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Background and Objective: Occlusal trauma is considered to be a contributing factor to bone loss associated with inflammatory periodontal disease. We hypothesized that pyroptosis, a recently discovered inflammation-induced programmed cell death pathway, plays a role in occlusal trauma., Materials and Methods: The occlusal trauma model was established using a cemented 1-mm elevated computer-aided design and manufacturing (CAD/CAM) metal crown. The periodontitis model was established by periodontal wire ligation with lipopolysaccharide (LPS) injection. The rats were sacrificed at 1, 2, 3, and 4 weeks. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze the expression of pyroptosis-, inflammation-, and osteoclast-related markers. Micro-computed tomography (micro-CT) was used to determine bone morphology parameters. Tissue morphology was evaluated using hematoxylin and eosin staining (H&E). Osteoclasts were identified using tartrate-resistant acid phosphatase (TRAP) staining. The expression and distribution of factors related to pyroptosis and inflammation were evaluated by immunohistochemistry (IHC). The colocalization of dead cells and cysteinyl aspartate-specific proteinase-1 (caspase-1)-positive cells was analyzed by immunofluorescence., Results: Quantitative real-time polymerase chain reaction and IHC results showed that occlusal trauma induced the expression of pyroptotic factors during the early stages, while occlusal trauma with periodontitis upregulated the expression of pyroptotic factors at the later stages. The results of qRT-PCR, TRAP staining, and micro-CT showed that occlusal trauma with periodontitis increased the production of proinflammatory cytokines, leading to severe bone loss. Glyburide, an NOD-like receptor pyrin domain containing protein 3 (NLRP3)inhibitor, reduced the expression of pyroptosis markers induced by occlusal trauma with periodontitis and reversed bone resorption., Conclusions: Pyroptosis was involved in bone loss induced by occlusal trauma with or without periodontitis, while glyburide reversed inflammation and bone resorption., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Observational studies have indicated that crestal bone level changes at implants are typically associated with clinical signs of inflammation, but still mechanical overload has been described as possible factor leading to hard-tissue deficiencies at implant sites without mucosal inflammation. The aim of this paper was systematically review the literature regarding the possible effect of traumatic occlusal forces on the peri-implant bone levels. Literature search was conducted using PubMed, Scielo and Lilacs, including the following terms: oral OR dental AND implant$ AND (load OR overload OR excessive load OR force$ OR bruxism) AND (bone loss OR bone resorption OR implant failure$). Databases were searched for the past 10 years of publications, including: clinical human studies, either randomized or not, cohort studies, case control studies, case series and animal research. Exclusion criteria were review articles, guidelines and in vitro and in silico (finite element analysis) research, as well as retrospective studies. The PICO questions formulated was: "does traumatic occlusal forces lead to peri-implant bone loss?" The database searches as well as additional hand searching, resulted in 807 potentially relevant titles. After inclusion/exclusion criteria assessment 2 clinical and 4 animal studies were considered relevant to the topic. The included animal studies did not reveal an association between overload and peri-implant bone loss when lower overloads were applied, whereas in the presence of excessive overload it seemed to generate peri-implant bone loss, even in the absence of inflammation. The effect of traumatic occlusal forces in peri-implant bone loss is poorly reported and provides little evidence to support a cause-and-effect relationship in humans, considering the strength of a clinically relevant traumatic occlusal force.

Purpose: Occlusal trauma, resulting in the destruction of alveolar bone, is a form of periodontal disease caused by excessive mechanical stress (MS) during hyperocclusion. Previously, we showed that CC chemokine ligand (CCL) 2/CCR2 receptor axis plays a crucial role in MS-dependent osteoclastogenesis. However, in the previous work, we were unable to precisely measure changes in alveolar bone profiles. In the present study, we sought to establish a precise method for evaluating alveolar bone resorption induced by hyperocclusion using micro-computed tomography., Methods: Under anesthesia, a stainless steel wire was attached to the molars of 5-week-old C57/BL6 wild-type (WT) mice, CCL2 -/- mice, and CCR2 -/- mice to induce occlusal force overload. At days 0 and 7, hard tissue samples were harvested and analyzed by micro-computed tomography., Results: In the WT mice, bone mineral density of the alveolar bone was significantly decreased at day 7 as compared with day 0, with marked alveolar bone resorption observed. Similarly, significant alveolar bone resorption was observed in the CCL2 -/- and CCR2 -/- mice at day 7 as compared with day 0., Conclusions: Micro-computed tomographic images can be used to measure changes in bone mineral density in a mouse model of hyperocclusion. This method may be useful for further investigating bone changes in other periodontal disease research fields., (Copyright © 2017 Japan Prosthodontic Society. Published by Elsevier Ltd. All rights reserved.)

