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Biomedical subjects

C A McCulloch

Publications and source records attributed to C A McCulloch.

At least 91 records · Page 5Linked to original sources
PubMed1995

Origins and functions of cells essential for periodontal repair: the role of fibroblasts in tissue homeostasis.

OBJECTIVE: A review is undertaken of rodent model systems and cell culture studies that address the role of periodontal fibroblasts in tissue homeostasis in both normal function and after wound healing. RATIONALE: Fibroblasts are the predominant cells of the periodontal ligament (PL) and of healthy gingiva and have important roles in the development, function and regeneration of the tooth support apparatus. REVIEW: In normally functioning periodontal tissues cell turnover involves generation of new cells by proliferation which in turn is balanced by apoptopic cell death. Consequently PL fibroblasts comprise a renewal cell system in steady-state. PL cell progenitors can generate multiple types of more differentiated, specialized cells including large numbers of fibroblastic cells and more limited numbers of osteogenic or cementogenic cells. However PL fibroblasts constitutively block osteogenesis and thereby maintain the PL width. Proliferating progenitor cell populations of the PL are enriched in locations adjacent to blood vessels and in contiguous endosteal spaces from where they migrate to the body of the PL. Large increases of cell formation and cell differentiation occur after wounding but surprisingly, the cells that repopulate the PL adjacent to the root surface are largely post-mitotic. As PL cell populations comprise multiple lineages, it is likely that after wounding, the separate phenotypes repopulating the wound site will be selected by environmental factors. Further, the specific repopulating lineages will strongly influence the form and function of the nascent tissue. To illustrate the specificity of fibroblast functions, examples of migratory and contractile fibroblast phenotypes are provided which exhibit constitutively different levels of gelsolin and alpha-smooth muscle actin respectively, cytoskeletal proteins which are markers for these cell types. CONCLUSION: Fibroblasts contribute to PL homeostasis by their abilities to remodel tissues, to repopulate wounds, to influence the metabolism of other cell types and to create a new fibrous attachment.

Animals↗
PubMed1995

Magnetic fields applied to collagen-coated ferric oxide beads induce stretch-activated Ca2+ flux in fibroblasts.

The ability to apply controlled forces to the cell membrane may enable elucidation of the mechanisms and pathways involved in signal transduction in response to applied physical stimuli. We have developed a magnetic particle-electromagnet model that allows the application of controlled forces to the plasma membrane of substrate-attached fibroblasts. The system allows applied forces to be controlled by the magnitude of the magnetic field and by the surface area of cell membrane covered with collagen-coated ferric beads. Analysis by single-cell ratio fluorimetry of fura 2-loaded cells demonstrated large calcium transients (50-300 nM) in response to the magnetic force applications. Experiments using either the stretch-activated channel blocker gadolinium chloride or ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid to eliminate external calcium ions, or addition of extracellular manganese ions, indicated that there was a calcium influx through putative stretch-activated channels. The probability of a calcium influx in single cells was increased by higher surface bead loading and the degree of cell spreading. Depolymerization of actin filaments by cytochalasin D increased the amplitude of calcium response twofold. The regulation of calcium flux by filamentous actin content and by cell spreading indicates a possible modulatory role for the cytoskeleton in channel sensitivity. Magnetic force application to beads on single cells provides a controlled model to study mechanisms and heterogeneity in physical force stimulation of cation-permeable channels.

Actins↗
PubMed1995

Development of a computer program for teaching periodontal diagnosis based on clinical epidemiological principles.

Multimedia teaching tools in dental education are still rare. This paper describes the development of an inexpensive yet powerful computer program for instruction in the principles of clinical epidemiology. The application was developed in the context of periodontal diagnostic methodologies at the third year D.D.S. level. Principles of probabilistic thinking are invoked as the student is guided from the application of raw research data to the derivation of likelihood ratios and how they affect clinical decision making. A questionnaire was used to evaluate student satisfaction with the program and the responses indicated good acceptance of the concepts presented in the program and an interest in further computer-aided instruction.

Computer-Assisted Instruction↗
PubMed1994

Collagenolytic enzymes in gingival crevicular fluid as diagnostic indicators of periodontitis.

