Periodontal Tissue Breakdown Research Articles

Tumor Necrosis Factor‐α Induces Matrix Metalloproteinases‐3, ‐10, and ‐13 in Human Periodontal Ligament Cells

Various biologic mediators, including matrix metalloproteinases (MMPs), that are implicated in periodontal tissue breakdown can be induced by cytokines. MMPs are known to degrade periodontal ligament attachment, and bone matrix proteins and tissue inhibitors of metalloproteinase (TIMPs) inhibit the activity of MMPs. The aim of this study is to investigate the effect of tumor necrosis factor (TNF)-α on the expression of MMPs in human periodontal ligament (PDL) cells in vitro and establish which MMPs are expressed specifically in response to that stimulus. Cultured PDL cells were stimulated with TNF-α and analyzed with an MMP antibody array. Real-time polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and western blot with cell lysate and zymography were used to measure messenger RNA (mRNA) and protein levels of MMP-3, -10, and -13. To examine TNF receptor (TNFR) expression, PDL cells were examined by flow cytometry, and expression of MMP-3, -10, and -13 was observed after blocking the TNFR with an antagonist. Results from real-time PCR, ELISA, and western blot were analyzed by paired t test. The antibody array showed that the protein most strongly upregulated by TNF-α stimulation was MMP-3, followed by MMP-13 and MMP-10. The TNF-α receptor blocker specifically inhibited expression of MMP-3 and -13. In addition, TNF-α increased levels of MMP mRNAs in MMP-3, -13, and -10 (in decreasing order). However, ELISAs showed that MMP-13 was the most upregulated protein, followed by MMP-10 and MMP-3. Western blotting indicated that TNF-α increased MMP-3 and -13 levels but had no significant effect on the level of MMP-10, and zymography showed that TNF-α increased the activities of all forms of MMP-3 and -13, but MMP-10 was not detected. Flow cytometry demonstrated that the majority of PDL cells expressed TNFR1. TNF-α (10 ng/mL) upregulates levels of MMP-3, -10, and -13 in human PDL cells. These results suggest that these proteins play an important role in the inflammation of PDLs.

Effect of Low‐Dose Doxycycline on Serum Oxidative Status, Gingival Antioxidant Levels, and Alveolar Bone Loss in Experimental Periodontitis in Rats

Subantibiotic doses of doxycycline (low-dose doxycycline [LDD]) have been widely used in periodontal treatment for enzymatic inhibition and related anti-inflammatory properties. The aim of the present study is to verify the possible effects of LDD on oxidative stress in relation to periodontal attachment loss associated with ligature-induced experimental periodontal disease in rats. Thirty female Wistar albino rats were divided into three study groups as follows: 1) control (C) rats; 2) rats with experimental periodontitis (PED); and 3) rats with PED that were treated with doxycycline (PED + LDD). PED was induced by placing ligatures around the cervix of the maxillary second molars for 21 days. The PED + LDD group was treated orally with doxycycline (6 mg/kg) for 21 days after the ligature was placed. After 21 days, the rats were euthanized, and samples of the right maxilla were defleshed and used for histologic and morphometric analyses. The gingival tissue of the left maxilla was used for the analysis of lipid peroxidation (malondialdehyde [MDA]) and antioxidant enzymes (catalase, glutathione peroxidase, and superoxide dismutase). Levels of serum total antioxidant status (TAS)/total oxidant status (TOS) and oxidative stress index (OSI) were also analyzed. Alveolar bone loss was significantly higher in the PED group compared with the PED + LDD and C groups (P <0.05). Doxycycline exhibited the most prominent inhibition on gingival tissue levels of MDA and antioxidant enzymes (P <0.05). Doxycycline also significantly reduced TOS and OSI levels (P <0.05) but increased the TAS level. Doxycycline helps to prevent periodontal tissue breakdown by inhibiting local and systemic oxidative stress.