Objective: Besides inflammatory bone loss, trauma from occlusion (TO)-induced alveolar bone loss increases the risk of future tooth loss. We have shown that resveratrol, a polyphenol, possesses anti-inflammatory characteristics and a suppressive effect on osteoclastogenesis. Therefore, we investigated the effects of resveratrol on TO-induced bone loss in mice., Material and Methods: Trauma from occlusion was induced by overlaying composite resin onto the maxillary first molar of C57BL/6 mice. TO-induced mice were administered either resveratrol or vehicle for 15 days from 5 days before TO induction. The mice administered vehicle only served as controls. The effect of resveratrol on bone resorption was assessed histologically. Gene expression in gingival and periodontal ligament tissues was analyzed. In vitro effect of resveratrol on the differentiation of RAW 264.7 cells and bone marrow-derived macrophages into osteoclastic cells was analyzed., Results: Resveratrol administration significantly decreased the bone loss and suppressed the elevated expression of osteoclastogenesis-related gene in periodontal ligament tissue by TO. Resveratrol treatment also suppressed the differentiation of both RAW 264.7 cells and bone marrow-derived macrophages into osteoclastic cells., Conclusion: Resveratrol administration suppressed the TO-induced alveolar bone loss by suppressing osteoclast differentiation, suggesting that resveratrol is effective in preventing both inflammation and mechanical stress-induced alveolar bone resorption., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. All rights reserved.)

Context: A better understanding of the relation between traumatic dental occlusion and periodontal changes is needed., Aims: This study aimed to evaluate the pattern of osteoclastic activity in the periodontal bone in front of the traumatic dental occlusion in rat molars., Patients and Methods: Traumatic dental occlusion (TO) was induced in twenty rats, which were sacrificed after periods of 2, 5, 7, and 14 days. Transversal histological sections of both jaws were stained with tartrate-resistant acid phosphatase and hematoxylin and eosin. Mann-Whitney U-test was used for group comparison, and Pearson's correlation test was applied for the number of osteoclasts and bone area (BA)., Results: Traumatic dental occlusion caused an increase in the number of osteoclasts in the bone of the upper and lower right first molar from days 2-5 to 2-14, respectively. In the TO groups, the number of osteoclasts on the lamina dura and in the center of the alveolar bone septum, respectively, increased almost 4-fold and 9-fold in the lower jaw; and 3-fold and 5-fold in the upper jaw, during all periods. In the TO groups, the BA of the alveolar bone septum was substantially reduced. There was a negative correlation between the number of osteoclasts and BA in both jaws during all experimental periods., Conclusions: Traumatic dental occlusion increases osteoclast activity in the alveolar lamina dura and in the center of alveolar bone and stimulates a higher degradation in the center of the alveolar bone septum.