Periodontal diseases are associated with the production of several families of enzymes that are detectable in gingival crevicular fluid and that are released by stromal, epithelial or inflammatory cells. Measurement of collagen degrading enzymes in crevicular fluid could contribute to insights into pathogenesis of periodontal diseases and also provide a rational basis for the development of novel diagnostic tests. However, similar to the development of other diagnostic tests, the appropriate validation of collagenolytic enzymes as diagnostic indicators is dependent on clearcut demonstrations of the identity of the enzyme in the assay, and the reproducibility, diagnostic accuracy, and clinical utility of the test. If collagenolytic enzymes are to be of clinical usefulness, they should be easily measured over a broad range of disease severities and in varied clinical settings. Ideally, the diagnostic test should assay for an essential component of proposed pathogenic mechanisms. Neutrophil collagenase and gelatinase are promising enzymes for diagnostic tests because of (1) their apparently central role in periodontal attachment loss and disease progression; (2) demonstrations of positive associations between enzyme levels and attachment loss and inflammation; and (3) availability of sensitive and specific assays to quantify these enzymes. However, much less data exist on reproducibility, diagnostic accuracy, and clinical use in longitudinal studies. In the future, more emphasis must be placed on the importance of appropriate study design for establishing the efficacy of collagenolytic enzymes as diagnostic tests.

Amino Acid Sequence↗
PubMed1994

Proliferative responses of endothelial cell populations to experimentally induced inflammatory lesions of gingival connective tissues in the cynomolgus monkey (Macaca fascicularis).

BACKGROUND: Endothelial cells exhibit heterogeneous and tissue-selective responses to injury and inflammation. The regulation of the size of endothelial populations in specific tissue sites is poorly characterized, particularly in soft connective tissues adjacent to bone. To investigate the effect of a primarily lymphocytic infiltrate on endothelial cell proliferation and growth of blood vessels, a primate model was used that reliably exhibits localized, distinct inflammatory, and destructive lesions in isolated sites of mucosal connective tissues adjacent to bone and epithelium around teeth. METHODS: Three Cynomolgus monkeys with healthy periodontium and two with spontaneously occurring inflammation or induced connective tissue destruction were pulse labeled with 3H-thymidine. Morphometric analyses of radioautographs from mid-sagittal supra-alveolar gingival connective tissues of incisor teeth were performed in sites subjacent to junctional, sulcular, and oral epithelium, in the body of the lamina propria and just superior to the alveolar bone crest. RESULTS: Subjacent to the sulcular epithelium there was a statistically significant (P < 0.01) increase in lymphocyte density between health and inflammation. The percentage of endothelial cells incorporating 3H-thymidine label (LI) and the number of blood vessels per unit area were significantly increased in this same site in inflamed samples (P < 0.02) but were not elevated further in lesions in which there was destruction of soft connective tissues. However, there was no increase of the numbers or the cross-sectional areas of blood vessels between samples of inflamed and destroyed tissues. CONCLUSIONS: 1) Experimentally induced inflammation and connective tissue destruction in the gingival connective tissues of Cynomolgus monkeys is associated with site-specific perturbations in the turnover of endothelial cells that is closely linked to lymphocytic infiltration; 2) the vascular response is a generalized increase in endothelial cell proliferation and blood vessel numbers but not lumen size or number of endothelial cells, suggesting the existence of homeostatic controls for preservation of the whole population in a steady state.

Animals↗
PubMed1994

Differentiation of periodontal ligament fibroblasts into osteoblasts during socket healing after tooth extraction in the rat.

BACKGROUND: The entire socket after tooth extraction is filled with new bone formed by osteoblasts (Obs), but the origin of these Obs remains unknown. Thus, the proliferation and migration of paravascular and endosteal fibroblastic cells and periodontal ligament (PDL) fibroblasts (Fbs) and their differentiation into Obs during socket healing after extraction of the first maxillary molars of the rat were investigated. METHODS: The proliferative activity and migration of these cells in the sockets after tooth extraction were studied using radioautography and immunohistochemistry after injection of 3H-thymidine and 5-bromo-2'-deoxyuridine (BrdU), respectively. Their morphological changes during differentiation was investigated by transmission electron microscopy. RESULTS: One day after tooth extraction, PDL Fbs were the major cell type in the PDL remnant of the socket. Proliferation was low (labeling index (LI) = approximately 2%) until 16 h after tooth extraction but dramatically increased to a maximum level 1 day postextraction (LI = 23%). Between 1 and 2 days, numerous PDL Fbs in the PDL remnant actively migrated into the coagulum and continued to proliferate. On the basis of the high proliferative activity and small number of cellular organelles responsible for procollagen synthesis, these cells appear immature. At 3 days, Fbs contained more cellular organelles and deposited more collagen fibers as they replaced the coagulum with dense connective tissue and the LI declined. At 4 and 5 days, some of the Fbs began to differentiate into Obs, and the proliferation of Fbs dramatically decreased to baseline values. The migration of PDL Fbs and their differentiation into Obs were investigated by labeling with 3H-thymidine or BrdU 1 day after tooth extraction. Heavily labeled Fbs were observed in the PDL remnant at 1 day, in the coagulum at 2 days, and in the dense connective tissue at 3 days. Labeled Obs associated with new bone were seen 4 days after injection. Endosteal and paravascular Fbs also proliferated, but at a lower level and at later time periods than the PDL Fbs. Surprisingly, endosteal and paravascular Fbs contributed only a small population of Fbs to socket healing. CONCLUSIONS: These results indicate that PDL Fbs after tooth extraction actively proliferative, migrate into the coagulum, form dense connective tissue, and differentiate into Obs which form new bone during socket healing.

