Apical Migration Of Junctional Epithelium Research Articles

Stage III Grade A Mandibular Anterior Tooth Periodontitis Treatment

Chronic periodontitis is inflammation caused by periodontopathogenic microorganisms characterized by alveolar bone resorption, loss of attachment and apical migration of junctional epithelium. Non-surgical and surgical periodontitis treatments including curettage are performed to reduce inflammation and form new attachments before flap surgery. The purpose of this writing is to treat periodontitis before flap surgical treatment is carried out. Case report: Female, 39 years old, came to RSGM UMY with complaints of loose lower front teeth and gums that bleed easily when brushing her teeth. The patient had no history of systemic disease. Intra-oral examination at the first visit revealed that the gingiva of the mandibular anterior teeth was reddish, unstippling and loose texture grade 2, OHI 7.3 (poor), PD 8 mm, PI score 30%, CAL 8 mm, and 3 tooth loss due to periodontitis. X-ray results showed resorption of the alveolar bone horizontally in the apical 1/3. DHE treatment plan, scaling and root planning, occlusal adjustment, splinting, curettage, flap surgery. Results: Control 2 weeks after curettage, gingiva was coral pink and PD was reduced. Conclusion: Curettage treatment in periodontitis cases reduces the depth of periodontal pockets and there are changes in clinical attachment levels (CAL) in mandibular anterior teeth. Surgical flap treatment is required in this case after curettage

Influences of standardized clinical probing on peri-implant soft tissue seal in a situation of peri-implant mucositis: A histomorphometric study in dogs.

Clinical probing is commonly recommended to evaluate peri-implant conditions. In a situation of peri-implant mucositis or peri-implantitis, the peri-implant seal healing from the disruption of soft tissue caused by probing has not yet been studied. This study aimed to investigate soft tissue healing after standardized clinical probing around osseointegrated implants with peri-implant mucositis in a dog model. Three transmucosal implants in each hemi-mandible of six dogs randomly assigned to the peri-implant healthy group or peri-implant mucositis group were probed randomly in the mesial or distal site as probing groups (PH or PM), the cross-sectional opposite sites as unprobed control groups. Histomorphometric measurements of implant shoulder (IS)-most coronal level of alveolar bone contact to the implant surface (BCI), apical termination of the junctional epithelium (aJE)-BCI, mucosal margin (MM)-BCI, and MM-aJE were performed at 1day, 1week, and 2weeks after probing. Apoptosis, proliferation, proinflammatory cytokines, and matrix metalloproteinases (MMPs) of peri-implant soft tissue were estimated by immunofluorescent analysis. In the PM group, apical migration of junctional epithelium was revealed by significantly decreased aJE-BCI from 1day to 2weeks in comparison to unprobed sites (p<0.05), while no significant differences were found in the PH group. Immunofluorescent analysis showed higher levels of interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), MMP-1, and MMP-8, together with exaggerated apoptosis and proliferation of peri-implant soft tissue in the PM group. Within the limitations, standardized clinical probing might lead to apical migration of the junctional epithelium in a situation of peri-implant mucositis.

The Role of Lactic Acid on Wound Healing, Cell Growth, Cell Cycle Kinetics, and Gene Expression of Cultured Junctional Epithelium Cells in the Pathophysiology of Periodontal Disease.

Lactic acid (LA) is short-chain fatty acid, such as butyric acid and propionic acid, that is produced as a metabolite of lactic acid bacteria, including periodontopathic bacteria. These short-chain fatty acids have positive effects on human health but can also have negative effects, such as the promotion of periodontal disease (PD), which is caused by periodontal pathogens present in the gingival sulcus. PD is characterized by apical migration of junctional epithelium, deepening of pockets, and alveolar bone loss. Thus, the junctional epithelial cells that form the bottom of the gingival sulcus are extremely important in investigating the pathophysiology of PD. The aim of this study was to investigate the effect of LA on wound healing, cell growth, cell cycle kinetics, and gene expression of cultured junctional epithelium cells. The results showed that stimulation with 10 mM LA slowed wound healing of the junctional epithelial cell layer and arrested the cell cycle in the G0/G1 (early cell cycle) phase, thereby inhibiting cell growth. However, cell destruction was not observed. LA also enhanced mRNA expression of integrin α5, interleukin (IL)-6, IL-8, intercellular adhesion molecule-1, and receptor activator of nuclear factor kappa-B ligand. The results of this study suggest that stimulation of junctional epithelial cells with high concentrations of LA could exacerbate PD, similarly to butyric acid and propionic acid.

