Undiagnosed intrusion of a maxillary primary incisor tooth: 15-year follow-up.
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Child↗
Biomedical subjects
Z Schwartz
Publications and source records attributed to Z Schwartz.
An approach to the treatment of advanced periodontal disease: a compromise.
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Adult↗
The effects of insulin and glucose on bone modelling in vitro.
The direct effects of insulin and glucose on bone modelling was studied in an in vitro system. 16 day old mice fetal radii and ulnae prelabelled with 45Ca were cultured for 48 hr in BGJ medium supplemented with either 4 mg/ml of human serum albumin or 10% fetal calf serum. Insulin at concentrations of 10(-8)-10(-10) M induced an increase in the periosteal bone formed as well as in calcium, phosphate and hydroxyproline content. Glucose at concentrations of 200-800 mg/dl decreased bone length, calcium, phosphate and hydroxyproline content. There was no change in the 45Ca released into the medium, by either insulin or glucose, implying that these substances have no effect on bone resorption. The results of this study imply that insulin and glucose have a direct effect on bone modelling and that they may be important factors in growth disturbances occurring during diabetic pregnancy.
Animals↗
Management of puerperal separation of the symphysis pubis.
Thirteen post-partum patients with symphysiolysis were treated by intra-symphysial injection of a combination of hydrocortisone, chymotrypsin and lidocain. The injection was given once a day and the full treatment consisted of between three to seven injections according to the severity of the symptoms. No other medication was given. Immediate relief was obtained in all cases after the first injection and all symptoms disappeared after the completion of treatment. The average time of hospitalization was 9.8 days. No complications were seen as a result of the treatment and the patients resumed their normal activities after being discharged from hospital. In comparison with other modes of treatment, the intra-symphysial injection of the above drug combination shortened the time of morbidity and effected complete recovery.
Adult↗
Second primary malignancy in endometrial carcinoma patients.
An epidemiologic study of multiple primary malignant neoplasms in endometrial cancer patients in Israel is presented. During the 7-year period of the study, 104 patients (10.3%) out of 1007 patients diagnosed as having endometrial cancer had another primary cancer. There was a significant difference in the incidence of multiple primary cancers between various ethnic groups, women of European/American origin having higher incidence than women of Asian/African origin. A significantly higher than expected incidence of second primary cancers occurred at the following sites: breast (relative risk, 4.1), ovary (relative risk, 11.6), cervix (relative risk, 5.1), and colon (relative risk, 5.9). The prognosis was mainly influenced by the site of the second primary cancer. The increased incidence of multiple primary malignancies justifies a high level of alertness to the possibility of second primary cancer in endometrial cancer patients.
Adult↗
Uterine sarcoma in Israel: a study of 104 cases.
Data gathered during the first epidemiologic study of sarcoma of the uterus in Israel are presented. In the 7-year period of this survey, 104 new cases of sarcoma of the uterus were diagnosed, representing an incidence of 1.55/100,000 females over the age of 20. Half of the patients were in their fifth and sixth decades of life at the diagnosis of the tumor. Uterine sarcomas were more prevalent in women of European-American origin than in those of Asian-African descent. In 54.9% of the patients the diagnosis was made while the disease was in stage I. A definite correlation between sarcoma of the uterus, diabetes, hypertension, and obesity was not found. The 5-year survival rate in the present survey was 38%. Factors affecting prognosis were the clinical stage of the disease at diagnosis, histologic type, and the method of treatment.
Adult↗
A novel approach to the analysis of risk factors in endometrial carcinoma.
Early diagnosis of endometrial carcinoma enables one to achieve a cure rate of 80%. The purpose of this study is to characterize the patients who are prone to develop adenocarcinoma by simple epidemiologic and clinical data. The data of 109 consecutive patients who developed adenocarcinoma were compared with those of 146 control hysterectomy patients using logistic regression analysis. The following characteristics of patients who developed adenocarcinoma were identified: parity (P less than 0.0001), diabetes mellitus (P less than 0.003), hypertension (P less than 0.0001), obesity (P less than 0.0006), treatment with exogenous estrogen (P less than 0.001), and second primary tumor. The logistic regression formula classified correctly 77% of all patients to their actual group. The study showed that the relative risk of a patient to develop adenocarcinoma can be estimated from simple and readily available epidemiologic and clinical data.
Adenocarcinoma↗
An in vitro assay of bone development using fetal long bones of mice: morphological studies.