Animals↗
PubMed1994

Dependence of collagen remodelling on alpha-smooth muscle actin expression by fibroblasts.

To study the relation between expression of the putative myofibroblast marker alpha-smooth muscle actin and the remodelling of extracellular matrix, immunocytochemical, gel electrophoresis, and collagen gel contraction studies were performed on two human fibroblast subtypes. Double immunolabelling for total actins and alpha-smooth muscle (sm) actin as well as affinity labelling of filamentous and monomeric actins in gingival fibroblasts demonstrated that alpha-sm was colocalized in stress fibres and in regions with high levels of monomeric actin throughout the cytoplasm. alpha-sm comprised up to 14% of total cellular actin as assessed by 2D gel electrophoresis. Thirteen different gingival and seven different periodontal ligament fibroblast lines constitutively expressed on alpha-sm actin. These cells exhibited up to 60% inter-line variations of fluorescence due to alpha-sm actin and up to 70% and 45% inter-line variation in the rate of collagen gel contraction. Quantitative, single cell fluorimetry of alpha-sm actin immunoreactivity demonstrated a linear relation between gel contraction and alpha-sm actin (correlation coefficients of 0.71 for gingival and 0.61 for periodontal ligament cells), but there was no detectable relationship between total actin content and gel contraction. In contrast, flow cytometry demonstrated that 99% of the total gated cells from cell lines exhibiting rapid gel contraction showed alpha-sm actin staining above background fluorescence as compared to only 35% of cells with slow rates of gel contraction. Contracting collagen gels stained with FITC-phalloidin showed cells with well-developed stress fibres that were progressively more compact and elongated during the time of maximal gel contraction. To examine the dependence of gel contraction on assembly of monomeric actin into actin filaments, cells were electroporated in the presence of phalloidin or cytochalasin D. Collagen gels exhibited up to 100% inhibition of gel contraction that was dose-dependent. Gel contraction was inhibited 93% by electroinjection of cells with alpha-sm actin antibody prior to incubation, but the antibody did not inhibit actin assembly after attachment and spreading on substrates. These data indicate that gel contraction is dependent on alpha-sm actin expression and that alpha-sm actin is a functional marker for a fibroblast subtype that rapidly remodels the extracellular matrix.

Actins↗
PubMed1994

Slow oscillations of free intracellular calcium ion concentration in human fibroblasts responding to mechanical stretch.

Calcium transients in single, human gingival fibroblasts were studied after mechanical stretching of flexible culture substrates. A model system was developed to reproducibly stretch and rapidly (<1 sec) refocus cells in the same focal plane so that changes in the concentration of free intracellular calcium ions ([Ca2+]i) were monitored without delay. Attached cells were grown on flexible bottom Petriperm dishes, loaded with fura-2/AM, and stretched by 1% or 2.8% of substrate area. The stretch caused no significant cell detachment or membrane lesions. A 1% stretch induce no calcium response, but a 2.8% stretch stimulated an initial calcium transient and the subsequent generation of [Ca2+]i oscillations of up to 2,000 sec. At 1% stretch, there was no calcium response. Cell shape and plating time were important determinants in the calcium response to mechanical stimulation: the responder cells were small and round without long processes. Major calcium transients were inhibited completely by 5 mM EGTA or by 10 microM gadolinium ions, by 50 microM nifedipine, or 250 microM verapamil, suggesting an influx of calcium through stretch-activated (SA) channels and L-type calcium channels. Depolarization by high KCl (144 mM) in the extracellular medium enhanced the amplitude of calcium transients by 54%. Calcium oscillations were not inhibited by preincubation with thapsigargin, caffeine, cholera toxin, staurosporine or 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), indicating that IP3 sensitive pools, IP3 insensitive pools, GS alpha subunits, and protein kinase C, respectively, were not involved in the generation of calcium oscillations. Pretreatment with genistein, a specific tyrosine kinase inhibitor or cytochalasin D, an inhibitor of actin polymerization, or pertussis toxin, an inhibitor of Gi alpha and G(o) alpha subunits, completely abolished calcium transients and oscillations. These results indicate that Ca2+ flux due to mechanical stretching is likely mediated through SA ion channels and is dependent on tyrosine kinases, pertussis toxin-sensitive subunits of G-proteins, and actin filaments.

