Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty percent of postoperative wound infections result from bacteria acquired elsewhere than in the operating room. Concomitant infections--such as dermatitis; periodontitis; infections of the respiratory, gastrointestinal, or urinary tracts--are not identified preoperatively, despite a threat to the patient greater than that of anesthesia and surgery combined. Isolation of overt infection is neglected. The entire hospital becomes a reservoir of bacterial debris that is reflected in the carriage of pathogens by personnel and patients. Infections are often initiated by medical devices that invade the vascular system, respiratory tract, or urinary bladder. Professional leadership at the bedside is the key to detecting and correcting breaches in technique and setting an example of a philosophy of total patient care.
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PMID:The surgeon's responsibility for asepsis. 71 99

Anaerobic Gram-negative bacteria dominate in periodontitis locations, while Gram-positive bacteria characterize healthy sites. A well-established Gram-positive flora might therefore inhibit the colonization of Gram-negative pathogens. The purpose of the present investigation was to examine whether endogenous S. sanguis could prevent, or reduce, periodontal bone loss in rats infected with a virulent P. gingivalis strain. Sixty specific pathogen-free Wistar rats were divided into 6 groups. Doxycycline was administered in the drinking water for 2 weeks to the groups A, B, C, and D to suppress the preexisting microflora in the mouth. Rats in groups A and C were subsequently inoculated with an S. sanguis strain, isolated from one of the rats, once a day for 5 d. Infection with P. gingivalis 381 was then carried out for 5 d in groups A, B, and E. Group F was not treated with doxycycline nor infected with bacteria and served as untreated control. Six weeks after the P. gingivalis inoculation, the rats were killed. Periodontal bone levels were assessed radiographically and morphometrically, and serum antibody against P. gingivalis 381 was determined by a fluorescence immunoassay. Periodontal bone support, determined radiographically, was reduced in group B (doxycycline-treated, P. gingivalis-inoculated) compared with the other groups. In contrast, the morphometric determination showed no differences between the groups. In group B antibody levels against two different P. gingivalis 381 cell surface antigens were significantly elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Periodontal bone loss in Porphyromonas gingivalis-infected specific pathogen-free rats after preinoculation with endogenous Streptococcus sanguis. 133 45

Complement components C3 and C5 are susceptible to limited proteolysis by an arginine-specific cysteine proteinase isolated from Porphyromonas gingivalis. This bacterium is an anaerobe commonly associated with severe periodontal disease. Infection by P. gingivalis is accompanied by an acute inflammatory response, complete with extensive neutrophil involvement. This prompted us to investigate a possible direct role for complement in periodontitis evoked by P. gingivalis. Exposure of C3 and C5 to the cysteine proteinase at molar ratios between 1:25 and 1:100 (enzyme to substrate ratios) resulted in a time-dependent, limited degradation of each component. C3 was converted in a stepwise manner to C3a-like and C3b-like fragments with evidence of extensive further degradation of the C3a-like portion of the molecule. We were unable to demonstrate C3a activity in the C3 digestion mixtures. C3 degradation appears to involve primarily the alpha-chain. Proteolysis of C5 also progresses in a stepwise manner producing an initial internal cleavage of the alpha-chain to generate 30- and 86-kDa fragments. Further digestion of the 86-kDa amino-terminal fragment of the alpha-chain leads to the release of C5a or a C5a-like fragment that is biologically active for neutrophil activation. The fact that a potent chemotactic factor, i.e. C5a, can be generated from C5 by a proteinase derived from P. gingivalis suggests a recruiting mechanism for attracting neutrophils to the gingival lesion site in periodontal disease.
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PMID:Activation of complement components C3 and C5 by a cysteine proteinase (gingipain-1) from Porphyromonas (Bacteroides) gingivalis. 152 18