Inhibitory effects of sword bean extract on alveolar bone resorption induced in rats byPorphyromonas gingivalisinfection

The domesticated legume, Canavalia gladiata (commonly called the sword bean), is known to contain canavanine. The fruit is used in Chinese and Japanese herbal medicine for treating the discharge of pus, but its pharmacological mechanisms are still unclear. This study examined the effect of sword bean extract (SBE) on (i) oral bacteria and human oral epithelial cells in vitro, and (ii) the initiation and progression of experimental Porphyromonas gingivalis-induced alveolar bone resorption in rats. A high-performance liquid chromatography/ultraviolet method was applied to quantitate canavanine in SBE. By assessing oral bacterial growth, we estimated the minimum inhibitory concentration and minimum bactericidal concentration of SBE, canavanine, chlorhexidine gluconate (CHX) solution. The cytotoxicity of SBE, canavanine, CHX, leupeptin and cystatin for KB cells was determined using a trypan blue assay. The effects of SBE, canavanine, leupeptin and cystatin on Arg-gingipain (Rgp) and Lys-gingipain (Kgp) were evaluated by colorimetric assay using synthetic substrates. To examine its effects on P.gingivalis-associated periodontal tissue breakdown, SBE was orally administered to P.gingivalis-infected rats. Sword bean extract contained 6.4% canavanine. SBE and canavanine inhibited the growth of P.gingivalis and Fusobacterium nucleatum. The cytotoxicity of SBE, canavanine and cystatin on KB cells was significantly lower than that of CHX. Inhibition of Rgp with SBE was comparable to that with leupeptin, a known Rgp inhibitor, and inhibition of Kgp with SBE was significantly higher than that with leupeptin at 500μg/mL ( p<0.05). P.gingivalis-induced alveolar bone resorption was significantly suppressed by administration of SBE, with bone levels remaining comparable to non-infected animals ( p<0.05). The present study suggests that SBE might be effective against P.gingivalis-associated alveolar bone resorption.

Role of insulin sensitivity and beta cell function in the development of periodontal disease in adults without diabetes

The goal of this study was to explore whether insulin resistance and beta cell function are related to periodontal pocket formation, indicative of infectious periodontal disease in non-smoking adults without manifest diabetes. We analysed data from a Health 2000 Survey consisting of dentate subjects without any indication of diabetes, aged between 30 and 64, who had never smoked and who had participated in the Follow-up Study on Finnish Adults' Oral Health about 4years later (n=157). The Homeostasis Model Assessment Indices were used to measure insulin resistance (HOMA-IR) and β-cell function (HOMA-B). The development of periodontal disease was measured by means of the incidence of deepened periodontal pockets (4mm deep or deeper) during the follow-up period. Incidence rate ratios (IRR) were estimated using Poisson regression models. Both HOMA-IR and HOMA-B indices were associated with periodontal pocket formation during the 4-year follow-up. The results of this follow-up study suggest that impaired glucose metabolism measured as insulin resistance and altered beta cell function predict the breakdown of periodontal tissues. Further studies about their role in the pathogenesis of periodontal diseases are needed.

Herpes virus: A key missing piece of the periodontopathogenic jigsaw puzzle

A solid understanding of the etiology of periodontitis is critical for developing therapies that can ensure long-lasting disease control. Research during the past 15 years has implied that herpes viruses are involved in the etiopathogeny of destructive periodontal disease. Because of the high copy counts of Epstein-Barr virus and cytomegalovirus in aggressive and chronic periodontitis, it is unlikely that these pathogenic viruses are acting merely as innocuous bystanders present in proportion to the severity of the underlying periodontal pathosis. However, herpes viruses are probably not stand-alone periodontopathic agents but cooperate with specific bacteria in periodontal tissue breakdown. A coinfection of active herpes viruses and periodontopathic bacteria may constitute a major cause of periodontitis and explain a number of the clinical characteristics of the disease. The purpose of this review is to evaluate the evidence supporting the hypothesis that viral infection plays a role in the development of periodontitis.

Successful stabilization of periodontal disease and preprosthetic implant site preparation using autogenous mandibular symphysis block bone grafting in aggressive periodontitis

Aggressive periodontitis is the disease affecting the periodontium, leading to rapid attachment and alveolar bone loss in an otherwise systemically healthy individual. The rate of periodontal connective tissue and alveolar bone breakdown is further influenced by hereditary, genetic, and familial compounding factors. This case report highlights the sequential treatment strategy employed to achieve an esthetic and functioning dentition for an aggressive periodontitis patient, involving stabilization of the periodontal condition and preprosthetic site preparation by horizontal ridge augmentation using autogenous mandibular block bone grafting procedure.