Actins↗
PubMed1994

Host enzymes in gingival crevicular fluid as diagnostic indicators of periodontitis.

Host responses to periodontal infections include the production of several families of enzymes that are released by stromal, epithelial or inflammatory cells. Study of these enzymes in gingival crevicular fluid may lead to insights into pathogenesis and may provide a rational basis for the development of novel diagnostic tests. However, analogous to other diagnostic interventions in dentistry and medicine, validation of host enzymes as diagnostic indicators is dependent on clear-cut demonstrations of the identity of the enzyme, reproducibility, diagnostic accuracy and clinical utility. The enzyme of interest should be readily measured over a broad range of disease severity and in varied clinical settings. Ideally, the enzyme should also be an essential component of proposed pathogenic mechanisms. In this context, the connective tissue matrix degrading enzymes elastase, collagenase and gelatinase are promising because of their apparently central role in periodontal attachment loss and disease progression. Sensitive and specific assays are also available to quantify these enzymes. Other work on enzymes associated with cell death (aspartate aminotransferase, lactate dehydrogenase) and several neutrophil lysosomal enzymes (beta glucuronidase, arylsulphatase, cathepsins) has demonstrated positive associations between enzyme levels and attachment loss and inflammation. While numerous cross-sectional studies have indicated that the levels of hydrolytic enzymes in gingival crevicular fluid parallel the severity of periodontal lesions, there are much less data on reproducibility, diagnostic accuracy and clinical utility in longitudinal studies. As appropriate study design is an essential prerequisite for establishing the efficacy of host enzymes as diagnostic tests, future clinical investigations should include: (1) individuals who would most likely benefit by early diagnosis, i.e., rapidly progressive and recurrent periodontitis cases; (2) longitudinal, cohort study designs to show that attachment loss is temporally linked with large increases in enzyme activity; (3) the use of a battery of tests to overcome intrinsic problems of low predictive values when prevalence of active disease is low. In the final analysis, the utility of host enzymes as diagnostic indicators will need to be examined in randomized controlled trials in which the question is asked: are patients better off as a result of testing?

Esterases↗
PubMed1994

Cellular origins and differentiation control mechanisms during periodontal development and wound healing.

In the context of cellular origins, odontogenic epithelium and oral epithelium are the sources for junctional epithelium during development and during wound healing respectively. In contrast, both odontogenic and non-odontogenic mesenchyme contain the progenitors for gingival fibroblasts in developing tissues while in wounded tissues, gingival fibroblasts are derived from gingival connective tissues and comprise a heterogeneous population of cells with diverse properties and functions. Periodontal ligament, bone and cementum cell populations apparently originate from dental follicle progenitor cells during development, but during wound healing derive from ancestral cells in periodontal ligament and bone. Cellular differentiation in developing periodontium is governed in part by epithelial-mesenchymal interactions that generate specific signals which regulate selective cell populations in time and space. On the other hand, differentiation during wound healing and regeneration is regulated by a vast array of extracellular matrix informational molecules and by cytokines that induce both selective and non-selective responses in the different cell lineages and their precursors. Further, several important signalling systems are irretrievably lost after development is complete. Thus, in the context of cellular origins and differentiation, developing and wounded periodontal tissues exhibit fundamental differences. Future prospects for improved healing and regeneration of periodontal tissues may derive from identification and isolation of informational molecules that are stored in connective tissue matrices. These molecules and elucidation of their functions may open new perspectives in our understanding of the biology of periodontal wound healing and may provide novel approaches to periodontal regeneration.

