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

Immunohistochemical methods have been used to study the occurrence of neuronal markers in human gingiva from periodontitis-affected sites. In periodontitis-affected buccal gingiva densely distributed neurofilament (NF)-immunoreactive (IR) fiber bundles were observed in the deeper parts of the propria, while NF-IR single fibers occurred in the superficial propria and occasionally in the buccal epithelium. Periodontitis-affected gingiva obtained from interproximal sites showed only sparsely distributed NF-IR fibers. Single nerve fibers immuno-reactive to the peptides substance P and calcitonin gene-related peptide occurred close to or within the epithelium in both buccal and interproximal gingiva. Around blood vessels neuropeptide Y-, peptide histidine-isoleucine amide- and vasoactive intestinal polypeptide-IR fibers were occasionally observed, while clusters of gamma-melanocyte-stimulating hormone-IR cells were found in the propria, in addition to gamma-melanocyte-stimulating hormone IR nerve fibers. Somatostatin-IR dendritic cells were seen in epithelium and propria of buccal and interproximal gingiva, although a high variability in the number of SOM-IR cells was observed. All neuronal markers studied showed a similar distribution in material obtained from young patients with clinically healthy gingivae, although the number of NF-IR fibers in the propria in these subjects was lower. The results demonstrate that in gingiva obtained from periodontitis-affected sites several different biologically active peptides occur in both nerve fibers and cells. At least some of these substances could possible play a role in the inflammatory process. However, since clinically normal gingiva was shown to contain nerve fibers and cells expressing immunoreactivity to the substances studied, no unique periodontitis-induced expression of the neuronal markers studied was found. Thus, any alteration of these substances during the periodontitis process remains to be elucidated.
 ...
PMID:Immunohistochemical study of neurochemical markers in gingiva obtained from periodontitis-affected sites. 257 Aug 28

The effect of bradykinin and desArg9-bradykinin on bone was studied in cultures of calvarial bones taken from 6-7-day-old mice. Bradykinin, at and above a 3-nM concentration, caused a dose-dependent stimulation of bone mineral mobilization and matrix degradation. Bradykinin-stimulated resorption was inhibited by calcitonin, an increased concentration of phosphate in the culture medium, hydrocortisone, dexamethasone, indomethacin, meclofenamic acid, naproxen, and 5, 8, 11, 14-eicosatetraenoic acid. The results suggest that bradykinin stimulates osteoclast-mediated bone resorption by a process that is dependent on endogenous prostaglandin production. The stimulatory effect of bradykinin, but not of parathyroid hormone and prostaglandin E2, was potentiated by the angiotensin-converting enzyme inhibitor, BPP5a. Treatment with carboxypeptidase B did not affect the capacity of the peptide to stimulate 45Ca release. DesArg9-bradykinin (1 mumole/liter) stimulated 45Ca release to the same degree as did bradykinin. Bradykinin (3 microM) did not affect the degradation of cartilage proteoglycans, as assessed by the release of 35S-sulfate from prelabeled calf articular cartilage in organ culture. These findings suggest that generation of bradykinin in inflammatory lesions of rheumatoid arthritis and periodontitis may contribute to the bone resorptive process seen in the joints and alveolar bone; however, bradykinin does not directly activate chondrocytes into a catabolic state.
 ...
PMID:Bradykinin, a new potential mediator of inflammation-induced bone resorption. Studies of the effects on mouse calvarial bones and articular cartilage in vitro. 359 36

The action on bone remodelling of indomethacin, a potent inhibitor of prostaglandin (PG) synthesis, was determined in hamster periodontitis and compared to that of calcitonin. The two treatments reduced the extent of bone resorption considerably but not significantly (NS). The reversal phase, the intermediate step between resorption and formation, was decreased by 33 per cent (NS) by indomethacin and 75 per cent by calcitonin (p less than 0.02). Bone formation was increased by 270 per cent with indomethacin (p less than 0.05) and by 400 per cent with calcitonin (p less than 0.03), compared with untreated animals. This exceeded the extent of bone formation activity in control animals. These data strongly suggest that PG are involved in the mechanism of bone destruction in hamster periodontitis and that PG are potent in vivo uncouplers of bone remodelling as they participate both in an increase in bone resorption and a decrease in bone formation. A partial decrease in reversal lacunae indicates that other factors, also acting as uncouplers, probably take part in the mechanism of bone destruction.
 ...
PMID:A histometric study of the effect of indomethacin and calcitonin on bone remodelling in hamster periodontitis. 659 87