Background and Objective: Occlusal trauma (OT) and smoking are both factors that alter alveolar bone metabolism and therefore could synergistically act on alveolar bone loss. The aim of this experimental study was to evaluate the influence of short-term cigarette smoke inhalation (CSI) on inter-radicular alveolar bone loss promoted by primary OT in a rat model., Material and Methods: Forty-eight animals were randomly assigned to one of three groups based on treatment type: OT + CSI (n = 16), animals were exposed to CSI three times per day, for 8 min per exposure, and they concomitantly received unilateral vertical augmentation creating an occlusal interference inducing experimental OT; OT (n = 16), animals received only unilateral vertical augmentation; negative control (NC; n = 16), animals maintained for equal periods to achieve periodontal baseline values of periodontal ligament dimension. Each group was divided into two subgroups (n = 8) based on treatment length: 7 or 14 d., Results: After 7 d, the OT + CSI group exhibited significantly higher bone loss compared to the NC group (p = 0.0022). After 14 d, the OT (p < 0.0001) and OT + CSI (p < 0.0001) groups presented significantly higher bone loss compared to the NC group, and OT + CSI resulted in significantly higher bone loss than OT alone (p = 0.0241). The number of tartrate-resistant acid phosphatase-positive cells on the linear surface of the bone crest after 7 d was significantly higher in the OT + CSI group as compared to the NC and OT groups (p < 0.0001 and p = 0.0045, respectively) and remained significantly higher in the OT + CSI group after 14 d, compared to the OT group (p < 0.0001)., Conclusion: Short-term CSI increases early bone loss in association with OT after 7 d, and this worsens in severity after 14 d of exposure., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Diabetes mellitus (DM) involves metabolic changes that can negatively influence periodontal tissues, resulting in more prevalent and severe periodontitis and impaired bone formation. Occlusal trauma (OT) is an injury of the supportive periodontium that results in bone loss. It can be hypothesized that DM would increase bone loss after OT, mainly when associated with periodontitis. Thus, the aim of the present study is to evaluate the influence of DM on bone response in the furcation area of teeth subjected to OT in the presence, or absence, of experimental periodontitis (EP) in the rat model., Methods: Thirty-two male Wistar rats were assigned to four groups: 1) group 1 (G1): DM+OT+EP (n = 8); 2) group 2 (G2): DM+OT (n = 8); 3) group 3 (G3): OT+EP (n = 8); and 4) group 4 (G4): OT (n = 8). G1 and G2 received a single intraperitoneal injection of streptozotocin (STZ). After 10 days, G1 and G3 were subjected to EP by ligature placement. Fifteen days after the start of EP, OT was induced by the creation of a premature contact. The animals were euthanized 35 days after DM induction., Results: DM enhanced bone loss in the presence of OT combined with EP, but did not increase bone loss in teeth subjected to OT alone. EP caused greater bone loss when associated with OT., Conclusion: Within the limits of this animal study, it can be concluded that DM enhances bone loss in the presence of occlusal trauma associated with EP.

Objective: To elucidate the effect of sympathetic nervous activity on alveolar bone loss induced by occlusal hypofunction in rat molars., Design: Occlusal hypofunction in the molar area was produced by attaching appliances to rat maxillary and mandibular incisors. In addition, a non-selective β-adrenergic receptor antagonist, propranolol, was administered orally to rats in drinking water to pharmacologically suppress sympathetic nervous activity. After 1 week, alveolar bones in all groups were examined by micro-CT, histomorphometry and histology to determine their trabecular bone phenotypes and histological changes., Results: The marrow spaces of the interradicular alveolar bone of rat mandibular first molars (M1) increased in the occlusal hypofunction group (Group H) but not in the control group (Group C), whilst these decreased in rats in the occlusal hypofunction group that were administered propranolol (Group HB). Bone volume/tissue volume (BV/TV), trabecular thickness (Tb.Th) and trabecular number (Tb.N) for interradicular alveolar bone in M1 in Group H were significantly lower than those in Group C, whereas those in Group HB remained as high as those in Group C. The number of TRAP-positive cells in Group H increased compared to that in Group C, whereas it significantly decreased in Group HB., Conclusions: These results suggest that sympathetic nervous activity may influence the alveolar bone loss induced by occlusal hypofunction., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Background: This study systematically evaluates the effect of occlusal overload (OV) on peri-implant tissue health in animal studies., Methods: MEDLINE, EMBASE, and LILACS databases were searched for articles published up to and including January 2010. Studies that reported outcomes of non-splinted titanium dental implants submitted to OV were eligible for inclusion. Probing depth (PD), clinical attachment level (CAL), radiographic and histologic distances from the implant base to the most coronal point of bone-to-implant contact (RDIB and DIB, respectively), and bone density (BD) were the main outcomes of interest., Results: Two controlled trials were included in this review and both were considered at a high risk of bias. The marked heterogeneity between studies did not allow data to be combined for meta-analyses. Two studies reported no association between OV and peri-implant tissue breakdown in the absence of dental plaque, with PD and CAL varying from 2 to 3 mm at the end of the experiments. In the presence of plaque accumulation, OV played a key role in peri-implant tissue breakdown (PD change: 5.3 mm; DIB: 6.0 mm). Trends suggested that OV may increase BD., Conclusions: Data on OV on stable implants are limited and conflicting. OV may lead to bone loss in the presence of dental plaque and to an increase in BD in areas where plaque control is performed.