Animals↗
PubMed1994

Degradation of endogenous plasma membrane fibronectin concomitant with Treponema denticola 35405 adhesion to gingival fibroblasts.

Treponema denticola adhesion and degradation of fibronectin (Fn) on human gingival fibroblasts (HGF) were studied by immunofluorescence and enzyme-linked immunosorbent assays. The number of adherent bacteria increased and the amount of immunoreactive Fn decreased as a function of increasing T. denticola concentration. The distribution of cell-bound Fn was punctate in micrographs. Anti-human Fn impaired bacterial adhesion to HGF. Phenylmethylsulfonyl fluoride inhibited Fn degradation but not adhesion. Sonicated extracts and diluted spent growth medium degraded HGF Fn but, unlike intact T. denticola cells, they hardly stimulated F-actin rearrangements.

Bacterial Adhesion↗
PubMed1994

Regulation of cell volume and [Ca2+]i in attached human fibroblasts responding to anisosmotic buffers.

Alteration of the cell volume of attached fibroblasts with anisosmotic buffers was used to examine the relationship between cell membrane perturbation and intracellular Ca2+ concentration ([Ca2+]i) and to study pathways that may be involved in transducing this response. Human periodontal ligament gingival fibroblasts grown on cover slips were loaded with fura 2-acetoxymethyl ester. The relative cell volume change of single fibroblasts was estimated by measurement of fluorescence intensity at the isosbestic wavelength (356 nm), and [Ca2+]i was calculated from ratiometric fura 2 emission with excitation at 345 and 380 nm. Isotonic buffer (300 mosmol/kgH2O) was substituted with either hypertonic (600 mosmol/kgH2O) or hypotonic (150 mosmol/kgH2O) buffer after baseline recordings. Attached cells exhibited a rapid decrease in cell volume and [Ca2+]i after hypertonic buffer treatment, which was associated with an increase in filamentous actin staining. In contrast, cells treated with hypotonic buffers demonstrated an increase in cell volume (mean approximately 10%), a significant decrease in filamentous actin staining, and a rapid transient elevation in [Ca2+]i (mean approximately 280 nM). This [Ca2+]i rise was significantly inhibited by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, gadolinium ions (P < 0.05), and inhibitors of actin assembly. These results indicate that [Ca2+]i fluxes in response to hypotonic cell swelling in attached fibroblasts are mediated by stretch-activated ion channels and are dependent on actin filaments.

Actins↗
PubMed1994

Serum deprivation induces apoptotic cell death in a subset of Balb/c 3T3 fibroblasts.

Little is known about the regulation of apoptosis in fibroblasts although several model systems including serum deprivation and treatment with staurosporine or topoisomerase inhibitors have been used to induce apoptosis in vitro. To validate a reproducible in vitro model for the study of apoptosis in fibroblasts, we cultured density-inhibited monolayer cultures of Balb/c 3T3 fibroblasts in Dulbecco's modified essential medium plus 15% fetal calf serum and then withdrew serum. Time-lapse video microscopy demonstrated that within minutes of serum withdrawal, cells lost substrate attachment and floated to the top of the liquid growth medium. There was a time-dependent increase in the number of non-adherent cells. Some of these cells regained attachment and spread momentarily, but they eventually rounded up and lost attachment permanently. In contrast to serum-containing cultures in which similar morphological changes were followed by mitosis, in serum-free cultures repeated attempts at mitosis were followed by permanent attachment loss and presumably cell death. To assess whether all the non-adherent cells were in fact dead, the percentages of cells that continued to proliferate upon return to serum-supplemented conditions was computed. After various periods of serum starvation a decreasing proportion (approx. 75% at 30 minutes; < 2% at 24 hours) of the non-adherent cells could be rescued by addition of serum. Transmission electron microscopy of cells 3 hours after serum withdrawal showed that the majority (approximately 60%) of non-adherent cells exhibited marked intranuclear chromatin condensation but maintained integrity of cell and nuclear membranes and cell organelles, morphological changes consistent with those of apoptotic cell death. Scanning electron microscopy of cultures 3 hours following serum withdrawal showed rounded cells with marked surface blebbing. Fluorescence and confocal microscopy revealed increased intensity of nuclear staining with DAPI while actin filaments became indistinct or collapsed around the nucleus. After cycloheximide treatment to inhibit protein synthesis, there was no reduction of apoptosis. Gel electrophoresis of DNA from both control and 3 hour-serum-deprived cells showed intact DNA with no oligonucleosomal length fragmentation. After serum withdrawal, intracellular calcium was reduced by about 32% over 5 minutes as measured by fura2 ratio fluorimetry in single cells. Serum-starved cells showed a time-dependent shrinkage in mean cell diameter compared to trypsinized, adherent control cells (at 0 hours, mean diameter = 18.0 microns--viable; at 4 hours, mean diameter = 15.5 microns--apoptotic). Flow cytometric analysis showed increased propidium iodide staining and reduced fluorescein diacetate uptake over 3 hours, changes that were contemporaneous with the reduction of cell diameter.(ABSTRACT TRUNCATED AT 400 WORDS)