The Effects of NF-kB Inhibition with p65-TMD-Linked PTD on Inflammatory Responses at Peri-implantitis Sites

The objective of this study was to find out if suppression of NF-kB complex function by p65-TMD-linked PTD could reduce host inflammation and bone resorption at peri-implantitis sites in rats. Twenty-one male 5-week-old SD rats were divided into three groups: untreated control group (A), silk-induced peri-implantitis group (B), and nt (nucleus transducible)-p65-TMD-treated, silk-induced peri-implantitis group (C). Implant sulcus of a rat in group C were divided into two groups, namely group Cp and Cb. Palatal implant sulcus where nt-p65-TMD solution was applied with an insulin syringe were assigned to group Cp. Buccal implant sulcus without topical nt-p65-TMD application were assigned to group Cb. H&E staining, TRAP staining, and immunohistological staining were done. The crestal bone levels of group A were significantly higher than those of group B at p<0.01. The crestal bone levels of group Cp were significantly higher than those of group Cb at p<0.05. H-E staining showed increased apical migration of junctional epithelium and inflammatory cells in group Cb. TRAP staining revealed more multinucleated osteoclasts in group Cb. As for immunohistological staining, group Cb showed many IL-6-positive cells while group Cp had none. In this study, p65-TMD-linked PTD inhibited NF-kB functions and reduced inflammation and bone resorption at peri-implantitis sites in rats.

Sequential colonization of periodontal pathogens in induction of periodontal disease and atherosclerosis in LDLRnull mice.

Periodontal disease (PD) and atherosclerotic vascular disease (ASVD) are both chronic inflammatory diseases with a polymicrobial etiology and have been epidemiologically associated. The purpose is to examine whether periodontal bacteria that infect the periodontium can also infect vascular tissues and enhance pre-existing early aortic atherosclerotic lesions in LDLRnull mice. Mice were orally infected with intermediate bacterial colonizer Fusobacterium nucleatum for the first 12 weeks followed by late bacterial colonizers (Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia) for the remaining 12 weeks mimicking the human oral microbiota ecological colonization. Genomic DNA from all four bacterial was detected in gingival plaque by PCR, consistently demonstrating infection of mouse gingival surfaces. Infected mice had significant levels of IgG and IgM antibodies, alveolar bone resorption, and showed apical migration of junctional epithelium revealing the induction of PD. These results support the ability of oral bacteria to cause PD in mice. Detection of bacterial genomic DNA in systemic organs indicates hematogenous dissemination from the gingival pockets. Bacterial infection did not alter serum lipid fractions or serum amyloid A levels and did not induce aortic atherosclerotic plaque. This is the first study examining the causal role of periodontal bacteria in induction of ASVD in LDLRnull mice.

Bis-enoxacin blocks rat alveolar bone resorption from experimental periodontitis.

Periodontal diseases are multifactorial, caused by polymicrobial subgingival pathogens, including Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Chronic periodontal infection results in inflammation, destruction of connective tissues, periodontal ligament, and alveolar bone resorption, and ultimately tooth loss. Enoxacin and a bisphosphonate derivative of enoxacin (bis-enoxacin) inhibit osteoclast formation and bone resorption and also contain antibiotic properties. Our study proposes that enoxacin and/or bis-enoxacin may be useful in reducing alveolar bone resorption and possibly bacterial colonization. Rats were infected with 109 cells of polymicrobial inoculum consisting of P. gingivalis, T. denticola, and T. forsythia, as an oral lavage every other week for twelve weeks. Daily subcutaneous injections of enoxacin (5 mg/kg/day), bis-enoxacin (5, 25 mg/kg/day), alendronate (1, 10 mg/kg/day), or doxycycline (5 mg/day) were administered after 6 weeks of polymicrobial infection. Periodontal disease parameters, including bacterial colonization/infection, immune response, inflammation, alveolar bone resorption, and systemic spread, were assessed post-euthanasia. All three periodontal pathogens colonized the rat oral cavity during polymicrobial infection. Polymicrobial infection induced an increase in total alveolar bone resorption, intrabony defects, and gingival inflammation. Treatment with bis-enoxacin significantly decreased alveolar bone resorption more effectively than either alendronate or doxycycline. Histologic examination revealed that treatment with bis-enoxacin and enoxacin reduced gingival inflammation and decreased apical migration of junctional epithelium. These data support the hypothesis that bis-enoxacin and enoxacin may be useful for the treatment of periodontal disease.