Pre-prosthetic minor tooth movement with elastic separating ring &amp; provisional restoration modification: case report

Proximal caries or coronal defect in posterior teeth may result in the loss of proximal space and drifting of neighboring teeth, which makes restoration difficult. Inability to restore proper contours and to align tooth axis properly are commonly encountered problems when planning tooth restoration. Moreover, tilted teeth aggravate periodontal tissue breakdown, such as pseudo-pocket, and angular osseous defect. The purpose of this case presentation is to describe a simple technique for inducing minor tooth movement with orthodontic separating ring and provisional restoration modification. This method was used to create crown placement space on mesially tilted molar. This method is easy, simple and efficient technique which could be used in interproximal space gaining in selected situation.

Fibroblast growth factor‐2 stimulates directed migration of periodontal ligament cells via PI3K/AKT signaling and CD44/hyaluronan interaction

Fibroblast growth factor-2 (FGF-2) regulates a variety of functions of the periodontal ligament (PDL) cell, which is a key player during tissue regeneration following periodontal tissue breakdown by periodontal disease. In this study, we investigated the effects of FGF-2 on the cell migration and related signaling pathways of MPDL22, a mouse PDL cell clone. FGF-2 activated the migration of MPDL22 cells and phosphorylation of phosphatidylinositol 3-kinase (PI3K) and akt. The P13K inhibitors, Wortmannin and LY294002, suppressed both cell migration and akt activation in MPDL22, suggesting that the PI3K/akt pathway is involved in FGF-2-stimulated migration of MPDL22 cells. Moreover, in response to FGF-2, MPDL22 showed increased CD44 expression, avidity to hyaluronan (HA) partly via CD44, HA production and mRNA expression of HA synthase (Has)-1, 2, and 3. However, the distribution of HA molecular mass produced by MPDL22 was not altered by FGF-2 stimulation. Treatment of transwell membrane with HA facilitated the migration of MPDL22 cells and an anti-CD44 neutralizing antibody inhibited it. Interestingly, the expression of CD44 was colocalized with HA on the migrating cells when stimulated with FGF-2. Furthermore, an anti-CD44 antibody and small interfering RNA for CD44 significantly decreased the FGF-2-induced migration of MPDL22 cells. Taken together, PI3K/akt and CD44/HA signaling pathways are responsible for FGF-2-mediated cell motility of PDL cells, suggesting that FGF-2 accelerates periodontal regeneration by regulating the cellular functions including migration, proliferation and modulation of extracellular matrix production.

The effect of chlorhexidine on the receptor activator of NF-kB ligand (RANKL) and osteoprotegerin (OPG) expression in chronic periodontitis in humans and companion animals

Periodontal disease is a chronic, multi-factorial disease of the tissues supporting the teeth. Periodontitis in companion animals is an almost identical disease to that in humans in terms of disease course and clinical presentation. Receptor activator of NF-kB ligand (RANKL) and osteoprotegerin (OPG) are bioactive molecules that control bone resorption. This study aims to evaluate the effect of Chlorhexidine (CXD) on the RANKL and OPG expressions in gingival crevicular fluid (GCF) collected from subjects with chronic periodontitis. GCF was obtained from subjects with chronic periodontitis.10 subjects (CXD1) rinsed the mouth with 0.12% CXD, 10 subjects (CXD2) utilized 0.20% CXD and the last 10 (PL) used Placebo solution for 7 days. RANKL and OPG concentrations in GCF were measured by enzyme-linked immunosorbent assays ELIat baseline and after 7 days. Periodontal clinical variables: clinical attachment loss (CAL), probing pocket depth (PPD), papilla-bleeding index (PBI) were evaluated in all groups. After 7 days in CXD1 and CXD2 group RANKL/OPG ratio exhibited a significant decrease (p<0.05) in contrast to the PL group where results showed similar values of RANKL/OPG ratio at baseline and after the observation period. RANKL/OPG ratio was positively correlated with PPD, CAL and PBI before and after the observation period in both Chlorhexidine (CXD1, CXD2) groups. In an existing inflammatory response, chlorhexidine reduced the level of periodontal inflammation, which leads to reduction of RANKL/OPG relative ratio. Decrease of RANKL/OPG ratio will apparently induce maintenance of alveolar bone and slow down periodontal tissue breakdown.