ODU Plaque-susceptible rats (ODUS/Odu) exhibit markedly heavy plaque formation in the lower incisors and develop both periodontal pockets and gingivitis after being fed a commercially available powder diet. These rats have been established as an inbred strain. We have demonstrated that the ODUS/Odu are a very suitable experimental model for studying periodontitis. We already reported about the allelic distribution, changes of plaque formation and body weight, biochemical nature, toxic activity, vascular permeability factor and bradykinin inactivating factor of the plaque, histological and immunological studies, the pH in the periodontal pocket, amount of saliva, IgA in the saliva, salivary kallikrein, the relationship between sialic acid in the saliva and the serum, leukocyte functions (chemotaxis and superoxide anion) in ODUS/Odu, histamine, mast cell, free radicals, superoxide dismutase activities in gingiva and gingival nerve fibers with substance P or calcitonin gene-related peptide, and effect of diabetes. Streptozotocin-induced diabetic ODUS/Odu may be a useful tool for studying the pathological mechanisms in the development of periodontal tissue breakdown in diabetes. ODUS/Odu should help to further establish the utility of this strain as a model for experimental periodontal disease.
 ...
PMID:[Experimental periodontitis in rats]. 762 82

We have shown previously that platelet-activating factor (PAF), a potent inflammatory mediator, acts directly on isolated rat osteoclasts to elevate cytosolic free Ca2+ concentration ([Ca2+]i). The purpose of this study was to examine the effects of PAF on osteoclast function. Osteoclasts were isolated from the long bones of neonatal rabbits and studied in three ways. [Ca2+]i of fura-2-loaded osteoclasts was monitored by microspectrofluorimetry. In 9 out of 16 cells tested, PAF (10-100 nM) caused elevation of [Ca2+]i that peaked then returned to baseline. In contrast, the biologically inactive precursor and metabolite of PAF, lyso-PAF, was without effect. Using time-lapse videomicroscopy, we found that PAF elicited retraction of peripheral pseudopods. Although calcitonin induced sustained retraction and immobility, the response to PAF was transient and, within 30 min, pseudopods reformed. To assess effects of PAF on resorptive activity, osteoclasts were cultured on dentin slices for 48 h in the presence of vehicle, PAF (200 nM), or calcitonin (100 ng/ml). PAF increased the area of individual resorption pits (from control values of 1,660 +/- 110 to 2,240 +/- 200 microns2, P < 0.05) and the total planar area resorbed per unit area of substrate (from 7.6 +/- 1.6 to 14.5 +/- 3.1 x 10(4) microns2/cm2, P < 0.025). As expected, calcitonin significantly decreased resorptive activity. These data indicate that PAF activates osteoclastic resorption. PAF may play a role in mediating the resorption of bone and mineralized cartilage in inflammatory diseases such as rheumatoid arthritis and periodontitis.
 ...
PMID:Platelet-activating factor stimulates resorption by rabbit osteoclasts in vitro. 843 Jul 91

Inflammatory processes occurring in the vicinity of bone tissue often result in stimulation of osteoclast activity and loss of skeletal mass. The aim of the current study was to determine if inflammatory exudates collected from gingival pockets in patients with periodontitis contain factors capable of stimulating resorptive activity. The degree of bone mineral mobilization and bone matrix degradation was assessed by analysis of the release of 45Ca and 3H from bones prelabelled with 45CaCl2 and [3H]proline, respectively. Gingival crevicular washings from six patients with signs of periodontitis stimulated 45Ca or 3H release from the calvarial bones. The stimulatory effect of the gingival crevicular washings on 45Ca release was concentration- and time-dependent, and reduced by calcitonin, a specific osteoclast inhibitor. These data demonstrate that crevicular fluid contains factor(s) which can stimulate osteoclastic degradation of bone in vitro. The bone resorbing activity was partially retained after extensive dialysis. Analysis of the concentrations of prostaglandin E2, interleukin-1alpha and interleukin-1beta in the crevicular fluids, and comparisons of these agents as stimulators of 45Ca release in the mouse calvarial assay, suggest that prostaglandin E2 is not the sole factor responsible for the bone resorbing activity of the exudates. The data indicate that other factors, such as IL-1, may play key roles in the stimulation of osteoclastic activity by gingival crevicular washings.
 ...
PMID:Gingival crevicular fluid from patients with periodontitis contains bone resorbing activity. 967

The aims of the present study were to investigate whether calcitonin gene-related peptide (CGRP) was present in gingival crevicular fluid in both periodontal health and disease and to study the relationship with periodontal inflammation. Gingival crevicular fluid (GCF) was collected from a healthy, a gingivitis and a periodontitis site in 18 subjects with periodontitis and from a healthy site in 19 subjects without periodontitis. The volume of GCF was measured and each sample subsequently analysed for CGRP by radioimmunoassay. In subjects with periodontitis, CGRP immunoreactivity (CGRP-IR) was not detected in any periodontitis sites, nor in 67% of gingivitis and 28% of periodontally-healthy sites. The total amount of CGRP-IR was significantly elevated in periodontally healthy (p=0.0015) and gingivitis (p=0.027) compared with periodontitis sites. CGRP-IR was present in 89% of the healthy sites sampled in control subjects at comparable levels to those in healthy sites in periodontitis subjects. It is concluded that in periodontal inflammation, particularly in deep pockets, constituents of GCF process and degrade CGRP.
 ...
PMID:Calcitonin gene-related peptide in gingival crevicular fluid in periodontal health and disease. 1022 91