Orally Administered Liposomal Lactoferrin Inhibits Inflammation‐Related Bone Breakdown Without Interrupting Orthodontic Tooth Movement

Bovine lactoferrin (bLF) modulates the production of tumor necrosis factor-alpha (TNF-α) and inhibits alveolar bone breakdown associated with periodontitis. This study is designed to examine the effects of orally administered liposomal bLF (LbLF) on orthodontic force (OF)-induced alveolar bone remodeling during experimental tooth movement. Two groups of male Wistar rats were treated with either LbLF or control solution in drinking water 7 days before OF application. Lipopolysaccharide (LPS) was injected into the gingival sulcus in half the rats in each group. Thus, four groups: OF, OF+LbLF, OF+LPS, and OF+LPS+LbLF were established. Orally administered LbLF significantly reduced apical migration of junctional epithelium in the OF and OF+LPS groups. In OF+LPS, osteoclast number in the alveolar crestal area was increased by LPS treatment, whereas osteoclast number was significantly reduced in OF+LPS+LbLF through suppression of TNF-α production. Osteoclastic induction in the middle part, mainly from OF application, was not affected by LbLF administration. Inhibition of tooth movement was not induced by LbLF. Orally administered LbLF significantly inhibits LPS-induced alveolar bone resorption but not OF-induced bone remodeling. LbLF could be a potent therapeutic and preventive agent to control periodontal inflammation in patients undergoing orthodontic treatment.

Stress and the Periodontium

ABSTRACTStress or tension is an unavoidable part of human life. It has been proven to cause not only health-related problems but problems pertaining to periodontium too. These include periodontal pocket formation, apical migration of junctional epithelium and delated wound healing. This paper connects the link between stress, its effect on general health and consequently on oral health.How to cite this articleSharma N, Gujjari SK, Kanagotagi S. Stress and the Periodontium. J Contemp Dent 2012;2(2):28-30.

Virulence of major periodontal pathogens and lack of humoral immune protection in a rat model of periodontal disease

This study was designed to test the hypothesis that periodontal pathogens Tannerella forsythia and Porphyromonas gingivalis are synergistic in terms of virulence potential using a model of mixed-microbial infection in rats. Three groups of rats were infected orally with either T. forsythia or P. gingivalis in mono-bacterial infections or as mixed-microbial infections for 12 weeks and a sham-infected group were used as a control. This study examined bacterial infection, inflammation, immunity, and alveolar bone loss changes with disease progression. Tannerella forsythia and P. gingivalis genomic DNA was detected in microbial samples from infected rats by PCR indicating their colonization in the rat oral cavity. Primary infection induced significantly high IgG, IgG2b, IgG1, and IgG2a antibody levels indicating activation of mixed Th1 and Th2 immune responses. Rats infected with the mixed-microbial consortium exhibited significantly increased palatal horizontal and interproximal alveolar bone loss. Histological examinations indicated significant hyperplasia of the gingival epithelium with moderate inflammatory infiltration and apical migration of junctional epithelium. The results observed differ compared to uninfected controls. Our results indicated that T. forsythia and P. gingivalis exhibit virulence, but not virulence synergy, resulting in the immuno-inflammatory responses and lack of humoral immune protection during periodontitis in rats.

Porphyromonas gingivalisandTreponema denticolaMixed Microbial Infection in a Rat Model of Periodontal Disease

Porphyromonas gingivalis and Treponema denticola are periodontal pathogens that express virulence factors associated with the pathogenesis of periodontitis. In this paper we tested the hypothesis that P. gingivalis and T. denticola are synergistic in terms of virulence; using a model of mixed microbial infection in rats. Groups of rats were orally infected with either P. gingivalis or T. denticola or mixed microbial infections for 7 and 12 weeks. P. gingivalis genomic DNA was detected more frequently by PCR than T. denticola. Both bacteria induced significantly high IgG, IgG2b, IgG1, IgG2a antibody levels indicating a stimulation of Th1 and Th2 immune response. Radiographic and morphometric measurements demonstrated that rats infected with the mixed infection exhibited significantly more alveolar bone loss than shaminfected control rats. Histology revealed apical migration of junctional epithelium, rete ridge elongation, and crestal alveolar bone resorption; resembling periodontal disease lesion. These results showed that P. gingivalis and T. denticola exhibit no synergistic virulence in a rat model of periodontal disease.

