Stochastic behavior of atrial and ventricular intrinsic cardiac neurons.

To quantify the concurrent transduction capabilities of spatially distributed intrinsic cardiac neurons, the activities generated by atrial vs. ventricular intrinsic cardiac neurons were recorded simultaneously in 12 anesthetized dogs at baseline and during alterations in the cardiac milieu. Few (3%) identified atrial and ventricular neurons (2 of 72 characterized neurons) responded solely to regional mechanical deformation, doing so in a tightly coupled fashion (cross-correlation coefficient r = 0.63). The remaining (97%) atrial and ventricular neurons transduced multimodal stimuli to display stochastic behavior. Specifically, ventricular chemosensory inputs modified these populations such that they generated no short-term coherence among their activities (cross-correlation coefficient r = 0.21 +/- 0.07). Regional ventricular ischemia activated most atrial and ventricular neurons in a noncoupled fashion. Nicotinic activation of atrial neurons enhanced ventricular neuronal activity. Acute decentralization of the intrinsic cardiac nervous system obtunded its neuron responsiveness to cardiac sensory stimuli. Most atrial and ventricular intrinsic cardiac neurons generate concurrent stochastic activity that is predicated primarily upon their cardiac chemotransduction. As a consequence, they display relative independent short-term (beat-to-beat) control over regional cardiac indexes. Over longer time scales, their functional interdependence is manifest as the result of interganglionic interconnections and descending inputs.

Role of P(1) purinergic receptors in myocardial ischemia sensory transduction.

OBJECTIVES: To characterize the role that cardiac sensory P(1) purinergic (adenosine A(1) or A(2)) receptors play in transducing myocardial ischemia. METHODS: Porcine nodose ganglion cardiac sensory neuron adenosine A(1) or A(2) receptor function was studied in situ during control states as well as in the presence of the peptides bradykinin and substance P or focal ventricular ischemia. The responses of porcine nodose ganglion cardiac and non-cardiac afferent neuronal somata to adenosine were also studied in vitro. RESULTS: Local application of A(1) or A(2) adenosine receptor agonists modified the activity generated by ventricular sensory neurites associated with 70 and 74% of identified nodose ganglion cardiac afferent somata in situ, respectively, exciting most neurons. In contrast, adenosine reduced the excitability of nodose ganglion cardiac afferent neuronal somata in vitro. Bradykinin and substance P affected 56 and 63%, respectively, of tested afferent neurons. The capacity of ventricular sensory neurites to transduce signals relating to these peptides was virtually eliminated by the presence of P(1) purinergic receptor antagonists. So was their capacity to transduce focal ventricular ischemia. Since most cardiac sensory neurites responded differently to adenosine in vivo than did cardiac afferent neuronal somata in vitro, it appears that the transduction properties of cardiac afferent neurons need to be characterized in situ. CONCLUSIONS: Most ventricular sensory neurites associated with nodose ganglion afferent neurons possess adenosine A(1) and/or A(2) receptors that play a primary role in transducing myocardial ischemic events to central neurons. These data support clinical observations implicating cardiac sensory purinoceptors in transducing myocardial ischemic events.

Transduction capabilities of neonatal ventricular afferent neurons in vivo.

We sought to determine the capacity of ventricular sensory nerve endings (neurites) associated with neonatal nodose ganglion afferent neurons to transduce mechanical and chemical stimuli in situ. Spontaneous activity generated by 17 nodose ganglion cardiac afferent neurons was identified in 8 anesthetized neonatal pigs (10-21 days old) using extracellular recording recording techniques. The activity generated by afferent neurons was studied when their ventricular sensory neurites were exposed to local mechanical or chemical stimuli, following systemic administration of specific chemicals or during brief periods of apnea. Gentle mechanical distortion of their ventricular sensory fields enhanced the activity generated by 6 spontaneously active afferent neurons, while suppressing the activity generated by another 3 neurons. Afferent neuronal activity was either enhanced or suppressed when the following chemicals were applied to identified ventricular epicardial sensory fields: the sodium channel modifier veratridine (92% of tested neurons); the P1-purinoceptor agonist adenosine (92%); the neuropeptides angiotensin II (100%), bradykinin (90%) and substance P (90%); and the nitric oxide donor S-nitroso-N-acetylpenicillamine (100%). Epicardial application of isoproternol or nicotine induced modest neuronal responses. Cardiac afferent neurons were also affected when these chemicals were administered systemically. Apnea of 60-100 s duration modified (enhanced, n = 2; suppressed, n = 5) the activity generated by most identified afferent neurons. The estimated average conduction velocity of afferent axons associated with these neurons was 1.0 +/- 0.2 m/s. It is concluded that neonatal nodose ganglion cardiac afferent neurons respond to many of the chemicals known to modify adult cardiac afferent neurons. That cardiac afferent neurons are capable of sensing the mechanical and chemical milieu of the neonatal heart should be taken into account when considering altered neonatal cardiovascular status such as occurs during apnea.

Functional interdependence of neurons in a single canine intrinsic cardiac ganglionated plexus.