The purpose of this study was to examine the morphological changes in an in vitro system in which the two elements of bone modelling, formation and resorption, could be studied simultaneously. Pregnant mice were killed on days 15, 16 and 17 of gestation, the fetuses were removed and the radii and ulnae dissected free of soft tissue. The bones were cultured for 6 days in media (BGJ) supplemented with 20% fetal calf serum and 150 micrograms/ml vitamin C. Growth and mineralization were estimated by measuring the total length of the bone, and diaphysis, and by light and transmission electron microscopy (TEM). The results of this study indicate that there is a continuous measurable increase in the total length of fetal mouse long bones over the 6 days of culture. These bones show a continuous growth of periosteal bone, with mesenchymal tissue penetrating into the diaphyseal shaft, and development of bone marrow like tissue. TEM examination showed differentiation of mesenchymal cells to osteoblasts, formation of new bone matrix and bone mineralization similar to that found in developmentally matched controls. In the cartilagenous epiphyses, however, many hydroxyapatite crystals were not associated with matrix vesicles. In addition, some of the chondrocytes of the hypertrophic zone appeared to be dedifferentiating into mesenchymal cells with osteoblast-like features. In spite of the lack of osteoclasts in the 15- and 16-day explants, osteoclasts appeared in the diaphysis after 2 and 4 days in culture. Our results suggest that this system can serve as a good model for the study of bone formation and resorption as they occur, simultaneously, during bone modelling.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Correlative morphometric and biochemical analysis of purified extracellular matrix vesicles from rat alveolar bone.
Extracellular matrix vesicles were isolated from rat alveolar bone and purified by either gel filtration or discontinuous sucrose density gradient. Morphometric evaluation of electron-micrographs of pellets of purified and nonpurified vesicle fractions was correlated with the activity of vesicular enzymes. A high correlation was found between the percentage of area occupied by vesicles with electron-dense content (electron-dense vesicle fractional area) and the enzymatic activity. Highest enzymatic specific activities and electron-dense vesicle fractional area were recorded in the "light" vesicle-enriched fraction obtained after equilibrium density centrifugation. These parameters revealed lowest values in the "heavy" vesicle-enriched fraction resolved by the same methods. The combined electron-dense and electron-lucent fractional area (vesicular fractional area) was similar in the different purified fractions. It is therefore suggested that the fraction obtained by gel filtration contains both "light" and "heavy" vesicles. Morphometric study is proposed as an additional criterion for the degree of purification of matrix vesicle preparations.
Acid Phosphatase↗
Nongenomic regulation of chondrocyte membrane fluidity by 1,25-(OH)2D3 and 24,25-(OH)2D3 is dependent on cell maturation.
1,25-(OH)2D3 and 24,25-(OH)2D3 regulate rat costochondral chondrocyte cultures in a metabolite-specific manner; 1,25-(OH)2D3 targets primarily growth zone cells (GC) and 24,25-(OH)2D3 targets primarily resting zone cells (RC). Some of the effects are nongenomic, since incubation of isolated membrane fractions with the metabolites results in regulation of enzyme activities comparable to that seen in culture. This study examined whether changes in membrane fluidity might be one mechanism involved in the nongenomic regulatory pathway. Chondrocyte cultures were incubated with the vitamin D metabolites and changes in plasma membrane fluidity monitored using the fluorophore, TMA-DPH, which is specific for membranes exposed to external fluids. Isolated matrix vesicles were also incubated directly with the metabolites and anisotropy of the membrane, as well as alkaline phosphatase-specific activity, determined. 1,25-(OH)2D3 caused a rapid and constant increase in alkaline phosphatase-specific activity in GC matrix vesicles; 24,25-(OH)2D3 caused an increase in RC matrix vesicle enzyme activity that was both dose- and time-dependent. Matrix vesicles produced by GC had a lower degree of fluidity than their parent plasma membranes or RC plasma membranes and matrix vesicles. Fluidity of the GC membrane fractions was increased by 1,25-(OH)2D3 in a dose- and time-dependent manner. 1,25-(OH)2D3 had no effect on the fluidity of the RC membranes. 24,25-(OH)2D3 caused a decrease in fluidity in GC at later time points. This metabolite caused an increase in fluidity of RC plasma membranes that returned to normal levels by 6 h; however, the increase induced in the matrix vesicles remained elevated throughout the 24-h experimental period.(ABSTRACT TRUNCATED AT 250 WORDS)
24,25-Dihydroxyvitamin D 3↗
24,25-(OH)(2)D(3) regulates cartilage and bone via autocrine and endocrine mechanisms.
