. In inflamed gingival tissues, staining for t-PA was significantly increased in the extracellular matrix of the connective tissue, whereas staining for u-PA, PAT-I and PAI-2 was found to be slightly increased, but no significant difference was noted for staining when compared with the healthy gingival tissues. A granular distribution of t-PA, u-PA, PAI-1 and PAI-2 was noted around areas of inflammatory cell infiltration. These immunohistochemical findings indicate that the plasminogen activator system produced by fibroblasts may be influenced by the presence of the inflammatory mediator IL-1β. In addition, the significant increase of t-PA in inflamed connective tissue and the wide expression of these components around inflamed cells may contribute to connective tissue degradation and may relate to the migration and localization of monocytes/macrophages in inflamed tissue.     

Retrospective investigation of gingival invaginations

Many orthodontic treatments involve tooth extraction. Gingival invagination is a common side effect after orthodontic extraction space closure leading to compromised oral hygiene and the space closure being hampered. Even the long-term stability of the orthodontic treatment result may be jeopardized. The aim of this study was to identify risk factors for the development of gingival invagination and possible implications on oral health and orthodontic treatment results.A total of 30 patients presenting 101 tooth extractions and subsequent orthodontic space closure were investigated to detect the presence of gingival invagination. The time required until active space closure, the thoroughness of space closure, and probing depths mesial and distal to the extraction site in addition to age, gender and the Periodontal Screening Index were investigated. A new coding system to describe the extent of gingival invagination is introduced for the first time here.Gingival invagination developed more frequently in the lower jaw (50%) than the upper (30%). Complete penetration occurred in the upper jaw in 6% of the patients and in the lower jaw in 25%. All patients without gingival invagination revealed complete space closure, whereas only 70% in the group with gingival invagination did so. The time until initiation of space closure took significantly longer in patients with gingival invagination (7.5 ± 1.4 months) than in patients without (3.3 ± 0.8 months). Probing depths of the adjacent teeth were significantly greater in regions with invaginations.Thus, the time required until space closure was initiated and the extraction site are important risk factors for the development of gingival invagination. The consequences of gingival invagination are instable space closure and deeper probing depths mesial and distal to the extractions. However, no statements concerning the mid- to long-term effects on oral health can be made.     

Disposition of nifedipine in plasma and gingival crevicular fluid in relation to drug-induced gingival overgrowth

The present study investigates the relationship between the pharmacokinetic variables of nifedipine with the incidence and severity of gingival overgrowth in 9 adult male patients medicated with the drug for at least 6 months. Five of the patients had experienced significant gingival changes and were thus designated "responders". The remaining four patients exhibited no gingival overgrowth, and thus acted as a control. A baseline periodontal examination (plaque scores, bleeding index and gingival overgrowth assessment) was carried out on each patient, and confined to the upper and lower anterior teeth. Serial blood and gingival crevicular fluid samples were collected over an eight-hour investigation period. Samples were analyzed for nifedipine by gas chromatography. No significant difference (p>0.05) was seen between responders and non-responders with regard to drug therapy, periodontal parameters or plasma pharmacokinetics of nifedipine. Nifedipine was detected in the gingival crevicular fluid of seven subjects (all responders, and two non-responders). The peak concentration of nifedipine in crevicular fluid was 15–90 fold greater than levels observed in plasma.     

Synthesis of sulfated glycosaminoglycans by human gingival fibroblasts from phenytoin-induced gingival overgrowth in vitro

The in vitro synthesis of sulfated glycosaminoglycans (GAGs) was studied in gingival fibroblasts from two patients exhibiting phenytoin(PHT)-induced gingival overgrowth, i.e. pseudopockets, which required surgical excision, from one patient on PHT medication not exhibiting pseudopockets and from two normal controls. The results showed that the newly synthesized GAGs were distributed to the culture medium, to a pericellular pool and to the cell fraction. Gingival fibroblasts from the PHT-induced gingival overgrowth showed a significantly increased incorporation of 35SO4(2-) into GAGs compared to the other strains, and this increase was mainly confined to the dermatan sulfate fraction. These results are in accordance with our previous biochemical studies where increased amounts of GAGs were found in gingival biopsies from the PHT-induced lesion.     