The purpose of this case report is to demonstrate the relation between occlusal overload and peri-implant bone loss and the reversal of the situation after removal of the offending forces. The placement of an unstable removable prosthesis on 3 well-integrated implants that had been stable for 9 years caused noticeable bone loss after 6 months. The elimination of the traumatic occlusion reversed the situation, and a remarkable healing of the peri-implant tissue occurred until the pretrauma condition was nearly restored. The condition has been stable for the past 4 years.

Background and Objective: Receptor activator of nuclear factor kappa B ligand (RANKL) is an important factor in osteoclast differentiation, activation and survival; however, its involvement in inflammatory bone resorption, with or without occlusal trauma, is unclear. The purpose of the present study was to investigate the distribution of RANKL-expressing cells in rat periodontium during lipopolysaccharide-induced inflammation with or without occlusal trauma., Material and Methods: Lipopolysaccharide was injected into rat gingiva of the lower left first molar to induce inflammation. In addition, the occlusal surface of the upper left first molar of rat was raised by placing a gold inlay to induce occlusal trauma in the lower left first molars. The distribution of RANKL-expressing cells was immunohistochemically observed., Results: In the inflammatory model, many osteoclasts were observed at the apical inter-radicular septum on day 5 and they were reduced by day 10. On the other hand, in the inflammatory model with occlusal trauma, many osteoclasts were still observed on day 10. RANKL expression was similar to the changes in osteoclast number. The expression of RANKL increased in endothelial cells, inflammatory cells and periodontal ligament cells., Conclusion: These findings clearly demonstrated that RANKL expression on endothelial cells, inflammatory cells and periodontal ligament cells is involved in inflammatory bone resorption and the expression is enhanced by traumatic occlusion. These results suggest that RANKL expression on these cells is closely involved in the increase of osteoclasts induced by occlusal trauma.

The relationship between occlusal overload and peri-implant bone loss remains a controversial topic in implant dentistry. A causal relationship between the incidence of marginal bone loss next to an implant and occlusal overload implies a treatment plan and occlusal scheme would benefit from a force management approach. A MEDLINE-assisted and hand search of peer-reviewed English literature and relative textbooks were used for a selective review of articles addressing biomechanical stress and bone loss in cellular biomechanics, engineering principles, mechanical properties of bone, animal studies, clinical reports, bone physiology, and implant design biomechanics. These papers demonstrate occlusal overload on implants may increase the incidence of marginal bone loss.

This clinical report presents the prosthodontic management of early peri-implant bone loss in a partially edentulous patient. Two narrow Brånemark implants (3.3 mm in diameter) were placed to retain a mandibular implant prosthesis in the area of the mandibular left second premolar and first molar. Two weeks after the prosthesis was put into function, the distal implant exhibited soft tissue reactions. Radiographically, bone corresponding to 4 threads and 7 threads was lost at the mesial and distal sites, respectively. After occlusal load reduction was made to the existing prosthesis, bone was observed to have regenerated sufficiently to restore the defect radiographically, though not to the original level. The bone remained at a similar level at 36 months after treatment.

This study, using 132 female rats, was designed to investigate whether oestrogen loss facilitates alveolar bone alterations induced by traumatic occlusion. Rats were ovariectomized (OVX) or underwent sham-operation (Sham). Seven days after surgery, half of the rats in each group were subjected to experimental traumatic occlusion (trauma), and the other half were left untreated. Thus, there were four groups: OVX+trauma, Sham+trauma, OVX, and Sham. Rats in each group were killed 1, 3, 5, 7, or 10 days after the introduction of occlusal trauma. The resected mandibles were processed without decalcification, and histomorphometric measurements were performed in the alveolar bone adjacent to the periodontal ligament of the first molar. The statistical assessment of the time- and group-specific differences by analysis of variance revealed significant differences between the OVX+trauma and Sham+trauma groups in the resorption parameters, but not in the formation parameters. The results show that the alveolar bone dynamics induced by traumatic occlusion are enhanced by oestrogen deficiency.