In the international literature it is shown the central role of root canal infection in the etiology of periapical lesions. As a matter of fact it has been proved (13) that sterile necrotic pulp tissue is completely unable to cause inflammatory reactions at the periapex. Infection of endodontic origin extends to the supporting tissues of the tooth only in the case of their acute inflammation (e.g. acute apical periodontitis, acute alveolar abscess, phoenix abscess). On the other hand in chronic inflammation bacteria remain confined in the endodontic space. Only few exceptions to this general rule have been experimentally proved. In endodontics we deal with a mixed infection which is composed by obligate anaerobes and by facultative anaerobes. The most frequently found obligate anaerobes are Bacteroides sp. and Fusobacterium sp. (Gram- rods) Anaerobic Diphtheroides (Gram+ rods) Peptostreptococcus sp. (Gram+ cocci) and Veilonella sp. (Gram- cocci). Actinomyces sp., Lactobacillus sp., Streptococcus sp., and Staphilococcus sp. are the facultative anaerobes most frequently found.
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PMID:[Significance of the bacterial flora in the etiology of apical periodontitis. Qualitative, quantitative and topographical aspects]. 213 40

Skin and mucous membranes including the oral mucosa are among the preferential locations of opportunistic infections and secondary neoplasms in patients infected with the human immunodeficiency virus (HIV). Infections of the oral mucosa such as thrush occur in a high percentage of AIDS patients, patients with AIDS-related complex or HIV-seropositive individuals. The clinical appearance of the infections (herpes virus infection, periodontitis) is often marked by aggressive expansion, frequent recurrences or resistance to therapy. Oral "hairy" leukoplakia is considered to be a characteristic lesion in HIV-infected individuals. Tumors like Kaposi's sarcoma, squamous cell carcinoma and non-Hodgkin lymphoma of the oral mucosa may cause marked morbidity in AIDS patients. Such oral lesions are frequently the first indication of an HIV-infection. Dentists should be aware of the oral manifestations of HIV-infection and initiate diagnostic and therapeutic measures in the interest of the patients and for epidemiologic reasons.
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PMID:[Oral manifestations of HIV infection]. 270 Apr 12

The different forms of periodontitis are all associated with a distinct bacterial flora. However, a clear relationship is described between localized juvenile periodontitis (LJP) and Actinobacillus actinomycetemcomitans. Eleven LJP patients all harboured A. actinomycetemcomitans. The arrest of LJP is often impossible, due to the inability to eliminate A. actinomycetemcomitans. Therefore, antibiotic treatment was introduced in combination with the initial treatment. We studied the effect of periodontal treatment on the microflora and clinical status of periodontal disease patients using different therapies. Group 3 attained the best results (initial treatment and a combination metronidazole and amoxicillin), the group to eliminate A. actinomycetemcomitans effectively.
Infection
PMID:The role of Actinobacillus actinomycetemcomitans in periodontal disease. 276 72

There is overwhelming evidence that bacteria cause periodontitis and that they do so by extending apically along the surfaces of the tooth roots and creating pockets. A very complex mixture of microbial species, mostly although not exclusively gram-negative, anaerobic, and motile, is involved. Infection probably occurs in a progressive and sequential manner. The bacteria involved include various species of Bacteroides, Actinobacillus, Eikenella, Fusobacterium, Capnocytophaga, and Eubacterium. Local oral conditions such as tooth position play an aetiologic role by affecting plaque accumulation and retention. Host defence factors, particularly the phagocytic cells and the immune system, play a determinative role in the aetiology by monitoring, controlling, and regulating microbial colonization and infection. These diseases begin as an acute inflammation of the marginal gingiva, and they progress through orderly stages to the formation of a gingival pocket. Transition from gingivitis to periodontitis is not well-understood, but it probably involves colonization by additional microbial species or invasion of the periodontal tissue by species already present. Progression of periodontal destruction is episodic, possibly as a consequence of successful host defence. In most patients, periodontal destruction occurs more infrequently than previously suspected. In both treated and untreated patients, a small subgroup accounts for most of the disease activity. The most important problem we now face is to develop diagnostic methods to identify individuals in this subgroup and devise ways to prevent and control their diseases.
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PMID:Current understanding of the aetiology and progression of periodontal disease. 353 87