3T3 Cells↗
PubMed1994

Relationship of oral malodor to periodontitis: evidence of independence in discrete subpopulations.

Associations between oral malodor, measures of periodontal disease, and trypsin-like activity of periodontal pathogens on tongue and teeth were examined in 127 subjects. Volatile sulphur compound (VSC) measurements were made with a portable sulphide monitor; oral malodor was also estimated by organoleptic methods. Measurements repeated one week apart indicated that steady-state VSC levels (r = 0.72; P = 0.0001) and peak VSC levels (r = 0.63; P = 0.0001) were reproducible but these r values were not significantly different (P > 0.1). There was a significant correlation between tongue odor and peak VSC levels (r = 0.40; P = 0.0001) and between tongue odor and whole mouth organoleptic measures (r = 0.55; P = 0.0001). To study the effect of reducing microbial colonization on oral malodor, chlorhexidine gluconate (0.2%) rinsing was prescribed for 7 days. Reductions of VSC levels were significant for both peak (37%) and steady-state (41%) data (P = 0.0001). Anaerobic periodontal pathogens on the tongue estimated by the proportions of positive BANA tests were reduced 19% (P = 0.001) and this was concomitant with a 40% (P = 0.0001) decrease in organoleptic measurement of the tongue dorsum. Mean pH measurements of the tongue dorsum showed large reductions from 6.9 initially to 6.3 post-treatment (P = 0.0001). Subjects were divided into periodontitis/no periodontitis based on periodontal inflammation and probing depth (> or = 5 mm). Of the 37 subjects with periodontitis, 23 had oral malodor whereas 52 out of 90 periodontally healthy subjects exhibited malodor. Chi square analysis comparing halitosis in subjects with and without periodontitis showed no statistically significant association (chi 2 = 0.208; P 0.65) between these two factors although the intensity of malodor as based on VSC concentration in periodontally healthy subjects was 19% less (mean = 111 ppb) than in subjects with periodontitis (mean = 136 ppb). The odds ratio was 1.2, indicating that oral malodor was not associated with periodontitis. These data indicate that a large proportion of individuals with oral malodor are periodontally healthy and that the mucosal surface of the tongue is a major site of oral malodor production.

Adult↗
PubMed1994

Probing velocity: novel approach for assessment of inflamed periodontal attachment.

Little is known about the biophysical characteristics of the dento-gingival junction in response to the development or resolution of inflammation. The Toronto automated periodontal probe (TAPP) provides an estimate of the biophysical integrity of the dento-gingival junction by measuring intrapocket probing velocity. Presence or absence of a plateau in displacement versus time plots were used to perform dichotomous analyses as a function of established parameters of inflammation. Plateaus were operationally defined as a 3 standard deviation reduction in the slope of the displacement versus time plot (probing velocity) and hence the plateau represents an increased resistance of the probe tip at the dento-gingival junction. The aim of the study was to measure the relationship between post-treatment reductions of gingival inflammation and the probability of plateau formation as measured by the TAPP. Twenty-nine subjects exhibiting gingival inflammation were provided with periodontal therapy consisting of subgingival scaling and root planing. Over a 2-month sampling period, 6 sites from each subject were monitored and these sites exhibited wide variations of inflammation. Logistic regression revealed a significant relationship between the probability of plateau formation and treatment (P = 0.002), plaque index (P = 0.002), the increased severity levels of gingival index (P > 0.05), or bleeding index (P > 0.05). The probability of plateau formation decreased with higher levels of crevicular fluid flow but there was no dependence of plateau formation on probing depth (P > 0.55). These data indicate a direct relationship between improved measures of clinical health and increased resistance to probe penetration near the base of the pocket.(ABSTRACT TRUNCATED AT 250 WORDS)

Case-Control Studies↗