歯周組織破壊の程度を表す新規指標（総合骨吸収率）の有用性：糖尿病の重症度との関連

歯周組織破壊の程度を表す新規指標（総合骨吸収率）の有用性：糖尿病の重症度との関連

Morphometric, Histomorphometric, and Microcomputed Tomographic Analysis of Periodontal Inflammatory Lesions in a Murine Model

Porphyromonas gingivalis is recognized as one of the major periodontal pathogens in chronic periodontitis, a common infectious disease characterized by inflammation and destruction of periodontal tissues. Several animal models with P. gingivalis have been used in periodontitis studies. Additionally, multiple approaches have also been applied to measuring alveolar bone loss in periodontitis models, including histomorphometry, morphometry, and radiography. The aims of this study were to assess periodontal inflammatory lesions after P. gingivalis-induced periodontitis and use this model to compare three approaches for assessing alveolar bone loss. Twelve-week-old male C57BL/6 mice were divided into two groups: 48 P. gingivalis-infected and 52 untreated control mice. Periodontitis was induced by wrapping P. gingivalis-soaked ligatures around the left maxillary second molar and changing the ligatures every other day. Mice were euthanized on days 0, 3, 7, and 10 after ligature placement, for a total of 12 experimental and 13 control mice per time point. Epithelial downgrowth, inflammation, and osteoclast activity were evaluated; alveolar bone loss was determined by histomorphometry, morphometry, and microcomputed tomography. The P. gingivalis-infected group showed significantly increased epithelial downgrowth (P <0.05), inflammation (P <0.05), alveolar bone loss (P <0.05), and osteoclast activity (P <0.05) throughout the experimental period compared to the controls. All three methods yielded efficient evaluation of alveolar bone loss. Our results show evidence that the P. gingivalis-soaked ligature-induced murine model mounts an adequate inflammatory response and exhibits periodontal tissue breakdown compatible with other models of periodontal disease. In addition, alveolar bone loss can accurately be quantified using any of the three alveolar bone analyses presented in this article.

Periodontal examination for alveolar bone resorption

Periodontitis is an inflammatory disease which is involved with gingival attachment loss and an alveolar bone resorption. Traditional methods for taking X-ray photograph or assessments of probing depth and clinical attachment level are provided the previous periodontal tissue breakdown, however, these methods are hard to confirm the disease activity and predict of the disease outcome. Therefore, the component or quality of gingival crevicular fluid (GCF), which is directly, reflects the gingival inflammation is noticed. It firstly describes that GCF containing the inflammatory mediator, cytokine, and bone markers are not only related to the bone resorption but also affected the periodontal disease activity. As the final part in the series it lastly discusses the possible uses of predictive diagnostic tests of periodontal disease activity in dental practice.

Role of bacteria in health and disease of periodontal tissues

The interaction between bacteria and eukaryotic cells is complex; active processes must exist that allow us to live harmoniously with the bacteria which normally live on and within our bodies. Periodontal diseases, a series of infections of the periodontal tissues which eventually can lead to loss of teeth, is a form of aberrant inflammation resulting from a complex biofilm of friendly commensal and periodontopathic bacteria and their products, triggering the human inflammatory response. A shift in microbial species in the gingival sulcus from gram-positive, facultative, fermentative microorganisms to predominantly gram-negative, anaerobic, chemoorganotrophic, and proteolytic organisms (214) has been strongly associated with periodontal tissue breakdown (65, 154). However, the level of periodontal breakdown has long been associated with the degree of host predisposition (59). A significant portion of the host predisposition to disease may relate to

Structure of periodontal tissues in health and disease*

The periodontium, defined as those tissues supporting and investing the tooth, comprises root cementum, periodontal ligament, bone lining the tooth socket (alveolar bone), and that part of the gingiva facing the tooth (dentogingival junction). The widespread occurrence of periodontal diseases and the realization that lost tissues can be repaired and, perhaps, regenerated has generated considerable interest in the factors and cells regulating their formation and maintenance. It is important to understand that each of the periodontal components has its very specialized structure and that these structural characteristics directly define function. Indeed, proper functioning of the periodontium is only achieved through structural integrity and interaction between its components. In recent years, a number of detailed descriptions of the structural and compositional features of periodontal tissues have been published (3, 5‐7, 9, 15, 17, 46, 50, 56, 58, 61); we refer the reader to these for a comprehensive description of the development, formation, and structure of periodontal tissues. The present review will focus on structure‐function relationships pertinent to understanding periodontal tissue breakdown and the repair ⁄ regeneration of affected structures.