The influence of experimental occlusal overload on peri-implantitis in monkeys (Macaca fascicularis) has been examined to explain the pathology of the disease that develops in the tissue around osseointegrated implants. In the first article of this series, it was reported that bone resorption was not observed around implants when occlusal trauma was produced by a super-structure that was in supraocclusal contact with an excess occlusal height of approximately 100 microns, provided there was no inflammation in the peri-implant tissue. In the second part of the study, experimental inflammation was created in the peri-implant tissue, and occlusal overload was produced by a superstructure with an excess occlusal height of 100 microns. Notable bone resorption was observed around the implant with the passage of time. These results suggested that, in addition to the control of inflammation in peri-implant tissue, traumatic occlusion may play a role in bone breakdown around the implant. In the present study, while the peri-implant tissue was kept in an inflammation-free state, bone level changes around the implants were investigated when various levels of traumatic force were exerted. The supraoccluding prostheses were defined as excessively high by 100 microns, 180 microns, and 250 microns, respectively. The heights were determined with an image analysis device, and the bone responses around the implants induced by the traumatic forces were investigated. The results showed that bone resorption around implants tended to increase with 180 microns or more excessive height of the superstructure. This suggests that the threshold of excessive height of the superstructures at which peri-implant tissue breakdown may start is approximately 180 microns. It is also suggested that there is a possibility of bone resorption around the implants caused by excess occlusal trauma, even when there is no inflammation in peri-implant tissue.

Purpose: To investigate in vivo the relationship of occlusal stress factors, periodontal health status, and acidic dietary patterns to the presence of non-carious cervical lesions (NCCL) in a convenience sample of undergraduate clinic, adult dental patients., Materials and Methods: Forty three subjects who met the entry criteria were admitted into the study; 178 teeth exhibiting NCCL were evaluated. A dietary assessment focusing on acidic food/beverage intake was used to evaluate nutritional intake over the most recent 24-hour period. Periodontal evaluation included intraoral measurement of gingival attachment loss, assessment of tooth mobility, and radiographic interpretation of percent bone loss using the Schei ruler method. Among the occlusal factors evaluated were shape and orientation of NCCL, presence and location of wear facets, and symptoms and characteristics of centric and eccentric occlusal function., Results: 95% of teeth examined exhibited functional wear facets, indicating a systematic relationship with presence of NCCL (Chi Square = 16.9, P < 0.0001); 48% displayed buccal or incisal facets; 64% were accompanied by balancing interferences in lateral excursion; 98.3% had mobility scores < or = 1; there was no significant association between mobility and facets present (Chi Square = 3.04, P = 0.21); and, no relationship with dietary patterns was found. Group function, that may evolve with age, and/or traumatic occlusion factors may be related to etiology of NCCL. Longitudinal controlled clinical trials are needed to confirm suspected etiologies and establish treatment guidelines for non-carious cervical lesions.

Breakdown of bone around oral implants following occlusal overload or plaque accumulation was evaluated in monkeys. 5 screw-type implants of pure titanium (Astra Tech) were inserted in the mandible of 4 monkeys (Macaca Fascicularis). 6 months after insertion of the implants a fixed partial prosthesis was mounted on the 2 implants in 1 of the lateral segments. The prosthesis was in supra-occlusal contact with an antagonizing splint and caused a lateral directed excessive occlusal load (overload). Implants retaining the prosthesis were brushed 1 x week and subgingival cleaning was performed 1 x month. The remaining implants were never cleaned and, additionally, a cotton cord was placed around the abutments of these implants to promote plaque accumulation. 6 out of 8 implants with occlusal overload became loose. 2 of these were lost, whereas the remaining 4 were retained in the jaws. After 18 months of occlusal load or plaque accumulation, the monkeys were sacrificed. Tissue blocks with the implants were infiltrated and embedded in acrylic resin. Approximately 50 microns thick sections of the implants and surrounding tissues were made. All implants with plaque accumulation were osseointegrated, but exhibited an average histologic marginal bone loss of 2.4 mm (range: 0.8-4.0 mm). Of the 6 implants with occlusal overload available for histologic analysis, 2 implants in 1 monkey had lost osseointegration completely and 2 other implants were osseointegrated in the apical part only, whereas the remaining 2 were still osseointegrated but exhibited a bone loss of 1.8-1.9 mm.