The influence of diabetes mellitus on periodontal tissues: a pilot study

PurposeThe purpose of this study was to preliminarily evaluate the influence of diabetes mellitus (DM) on periodontal tissue without establishment of periodontitis.MethodsSeven-week-old db/db mice were used for the diabetic experimental group and systematically healthy mice of the same age were used as controls. After 1 week of acclimatization, the animals were sacrificed for hard and soft tissue evaluation. The pattern of bone destruction was evaluated by stereomicroscope evaluation with alizarin red staining and radiographic evaluation by microscopic computerized tomography images. Histological evaluation was performed with hematoxylin and eosin stain for evaluation of soft tissue changes.ResultsIn both stereomicroscope evaluation and radiograph image analysis, aggressive form of bone destruction was observed in diabetic animals when compared to the systematically healthy controls. In histological evaluation, apical migration of junctional epithelium with slight inflammatory cell infiltration was observed with disarrangement of connective tissue fibers.ConclusionsWithin the limits of this study, diabetic animals presented distortion in periodontal attachment and an aggressive bone loss pattern when compared to the healthy controls, suggesting that DM has an independent effect on periodontal tissue destruction irrespective of the presence or absence of periodontal disease.

Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

Reactive oxygen species (ROS) production is an antimicrobial response to pathogenic challenge that may, in the case of persistent infection, have deleterious effects on the tissue of origin. A rat periodontal disease model was used to study ROS-induced chronic epithelial inflammation and bone loss. Lipopolysaccharide (LPS) was applied for 8 weeks into the gingival sulcus, and histological analysis confirmed the onset of chronic disease. Junctional epithelium was collected from healthy and diseased animals using laser-capture microdissection, and expression microarray analysis was performed. Of 19,730 genes changed in disease, 42 were up-regulated >/=4-fold. Three of the top 10 LPS-induced genes, monoamine oxidase B (MAO/B) and flavin-containing monooxygenase 1 and 2, are implicated in ROS signaling. LPS-associated induction of the ROS mediator H(2)O(2), as well as MAO/B and tumor necrosis factor (TNF)-alpha levels were validated in the rat histological sections and a porcine junctional epithelial cell culture model. Topical MAO inhibitors significantly counteracted LPS-associated elevation of H(2)O(2) production and TNF-alpha expression in vivo and in vitro, inhibited disease-associated apical migration and proliferation of junctional epithelium and inhibited induced systemic H(2)O(2) levels and alveolar bone loss in vivo. These results suggest that LPS induces chronic wounds via elevated MAO/B-mediated increases in H(2)O(2) and TNF-alpha activity by epithelial cells and is further associated with more distant effects on systemic oxidative stress and alveolar bone loss.

Impaired Phagosomal Maturation in Neutrophils Leads to Periodontitis in Lysosomal-Associated Membrane Protein-2 Knockout Mice

Inflammatory periodontal diseases constitute one of the most common infections in humans, resulting in the destruction of the supporting structures of the dentition. Circulating neutrophils are an essential component of the human innate immune system. We observed that mice deficient for the major lysosomal-associated membrane protein-2 (LAMP-2) developed severe periodontitis early in life. This development was accompanied by a massive accumulation of bacterial plaque along the tooth surfaces, gingival inflammation, alveolar bone resorption, loss of connective tissue fiber attachment, apical migration of junctional epithelium, and pathological movement of the molars. The inflammatory lesions were dominated by polymorphonuclear leukocytes (PMNs) apparently being unable to efficiently clear bacterial pathogens. Systemic treatment of LAMP-2-deficient mice with antibiotics prevented the periodontal pathology. Isolated PMNs from LAMP-2-deficient mice showed an accumulation of autophagic vacuoles and a reduced bacterial killing capacity. Oxidative burst response was not altered in these cells. Latex bead and bacterial feeding experiments showed a reduced ability of the phagosomes to acquire an acidic pH and late endocytic markers, suggesting an impaired fusion of late endosomes-lysosomes with phagosomes. This study underlines the importance of LAMP-2 for the maturation of phagosomes in PMNs. It also underscores the requirement of lysosomal fusion events to provide sufficient antimicrobial activity in PMNs, which is needed to prevent periodontal disease.