The purpose of this paper is to summarize recent advances in our understanding of the physiological role of 24(R),25(OH)(2)D(3) in bone and cartilage and its mechanism of action. With the identification of a target cell, the growth plate resting zone (RC) chondrocyte, we have been able to use cell biology methodology to investigate specific functions of 24(R),25(OH)(2)D(3) and to determine how 24(R),25(OH)(2)D(3) elicits its effects. These studies indicate that there are specific membrane-associated signal transduction pathways that mediate both rapid, nongenomic and genomic responses of RC cells to 24(R),25(OH)(2)D(3). 24(R),25(OH)(2)D(3) binds RC chondrocyte membranes with high specificity, resulting in an increase in protein kinase C (PKC) activity. The effect is stereospecific; 24R,25(OH)(2)D(3), but not 24S,25-(OH)(2)D(3), causes the increase, indicating a receptor-mediated response. Phospholipase D-2 (PLD2) activity is increased, resulting in increased production of diacylglycerol (DAG), which in turn activates PKC. 24(R),25(OH)(2)D(3) does not cause translocation of PKC to the plasma membrane, but activates existing PKCalpha. There is a rapid decrease in Ca(2+) efflux, and influx is stimulated. 24(R),25(OH)(2)D(3) also reduces arachidonic acid release by decreasing phospholipase A(2) (PLA(2)) activity, thereby decreasing available substrate for prostaglandin production via the action of cyclooxygenase-1. PGE(2) that is produced acts on the EP1 and EP2 receptors expressed by RC cells to downregulate PKC via protein kinase A, but the reduction in PGE(2) decreases this negative feedback mechanism. Both pathways converge on MAP kinase, leading to new gene expression. One consequence of this is production of new matrix vesicles containing PKCalpha and PKCzeta and an increase in PKC activity. The chondrocytes also produce 24(R),25(OH)(2)D(3), and the secreted metabolite acts directly on the matrix vesicle membrane. Only PKCzeta is directly affected by 24(R),25(OH)(2)D(3) in the matrix vesicles, and activity of this isoform is inhibited. This effect may be involved in the control of matrix maturation and turnover. 24(R),25(OH)(2)D(3) causes RC cells to mature along the endochondral developmental pathway, where they become responsive to 1alpha,25(OH)(2)D(3) and lose responsiveness to 24(R),25(OH)(2)D(3), a characteristic of more mature growth zone (GC) chondrocytes. 1alpha,25(OH)(2)D(3) elicits its effects on GC through different signal transduction pathways than those used by 24(R),25(OH)(2)D(3). These studies indicate that 24(R),25(OH)(2)D(3) plays an important role in endochondral ossification by regulating less mature chondrocytes and promoting their maturation in the endochondral lineage.
24,25-Dihydroxyvitamin D 3↗
1,25-(OH)2D3 modulates growth plate chondrocytes via membrane receptor-mediated protein kinase C by a mechanism that involves changes in phospholipid metabolism and the action of arachidonic acid and PGE2.
1,25-(OH)2D3 (1,25) exerts its effects on growth plate chondrocytes through classical vitamin D (VDR) receptor-dependent mechanisms, resulting in mineralization of the extracellular matrix. Recent studies have shown that membrane-mediated mechanisms are involved as well. 1,25 targets cells in the prehypertrophic and upper hypertrophic zones of the costochondral cartilage growth plate (GC cells), resulting in increased specific activity of alkaline phosphatase (ALP), phospholipase A2 (PLA2), and matrix metalloproteinases (MMPs). At the cellular level, 1,25 action results in rapid changes in arachidonic acid (AA) release and re-incorporation, alterations in membrane fluidity and Ca ion flux, and increased prostaglandin E1 and E2 (PGE2) production. Protein kinase C (PKC) is activated in a phospholipase C (PLC) dependent-mechanism, due in part to the increased production of diacylglycerol (DAG). In addition, AA acts directly on the cell to increase PKC specific activity. AA also provides a substrate for cyclooxygenase (COX), resulting in PGE2 production. 1,25 mediates its effects through COX-1, the constitutive enzyme, but not COX-2, the inducible enzyme. Time course studies using specific inhibitors of COX-1 show that AA stimulates PKC activity and PKC then stimulates PGE2 production. PGE2 acts as a mediator of 1,25 action on the cells, also stimulating PKC activity. The rapid effects of 1,25 on PKC are nongenomic, occurring within 3 min and reaching maximal activation by 9 min. It promotes translocation of PKC to the plasma membrane. When 1,25 is incubated directly with isolated plasma membranes, PKCalpha is stimulated although PKCzeta is also present. In contrast, when isolated matrix vesicles (MVs) are incubated with 1,25, PKCzeta is inhibited and PKCalpha is unaffected. These membrane-mediated effects are due to the presence of a specific membrane vitamin D receptor (mVDR) that is distinct from the classical cytosolic VDR. Studies using 1,25 analogs with reduced binding affinity for the classical VDR, confirm that rapid activation of PKC by 1,25 is not VDR dependent. The membrane-mediated effects of 1,25 are critical to the regulation of events in the extracellular matrix produced by the chondrocytes. MVs are extracellular organelles associated with maturation of the matrix, preparing it for mineralization. MV composition is under genomic control, involving VDR-mechanisms. In the matrix, no new gene expression or protein synthesis can occur, however. Differential distribution of PKC isoforms and their nongenomic regulation by 1,25 is one way for the chondrocyte to control events at sites distant from the cell. GC cells contain 1a-hydroxylase and produce 1,25; this production is regulated by 1,25, 24,25, and dexamethasone. 1,25 stimulates MMPs in the MVs, resulting in increased proteoglycan degradation in mineralization gels, and increased activation of latent transforming growth factor-beta 1 (TGF-beta1).