Infection by Porphyromonas gingivalis is strongly associated with adult periodontitis, with proteinases from this bacterium now considered to be important virulence factors. In order to investigate possible pathological functions of these enzymes, we examined the effect of both free and vesicle-bound forms of the two major cysteine proteinases (gingipains) of P. gingivalis on plasma clot formation by using thrombin time (TT) measurements. Both Lys-gingipain (gingipain-K) and Arg-gingipain (gingipain-R) prolonged plasma TT in a dose- and time-dependent manner, and this was also found with vesicles which are the biological carriers of P. gingivalis proteinases. The increase in plasma TT by vesicles could be completely reversed by treatment with nonspecific cysteine proteinase inhibitors but only partially by compounds selective for either gingipain-K or gingipain-R. Preincubation of vesicles with a gingipain-K-specific inhibitor (z-FK-ck) reduced plasma TT more than a gingipain-R-specific inhibitor (leupeptin), suggesting that under physiological conditions gingipain-K was more effective in fibrinogen destruction. Each purified enzyme also markedly increased fibrinogen TT, gingipain-R being fourfold more potent than gingipain-K. However, in plasma, gingipain-R was ineffective because of the inhibitory effect of albumin. These results imply that cysteine proteinases, especially gingipain-K, abrogate the clotting potential of fibrinogen and, therefore, may contribute to the bleeding tendency and to persistent inflammation in periodontitis sites infected with P. gingivalis.
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PMID:Effect of free and vesicle-bound cysteine proteinases of Porphyromonas gingivalis on plasma clot formation: implications for bleeding tendency at periodontitis sites. 759 Nov 49

Infection with Porphyromonas gingivalis is strongly associated with adult periodontitis, and proteinases are considered to be important virulent factors of the bacterium. In order to investigate the function of proteinases in disease development we examined vesicles, a biological carrier of these enzymes, for the generation of vascular permeability enhancement (VPE) activity, believed to correlate with the exudation of gingival crevicular fluid. The vesicles generated VPE activity from human plasma in a dose-dependent manner which could be inhibited 90% by antipain, a specific inhibitor of the Arg-specific cysteine proteinases (Arg-gingipains [RGPs] from P. gingivalis. Incubation of vesicles with high-molecular-weight-kininogen (HMWK)-deficient plasma did not result in VPE activity. On this basis, RGPs associated with vesicles were assumed to be responsible for most of the VPE activity generation via plasma prekallikrein activation and subsequent bradykinin production. The secondary pathway for VPE activity production was dependent on the direct release of bradykinin from HMWK by the concerted action of RGP and a Lys-specific cysteine proteinase (Lys-gingipain [KGP]), also associated with vesicles. These results indicate that RGP and KGP are biologically important VPE factors acting either via prekallikrein activation (RGP) and/or HMWK cleavage (RGP and KGP) to release BK and, thereby, contributing to the production of gingival crevicular fluid at periodontal sites infected with P. gingivalis.
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PMID:Dependence of vascular permeability enhancement on cysteine proteinases in vesicles of Porphyromonas gingivalis. 772 14

Infections due to Actinomycosis species are located in the cervico-facial region in 50 to 65 percent of the cases. Extra-cervical cutaneous lesions are exceptional. The most frequently encountered germ is Actinomyces israeli, observed in 85 percent of the cases. We report the case of an Actinomyces meyeri infection which presented as a leg abscess and a pulmonary lesion. There was no cervico-facial localization. There was however a chronic parodontitis. A second germ, Capnocytophaga sp. was isolated from the abscess. This case is of particular interest because of the extracervical localization and the rare species isolated (17 other cases of Actinomyces meyeri infection have been reported). The mechanism of the infection can be better understood in light of pulmonary lesions in the lower right lobe due to inhalation and the coexistence of a buccodental germ in the culture of the leg abscess: buccodental origin of the germ, pulmonary lesion secondary to inhalation, septicaemic dissemination with cutaneous metastases.
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PMID:[Actinomyces meyeri cutaneous actinomycosis with pulmonary localization]. 807 51


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