Initial Apical Migration of Junctional Epithelium in Rats Following Application of Lipopolysaccharide and Proteases

Apical migration of junctional epithelium (JE) occurs in association with periodontal pocket formation. The aim of this study was to investigate the gingival changes occurring during apical migration of the JE following application of factors associated with inflammatory periodontal disease pathogenesis. Six-week-old male Wistar rats were divided into six groups: three experimental groups to investigate gingival changes following 2, 4, and 8 weeks topical application of lipopolysaccharide (LPS) and proteases and three control groups using pyrogen-free water. After 2, 4 or 8 weeks, nuclear DNA fragmentation was detected in periodontal ligament (PDL) fibroblasts using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method, and proliferative activities of the basal cells and fibroblasts were evaluated through expression of proliferating cell nuclear antigen (PCNA). Collagen destruction was examined histologically. Gingiva treated with LPS and proteases showed an increase in PCNA-positive basal cells but not the fibroblasts. Collagen destruction was observed at 2 weeks; apical migration of the JE and TUNEL-positive fibroblasts was seen at 4 weeks. Following application of LPS and proteases to rat gingival sulci, the apical migration of the JE appears to occur simultaneously with the apoptosis of PDL fibroblasts, which in turn follows proliferation of the basal cells and collagen destruction.

Keratinocyte growth factor and scatter factor expression by regionally defined oral fibroblasts.

Keratinocyte growth factor (KGF) and hepatocyte growth factor/scatter factor (SF) are two signalling molecules thought to play important roles in regulating epithelial-mesenchymal interactions. Expression of both factors by fibroblasts in subepithelial connective tissue may play a role in maintaining epithelial integrity in health and in the apical migration of junctional epithelium in periodontitis. The aims of this study were (a) to compare expression levels of KGF and SF by periodontal ligament (PDL) and gingival fibroblasts; and (ii) to determine the effects of interleukin (IL)-1 beta, transforming growth factor (TGF)-beta 1, platelet-derived growth factor (PDGF)-BB and epidermal growth factor (EGF) on KGF/SF expression by these cell populations. Three paired PDL and gingival fibroblast strains were developed. The KGF and SF protein levels were analysed by enzyme-linked immunosorbent assay. Relative levels of KGF and SF mRNA in cytokine-treated cultures were determined using semiquantitative reverse transcriptase polymerase chain reaction. No differences in the levels of KGF and SF produced by PDL and gingival (SOG) populations were found. In both cell types IL-1 beta stimulated KGF and SF expression, while TGF-beta 1 significantly inhibited expression at both the mRNA and protein levels. Epidermal growth factor and PDGF-BB induced differing effects on expression, stimulating SF protein production but inhibiting KGF output in both fibroblast populations. Differences in response to EGF and PDGF were also seen between paired PDL and gingival fibroblasts.

Reactive change in proliferative activity of the junctional epithelium after topical application of lipopolysaccharide.

IT IS WELL ESTABLISHED THAT apical migration of junctional epithelium (JE) along a root surface is an important factor in periodontal pocket formation and deepening. However, the exact mechanism and, more specifically, the role of inflammatory products in influencing the activity of cells within the JE is not known. To address this issue lipopolysaccharide (LPS) was applied topically into rat molar gingival sulcus and then tissues evaluated immunohistochemically for expression of proliferating cell nuclear antigen (PCNA). Tissues were prepared for histological analysis at designated times. Histologically, infiltration of neutrophils with associated edema was noted in JE and gingival connective tissues 6 hours after LPS application and was prominent at 12 hours. These inflammatory changes persisted in the 2- and 3-day specimens, and disappeared at 5 days. In normal gingiva, before the LPS application, the JE showed few PCNA positive cells, while almost all cells in the basal and suprabasal cell layers of the oral gingival epithelium and the oral sulcular epithelium were PCNA positive. No increase in the number of PCNA positive cells in the JE beyond zero time was observed at 6 and 12 hours after LPS application. One day after LPS application, PCNA positive cells appeared in the basal cell layer of the JE, with a continued increase number of PCNA positive cells in the JE continued at 2 and 3 days. By day 5 the number of PCNA positive cells were decreasing with return to a normal range by 7 days. These results showed that 1) under normal physiological conditions, cells within the JE have minimal mitotic activity and 2) the JE cells can enter the proliferating cell cycle when exposed to LPS, and suggest that the enhanced proliferating activity in the JE is an important factor for the deepening of the periodontal pocket, if the connective tissue attachment is broken down.