Three case reports of treatment of the failing implant are presented. The implants were immobile but had lost a significant amount of osseous support. The cause of failure was determined to be a combination of bacterial and occlusal traumatogenic insult. The defects were debrided and the implant surface was detoxified with tetracycline. Decalcified freeze-dried bone allograft was implanted in the osseous defects and covered with expanded polytetrafluoroethylene material in accordance with principles of guided tissue regeneration. The barrier membrane was removed 6 to 8 weeks after placement. Eight months to 1 year posttreatment, all sites demonstrated a substantial reduction in probing depth, a gain in clinical attachment, and bone fill of the defects adjacent to the implant.

A series of destructive changes occurring in the jaws of patients wearing a complete maxillary denture opposed by a mandibular distal extension removable partial denture have been described as the combination syndrome. However, the syndrome does not occur in all patients. Those patients who have not developed signs of the combination syndrome and whose mandibular anterior teeth are well preserved and not overerupted may be treated conservatively with a mandibular removable partial denture. A properly designed removable partial denture that distributes occlusal stresses over hard and soft tissues minimizes the risk of developing the combination syndrome. Nevertheless, the overdenture seems to provide a more predictable prognosis, especially for patients who already have the combination syndrome or whose mandibular anterior teeth are structurally or periodontally compromised or overerupted. The treatment modality is determined by the apparent potential of the patient to develop the combination syndrome and by the condition of the remaining mandibular anterior teeth.

Histories and clinical evaluations were obtained from 230 postmenopausal women aged 48 to 56 years to determine whether the alveolar height in the edentulous anterior region of the maxillae is adversely affected by the presence of mandibular incisors. Many of these women lost their teeth in early adulthood. When all subjects were included, the height of the ridge in the anterior region of the maxillae was not significantly altered by presence of mandibular incisors. When the ridge height was compared among those who had been edentate in the maxillae for less than 30 years, the difference between dentate and edentate subjects was significant. This study indicates that the alveolar ridges in the anterior region of the maxillae where teeth were extracted early in life during the rapid phase of bone metabolism are less disposed to bite trauma caused by the presence of the mandibular incisors than are individuals who lost their teeth in middle or old age.

Loss of alveolar bone from the edentulous jaws is a serious and common clinical problem, especially among the elderly. The retention and stability of dentures are reduced, but little is known about the pathogenesis of this bone loss. The existing data suggest that either local factors, for instance occlusal trauma, or systemic factors such as postmenopausal osteoporosis, contribute to edentulous alveolar bone resorption. This paper reviews the evidence for the aetiology of residual ridge resorption following tooth extraction.

The present study was carried out by fabrication of microcorrosive resin cast to investigate the vascular changes of periodontium of dogs' mandibular incisors with severe mobility and deep pocket formation concomitant with suppuration and alveolar bone loss. With aid of the dissolution of soft tissues by protease, alveolar bone remained left with resin cast of specimen, which then was referred for scanning electron microscopic examination. Results were as follows: 1. The vasculature of inner gingival epithelium which originally appeared as a flat, mesh-like network underwent a conformational change and turned out to be a vasculature with glomerulus-like loops due to chronic inflammation. 2. No remarkable change was ever identified in vasculature of periodontal ligament surrounding cervix of tooth. 3. Certain parts of vasculature of periodontal ligament disappeared, which combining with the occlusion indicated the occurrence of occlusal trauma. 4. Exposed alveolar bone surface where the periodontal vasculature disappeared showed an amorphous, flat surface. Quite contrast to this, the surface of alveolar bone on which the vasculature is located appeared undergoing a resorptive process. 5. Accordingly, the damage occurred in periodontium was not merely due to chronic inflammation but to the accompanying occlusal trauma which was supposed to be a predominant factor.