Animals↗
The membrane effects of 17beta-estradiol on chondrocyte phenotypic expression are mediated by activation of protein kinase C through phospholipase C and G-proteins.
Growth plate chondrocytes from both male and female rats have nuclear receptors for 17beta-estradiol (E(2)); however, recent studies indicate that an alternative pathway involving a membrane receptor may also be involved in the female cell response. E(2) directly affects the fluidity of chondrocyte membranes derived from female, but not male, rats. In addition, E(2) activates PKC in a nongenomic manner in female cells, and chelerythrine, a specific inhibitor of PKC, inhibits E(2)-dependent alkaline phosphatase activity in these cells, indicating PKC is involved in the signal transduction mechanism. The aims of this study were: (1) to examine if PKC mediates the effect of E(2) on chondrocyte proliferation, differentiation, and matrix synthesis; and (2) to determine the pathway that mediates the membrane effect of E(2) on PKC. Confluent, fourth passage resting zone (RC) and growth zone (GC) chondrocytes from female rat costochondral cartilage were treated with 10(-10) to 10(-7) M E(2) in the presence or absence of the PKC inhibitor chelerythrine, and changes in alkaline phosphatase specific activity, proteoglycan sulfation, and [3H]thymidine incorporation were measured. To examine the pathway of PKC activation, chondrocyte cultures were treated with E(2) in the presence or absence of genistein (an inhibitor of tyrosine kinases), U73122 or D609 (inhibitors of phospholipase C [PLC]), quinacrine (an inhibitor of phospholipase A(2) [PLA(2)]), and melittin (an activator of PLA(2)). Alkaline phosphatase specific activity and proteoglycan sulfation were increased and [3H]thymidine incorporation was decreased by E(2). The effects of E(2) on all parameters were blocked by chelerythrine. Treatment of the cultures with E(2) produced a significant dose-dependent increase in PKC. U73122 dose-dependently inhibited the activation of PKC in E(2)-stimulated female chondrocyte cultures. However, the classical receptor antagonist ICI 182780 was unable to block the stimulatory effect of E(2) on PKC. Moreover, the classical receptor agonist diethylstilbestrol (DES) had no effect on PKC, nor did it alter the stimulatory effect of E(2). Inhibition of tyrosine kinase and PLA(2) had no effect on the activation of PKC by E(2). The PLA(2) activator also had no effect on PKC activation by E(2). E(2) stimulated PKC activity in membranes isolated from the chondrocytes, demonstrating a direct membrane effect for this steroid hormone. These data indicate that the rapid nongenomic effect of E(2) on PKC activity in chondrocytes from female rats is sex-specific and dependent upon a G-protein-coupled phospholipase C.
Alkaline Phosphatase↗
Matrix vesicle enzyme activity in endosteal bone following implantation of bonding and non-bonding implant materials.
The effect of bone bonding (KGy-Cera) and non-bone bonding (KGy-213) implant materials on primary mineralization was examined in endosteal bone repair following marrow ablation. Comparisons were made to determine implant effect on concentration and biochemical parameters of matrix vesicles, as contrasted to vesicles in normal bone healing. Matrix vesicle number was determined by high-resolution computerized morphometric analysis, and implant effect on the specific activity of alkaline phosphatase and phospholipase A2 was measured. Bone responses differed according to the composition of the implant material. The bone bonding implant in this study stimulated matrix vesicle formation, alkaline phosphatase specific activity, and, to a lesser extent, phospholipase A2 activity. The effect of the non-bonding implant on healing bone was of suppression of enzyme specific activities and reduced matrix vesicle production. The results indicate that the bone bonding implant material (KGy-Cera) promotes the initiation of primary mineralization, whereas failure of the KGy-213 to bond may be related to toxic materials that leach from the implant and inhibit the normal sequence of events in the mineralization cascade. The results also demonstrate that the implant materials alter the healing process distal to the injury site. Changes observed in the contralateral control limb mimic the changes observed in the injured limb, but at lower magnitude.
Adhesiveness↗
The effect of local application of a sustained release delivery system of chlorhexidine on plaque accumulation.
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Adult↗