Periodontal disease is a common multifactorial chronic inflammatory disease in humans. In inflammatory conditions that are known to be associated with changes in nociception, such as arthritis, the neuronal expression of the proinflammatory neuropeptides, substance P and calcitonin gene-related peptide is altered. In this study the expression of these neuropeptides' mRNAs has been studied in an inflammatory model that shows no behavioural evidence of altered nociception. Periodontitis was induced in male rats by intragingival injection of lipopolysaccharide adjacent to the second right mandibular molar. The animals were killed at various times after lipopolysaccharide injection and right and left trigeminal ganglia and brain were processed for in situ hybridization for beta-preprotachykinin and alpha-calcitonin gene-related peptide mRNAs. Expression of both neuropeptide mRNAs was significantly increased only in small neurons in the mandibular division of the trigeminal ganglion ipsilateral to the LPS injection from 3 to 10 days postinjection. Neuropeptide mRNA expression was also significantly increased in the contralateral trigeminal ganglion at day 10. No significant changes in neuropeptide mRNA levels were seen in the maxillary and ophthalmic divisions of the trigeminal ganglia or in the trigeminal mesencephalic nucleus. The up-regulation of substance P and CGRP mRNAs in periodontal disease suggests that this is associated with the inflammatory process rather than nociception, as this disease does not appear to result in altered nociception in either rats or humans. The contralateral alteration in neuropeptide mRNA expression suggests a role for neurogenic mechanisms in the development of periodontal disease.
 ...
PMID:Sensory neuropeptide mRNA up-regulation is bilateral in periodontitis in the rat: a possible neurogenic component to symmetrical periodontal disease. 1498 15

It is generally accepted that the nervous system contributes to the pathophysiology of peripheral inflammation, and a neurogenic component has been implicated in many inflammatory diseases, including periodontitis. Neurogenic inflammation should be regarded as a protective mechanism, which forms the first line of defense and protects tissue integrity. However, severe or prolonged noxious stimulation may result in the inflammatory response mediating injury rather than facilitating repair. This review focuses on the accumulating evidence suggesting that neuropeptides have a pivotal role in the complex cascade of chemical activity associated with periodontal inflammation. An overview of neuropeptide synthesis and release introduces the role of neuropeptides and their interactions with other inflammatory factors, which ultimately lead to neurogenic inflammation. The biological effects of the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), and neuropeptide Y (NPY) are summarized, and evidence for their involvement in the localized inflammatory lesions which characterize periodontitis is presented. In this context, the role of CGRP in bone metabolism is described in more detail. Recent research highlighting the role of the nervous system in suppressing pain and inflammation is also discussed.
 ...
PMID:NEUROPEPTIDES AND NEUROGENIC MECHANISMS IN ORAL AND PERIODONTAL INFLAMMATION. 1505 44

Proinflammatory neuropeptides, such as substance P and calcitonin gene-related peptide, are up-regulated in primary afferent neurons in acute and chronic inflammation. While these neuropeptides have been intensively studied, potentially anti-inflammatory and/or anti-nociceptive neuropeptides such as somatostatin (SS) have been less widely investigated. Endogenous somatostatin is thought to exert a tonic antinociceptive effect. Exogenous SS is anti-inflammatory and antinociceptive and is thought to exert these actions through inhibition of proinflammatory neuropeptide release. In this study we have compared the expression of somatostatin in two inflammatory models: arthritis, a condition associated with increased nociception, and periodontitis, in which there is little evidence of altered nociceptive thresholds. In acute arthritis (< 24 h) SS mRNA was down-regulated in ipsilateral dorsal root ganglia (DRG; 52 +/- 7% of control, P < 0.05), and up-regulated in contralateral DRG (134 +/- 10% of control; P < 0.05). In chronic arthritis (14 days) this pattern of mRNA regulation was reversed, with SS being up-regulated ipsilaterally and down-regulated contralaterally. In chronic mandibular periodontitis (7-10 days), SS mRNA was up-regulated in only the mandibular division of the ipsilateral trigeminal ganglion (TG) (day 7, 219 +/- 9% and day 10, 217 +/- 12% of control; P < 0.02) but showed no change in other divisions of the trigeminal ganglion or in the mesencephalic nucleus. These data show that antinociceptive and anti-inflammatory neuropeptides are also regulated in inflammation. It is possible that the degree of inflammation and nociception seen may depend on the balance of pro- and anti-inflammatory and nociceptive peptide expression in a particular condition.
 ...
PMID:Inflammation alters somatostatin mRNA expression in sensory neurons in the rat. 1565 50


1 2 Next >>