Rehabilitative Management Offered Nigerian Localized and Generalized Aggressive Periodontitis Patients

This paper highlights the typical clinical features of aggressive periodontitis (formerly known as juvenile periodontitis in the South Western region of Nigeria), the attending psychological effect following tooth loss, and the rehabilitative management offered which included periodontal therapy, psychotherapy, and prosthetic replacement of the missing teeth. The psychotherapy is the main distinguishing treatment in this study from previously reported modes of management of this disease entity. Subjects were from a part of the South Western region of Nigeria, and ages ranged from 15 to 22 years. They all presented very late with subsequent gross periodontal breakdown and subsequent psychological depression. The mean values of the probing depth (mm), degree of mobility, and the amount of bone fill (mm) from the periapical radiographs were recorded pre and post-operatively. The missing teeth were replaced with acrylic dentures, and psychotherapy was offered at three levels (individual, group, and conjoint-family psychotherapy). There was significant improvement of these clinical parameters six months after treatment, and the partial denture replacement of the missing teeth improved their appearance as expected but did not totally improve the initial depressive state. The psychotherapy offered gave the patients positive psychological effects that further restored their ability to socialize in their environment, which added to their positive experience of life. In conclusion the typical clinical features of localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP) patients in our environment are late presentation with gross periodontal tissue breakdown. Psychotherapy is an important aspect in the management of this group of patients in conjunction with the periodontal and prosthetic management, which gives total rehabilitation.

Specific pro-apoptotic fibronectin fragments modulate proteinase expression in periodontal ligament cells.

During inflammation and periodontal disease, the extra-cellular matrix protein fibronectin (FN) is degraded into fragments whose activities differ from those of the intact molecule. In periodontal ligament cells in vitro, some fragments elevate the expression of matrix metalloproteinases and serine proteinases, while others induce apoptosis through a mechanism regulated by caspase proteases and specific signaling pathways. In this study, we investigated whether the pro-apoptotic V+H- fibronectin fragment modulates proteinase expression as part of the apoptotic mechanism in periodontal ligament cells. The importance of this study is that a structurally similar fibronectin fragment found in vivo (40-kDa) is associated with periodontal disease status. However, the recombinant V+H- FN protein which is structurally and functionally similar to the in vivo 40-kDa fragment was chosen as the focus of these studies over the in vivo fragment because of the ability to readily produce and purify large quantities of recombinant fragments for detailed studies. Thus, findings from this study relate to our understanding of how the extracellular matrix of the periodontal ligament in an inflamed environment may contribute to periodontal disease and its progression. We used substrate zymography, reverse zymography, proteinase inhibitors, and partial sequencing to investigate whether the pro-apoptotic V+H- fibronectin fragment modulates proteinase expression as part of this apoptotic mechanism. Incubation with the V+H- fragment reduced the expression of all gelatinolytic proteinases and inhibitors commonly expressed by periodontal ligament cells. In the presence of caspase inhibitors, inhibitors known to suppress apoptosis, however, the reduced proteinase profile was rescued, showing that caspase inhibitors were able to reverse the reduced proteinase profile and indicating that caspase-mediated pathways are pertinent to fibronectin-fragment-mediated matrix metalloproteinase expression. In addition, the V+H- fragment also triggered the expression of a unique high molecular weight gelatinolytic proteinase of approximately 200 kDa. This proteinase was a serine proteinase, whose identity is not known. These findings suggest that matrix-degrading proteinases may be involved in apoptosis as part of a unique mechanism of periodontal tissue breakdown, in which novel proteinases may help execute the dissolution of the extracellular matrix.

Porphyromonas gingivalis 67-kDa fimbriae induced cytokine production and osteoclast differentiation utilizing TLR2

Porphyromonas gingivalis, a major etiological agent of adult periodontitis, has two distinctly different types of fimbriae on the cell surface. The major fimbriae, which consist of a 41-kDa fimbrillin of P. gingivalis ATCC 33277, have been known to induce inflammatory cytokine production in murine peritoneal macrophages. In this study, we examined the effects of the minor fimbriae of P. gingivalis, composed of a 67-kDa fimbrillin, on cytokine production in murine peritoneal macrophages and the ability to induce osteoclast differentiation. Murine peritoneal macrophages were stimulated with P. gingivalis 67-kDa minor fimbriae for 24 h, then the levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and IL-6 production were determined by enzyme-linked immunosorbent assay (ELISA). To estimate osteoclast differentiation, mouse osteoclast precursors were placed on dentine slices, and cultured with or without P. gingivalis 67-kDa minor fimbriae for 7 days. P. gingivalis 67-kDa minor fimbriae clearly induced IL-1β, TNF-α and IL-6 production in mouse macrophages. Furthermore, pit formations on the dentine slices were significantly extended when the osteoclast precursors were incubated with P. gingivalis 67-kDa minor fimbriae. Pretreatment with anti-Toll-like receptor 2 (TLR2) antibody significantly inhibited IL-1β, TNF-α and IL-6 induction ( P<0.05) in mouse macrophages and pit-forming activity of osteoclast precursor cells stimulated with P. gingivalis 67-kDa minor fimbriae. These results suggest that P. gingivalis 67-kDa minor fimbriae may provoke host inflammatory response and be involved in periodontal tissue breakdown.