The distribution of fibronectin and laminin in the murine periodontal membrane, indicating possible functional roles in the apical migration of the junctional epithelium

Periodontal tissue shows various morphological changes with ageing. A typical example of these changes is the apical migration of the junctional epithelium. The distribution of fibronectin and laminin was investigated by immunofluorescent and immunoelectron-microscope methods in mice to clarify any possible functional roles of these proteins in the apical migration of junctional epithelium. Apical migration begins in 20-week-old mice, and then progresses with increasing age until the mice reach 80 weeks. In the apical tip of the junctional epithelium, fibronectin was demonstrated in the subepithelial fibrillar matrix, preceding the progression of apical migration. Fibronectin was also demonstrated in association with the stromal side of focal contants between epithelial cells and basement membrane. Therefore, these focal contacts are assumed to be fibronectin receptors. There was no apparent relation between the localization of laminin and the migration of the junctional epithelium. These results suggest that the fibronectin provides a provisional matrix for the apical migration of junctional epithelium, but laminin does not appear to play a major part in that migration.

Loss of attachment in the marginal periodontium of the rat incisor under non-inflammatory conditions. Expression of alkaline phosphatase activity. Experimental Oral Biology Group.

Alkaline phosphatase (ALP) has been suggested to play a role in acellular cementum formation and maintenance of periodontal attachment. In an attempt to determine whether changes in attachment level are associated with altered expression of ALP-activity in the periodontium we induced natural loss of attachment in rats by pinning the lower incisor to the jaw bone. Previous studies have shown that this procedure results in regressive changes in the marginal periodontium without any inflammatory response. Six months after blockage of eruption the attachment level on the experimental (right) side had shifted about 700 microm in the apical direction. On the control (left) side the apical termination of the junctional epithelium had remained stationary with respect to the alveolar crest. Our observations have shown that during the first few weeks of the experiment loss of attachment is accompanied by considerable reduction of ALP-activity in the supracrestal part of the periodontium. At later time intervals, however, no distinct relation was found between apical migration of junctional epithelium and loss of ALP-activity in the supracrestal region, indicating that the two phenomena are not directly related to each other. The domain of the ALP-positive fibroblasts in the supracrestal extension of the periodontal ligament decreased in size and was replaced by ALP-negative connective tissue cells probably coming from the outer gingival domain. Since at all time intervals a distinct demarcation could be observed between the ALP-positive and ALP-negative areas, we interpret our data as indicating that ligament and gingival cells do not mix.

Electron Microscopical Evaluation of Connective Tissue Healing to Periodontally Involved Teeth

The present study was undertaken to examine if our novel root treatment for human periodontally involved teeth can facilitate a new connective tissue attachment. The novel treatment was in two parts: 1) planning and surface decalcification with citric acid on the coronal quarter of the exposed root corresponding to pocket, and 2) curettage of superficial cementum of the apical three quarters of the exposed root. The interface of the root surface and regenerating connective tissue was observed 2 and 3 weeks after surgery by light and electron microscopy. The apical migration of junctional epithelium was effectively prevented. The fibroblasts synthesized new fibrillar materials and collagen fibrils towards the curetted cementum. The results suggested the possibility that this treatment for periodontally involved teeth would provide ideal root surface conditions for the formation of new fibrous attachment.

Healing following implantation of periodontitis affected roots into bone tissue.

The aim of the present experiment was to study whether new connective tissue attachment can occur to root surfaces which have been exposed to the oral environment and subsequently implanted into bone tissue. Twelve teeth in three beagle dogs were subjected to progressive periodontal breakdown to half the root length by placing cotton floss ligatures around the neck of the teeth. Following crown resection and root hemisection, the teeth were root filled and the roots thoroughly scaled and planed. Each root was extracted and implanted into bone cavities prepared in edentolous areas of the jaws in such a way that epithelial migration into the wound and bacterial infection were prevented during healing. Root implantation and sacrifice of the animals were scheduled to allow for observation periods of 1, 2 and 3 months. The results demonstrated that new connective tissue attachment did not occur to root surfaces which had been exposed to the oral environment, but healing was characterized by repair phenomena, i.e. mainly root resorption and ankylosis. In those areas of the roots where periodontal ligament tissue was preserved following tooth extraction, a functionally oriented attachment apparatus was reformed. The results indicate that in addition to apical migration of junctional epithelium and regrowth of subgingival plaque, the type of cells which repopulate the wound area may jeopardize new connective tissue attachment.