The relationship of gingival crevicular fluid short chain carboxylic acid concentration to gingival inflammation

Abstract Short-chain carboxylic acids (SCCA; C≤5: e.g., lactic acid, propionic acid, butyric acid) are metabolic by-products of bacterial metabolism which accumulate in the gingival crevice, and exhibit significant biological activity, including the ability to alter gene expression. It has been hypothesized that among the activities of SCCAs are their ability to contribute to gingival inflammation. This concept complements the notion that specific periodontal pathogens are the causative agents of gingival inflammation. To begin testing these 2 hypotheses, we examined the relationship between SCCA concentrations, specific putative periodontal pathogens, and gingival inflammation in medically healthy periodontally diseased subjects. We reasoned that if SCCAs and/or specific periodontal pathogens were causative gingival inflammatory agents, gingival inflammation should increase with increasing concentration of the inflammatory mediator. We also recognized that other clinical variables needed to be controlled for, and an objective quantitative assessment of gingival inflammation used. To accomplish these tasks, sites within subjects were stratified by location and pocket depth, and the following quantified: bacteria] presence; SCCA concentration: and gingival inflammation. The results indicated that gingival inflammation directly and significantly correlated with SCCA concentrations in the maxillary and mandibular molars, incisors and canines (all r≥0.47; all p≤ 0.015; too few bicuspids were available for complete analysis). The relationship between gingival inflammation and SCCA concentration was best described by a natural log relationship. Gingival inflammation did not, however, correlate positively with either the total number of specific putative periodontal pathogens, or the sum of subsets of these pathogens (?0.31 ≤r≤ 0.39; 0.08 ≤p 0.75) for any of the locations. Finally, the SCCA concentration did not correlate with the level of individual or groups of pathogens. These data, together with historical work and other preliminary data, support the hypothesis that SCCA, rather than specific putative periodontal pathogens, may be a causative agent in gingival inflammation. This work may, in part, begin to explain the apparent lack of a direct relationship between current gingival inflammation and the prediction of bacterially mediated periodontal attachment loss.     

Fluid dynamics of gingival tissues

Gingival hydraulic interstitial pressure was measured with glass micropipettes in 18 anesthetized rabbits at the level of the free gingiva, attached gingiva and oral mucosa facing the incisors and molar teeth. Samples of gingival interstitial tissue fluid were also collected by inserting nylon wicks in the subepithelial layer of the oral mucosa. Colloid osmotic pressure of interstitial fluid samples was measured with an osmometer whose membrane had a molecular cutoff of 30 kD. Hydraulic interstitial pressure from the free gingiva, at an average distance of 300 μm from sulcular space, was - 1.3 ± 0.9 (SD) cmH₂O. Mean colloid osmotic pressure of gingival tissues interstitial fluid was 13.1 cmH₂O, corresponding to a protein concentration of 2.8 g/dl. The thickness of the sulcular epithelium and of the oral gingival epithelium (data from 2 rabbits) were ～ 100 μm; the minimal distance of microvessels from the surface of the sulcular epithelium was ～150 μum. Based on hydraulic and colloid osmotic data, the Starling balance of pressures causes fluid filtration from gingival capillaries to gingival interstitium; however, across the sulcular epithelium, the pressure gradient sustains fluid absorption from the sulcus into the gingival interstitium. Plasma proteins may leak from microvessels into gingival interstitium, down convective bulk flow and via a concentration dependent diffusive component. At sulcular level, proteins may leak into the sulcus down a concentration gradient. Thus, at sulcular level a peculiar condition occurs in that there is an absorption gradient for water but a filtration gradient for plasma proteins.     

Treatment of gingival recession in two surgical stages: Free gingival graft and connective tissue grafting

This report describes a clinical case of severe Miller Class II gingival recession treated by two stages of surgery that combined a free gingival graft and connective tissue grafting. First, a free gingival graft (FGG) was performed to obtain an adequate keratinized tissue level. Three months later, a connective tissue graft (CTG) was performed to obtain root coverage. The results indicated that the FGG allows for a gain in the keratinized tissue level and the CTG allows for root coverage with decreased recession level after 16 months. Therefore, for this type of specific gingival recession, the combination of FGG and CTG can be used.