Clinical Effect of the Subantimicrobial Dose of Doxycycline(SDD) on the Chronic Periodontitis

【Periodontal disease is a complex infectious disease caused by bacteria in the oral mucosa, which results in gingival inflammation, breakdown of periodontal tissues, bone resorption, and finally tooth loss. Mechanical plaque control methods-scaling and root planing are effective methods to stop the progression of such periodontal disease. It was reported that subantimicrobial dose of doxycycline(SDD) regimen could improve clinical conditions of periodontal tissues without causing the overgrowth of opportunistic organisms that was a typical antibiotic side effect. Therefore pharmacological therapy, used in conjunction with mechanical therapy could be considered a useful treatment modality in the treatment of chronic periodontal disease. In this study, 30 patients diagnosed as moderate to advanced chronic periodontitis were divided into 2 groups. In this double-blind, placebo-controlled study, the patients were administered 20mg doxycycline capsule or placebo capsule b.i.d. for 4months, after scaling and root planing. Clinical parameters-bleeding on probing, pocket depth and clinical attachment level were compared and evaluated between these groups at periods of first visit, 1 month, 2 months, 3 months, 4 months. The results were as follows ; 1. In case of moderate periodontitis, pocket depth showed significant reduction after treatment in both the control & experiment groups, when compared with the baseline values(p】

Inactivation of tissue inhibitor of metalloproteinases-1 (TIMP-1) by Porphyromonas gingivalis

In response to periodontal inflammation, host cells release matrix metalloproteinases (MMPs) that contribute to periodontal tissue breakdown unless the tissue inhibitors of metalloproteinases (TIMPs) neutralize their activity. In this study, the capacity of Porphyromonas gingivalis to inactivate TIMP-1 was investigated. Proteolytic digestion of TIMP-1 was monitored by SDS–PAGE and Western immunoblotting. Planktonic cells and biofilms of P. gingivalis degraded TIMP-1 with production of several lower molecular mass fragments. Incorporation of human serum in the assay mixture had no effect on the degradation of TIMP-1 by P. gingivalis, whereas a cysteine proteinase inhibitor caused a complete inhibition. Using a fluorogenic assay, it was found that TIMP-1 treated with P. gingivalis lost its capacity to inhibit MMP-9 activity. This study revealed the potential of P. gingivalis to inactivate TIMP-1 through proteolytic degradation. This phenomenon may contribute to increasing significantly the level of active MMPs in affected periodontal sites and subsequently favor tissue destruction.

Inactivation of tissue inhibitor of metalloproteinases-1 (TIMP-1) by Porphyromonas gingivalis.

In response to periodontal inflammation, host cells release matrix metalloproteinases (MMPs) that contribute to periodontal tissue breakdown unless the tissue inhibitors of metalloproteinases (TIMPs) neutralize their activity. In this study, the capacity of Porphyromonas gingivalis to inactivate TIMP-1 was investigated. Proteolytic digestion of TIMP-1 was monitored by SDS-PAGE and Western immunoblotting. Planktonic cells and biofilms of P. gingivalis degraded TIMP-1 with production of several lower molecular mass fragments. Incorporation of human serum in the assay mixture had no effect on the degradation of TIMP-1 by P. gingivalis, whereas a cysteine proteinase inhibitor caused a complete inhibition. Using a fluorogenic assay, it was found that TIMP-1 treated with P. gingivalis lost its capacity to inhibit MMP-9 activity. This study revealed the potential of P. gingivalis to inactivate TIMP-1 through proteolytic degradation. This phenomenon may contribute to increasing significantly the level of active MMPs in affected periodontal sites and subsequently favor tissue destruction.