To determine the activity characteristics displayed by different subpopulations of neurons in a single intrinsic cardiac ganglionated plexus, the behaviour and co-ordination of activity generated by neurons in two loci of the right atrial ganglionated plexus (RAGP) were evaluated in 16 anaesthetized dogs during basal states as well as in response to increasing inputs from ventricular sensory neurites. These sub-populations of right atrial neurons received afferent inputs from sensory neurites in both ventricles that were responsive to local mechanical stimuli and the nitric oxide donor nitroprusside. Neurons in at least one RAGP locus were activated by epicardial application of veratridine, bradykinin, the beta1-adrenoceptor agonist prenaterol or glutamate. Epicardial application of angiotensin II, the selective beta2-adrenoceptor agonist terbutaline and selective alpha-adrenoceptor agonists elicited inconsistent neuronal responses. The activity generated by both populations of atrial neurons studied over 5 min periods during basal states displayed periodic coupled behaviour (cross-correlation coefficients of activities that reached, on average, 0.88 +/- 0.03; range 0.71-1) for 15-30 s periods of time. These periods of coupled activity occurred every 30-50 s during basal states, as well as when neuronal activity was enhanced by chemical activation of their ventricular sensory inputs. These results indicate that neurons throughout one intrinsic cardiac ganglionated plexus receive inputs from mechano- and chemosensory neurites located in both ventricles. That such neurons respond to multiple chemical stimuli, including those liberated from adjacent adrenergic efferent nerve terminals, indicates the complexity of the integrative processing of information that occurs within the intrinsic cardiac nervous system. It is proposed that the interdependent activity displayed by populations of neurons in different regions of one intrinsic cardiac ganglionated plexus, responding as they do to multiple cardiac sensory inputs, forms the basis for integrated regional cardiac control.

Chemotransduction properties of nodose ganglion cardiac afferent neurons in guinea pigs.

To determine the chemotransduction characteristics of ventricular sensory neurites associated with nodose ganglion afferent neurons, various chemicals were applied individually to epicardial sensory neurites associated with individual afferent neurons in anesthetized guinea pigs. The following ion channel-modifying agents were tested: barium chloride, cadmium chloride, calcium chloride, the chelating agent EGTA, nickel chloride, potassium chloride, tetraethylammonium chloride, and veratridine. An acidic solution (pH 6.0) and oxygen-derived free radicals (H(2)O(2)) were tested. The following chemicals were also tested: adenosine, alpha- and beta-adrenergic agonists, angiotensin II, bradykinin, calcitonin gene-related peptide (CGRP), histamine, nicotine, the nitric oxide donor nitroprusside, substance P, and vasoactive intestinal peptide. A total of 102 cardiac afferent neurons was identified, of which approximately 66% were sensitive to mechanical stimuli applied to their epicardial sensory fields. Application of individual ion channel-modifying agents to epicardial sensory fields modified most associated afferent neurons, with barium chloride affecting each neuron studied. Ventricular sensory neurites associated with most identified neurons were also responsive to the other tested chemicals, with hydrogen peroxide, adenosine, angiotensin II, bradykinin, CGRP, clonidine, and nicotine inducing responses from at least 75% of the neurons studied. It is concluded that 1) the ventricular sensory neurites associated with nodose ganglion afferent neurons transduce a much wider variety of chemical stimuli than considered previously, 2) these sensory neurites employ a variety of membrane ion channels in their transduction processes in situ, and 3) adrenergic agents influence on sensory neurites associated with cardiac afferent neurons suggests the presence of a cardiac feedback mechanism involving local catecholamine release by adjacent sympathetic efferent postganglionic nerve terminals.

The heart reinnervates after transplantation.

BACKGROUND: Whether cardiac reinnervation occurs after transplantation remains controversial. If reinnervation does occur, how sympathetic and parasympathetic efferent neurons do this remains unknown. METHODS: Power spectral analysis of heart rate variability was assessed for 1 year after cardiac autotransplantation in 9 dogs. After induction of anesthesia 13 months after transplantation, cardiac and intrinsic cardiac neuronal responses elicited by both electrical stimulation of parasympathetic or sympathetic efferent neurons and systemic or local coronary artery administration of nicotine (5 microg/kg), angiotensin II (0.75 microg/kg), and tyramine (1.2 microg/kg) were studied. The transmembrane electrical properties of intrinsic cardiac neurons were studied in vitro. Ventricular tissue catecholamine content, alpha-tubulin expression, and beta-adrenergic receptor density and affinity were studied. The presence of axons crossing suture lines was sought histologically. RESULTS: Nerves were identified crossing suture lines. Electrical or chemical (ie, nicotine or angiotensin II) activation of sympathetic efferent neurons enhanced cardiodynamics, as did tyramine. Stimulating vagal efferent preganglionic axons induced bradycardia in half of the dogs. Functional reinnervation did not correlate with specific power spectra derived from rate variability in the conscious state. Responding to nicotine and angiotensin II in situ, transplanted intrinsic cardiac neurons generated spontaneous activity. These neurons displayed nicotine-dependent synaptic inputs in vitro. Ventricular tissue had normal beta-adrenergic receptor affinity and density but reduced catecholamine and alpha-tubulin contents. CONCLUSIONS: The intrinsic cardiac nervous system receives reduced input from extracardiac sympathetic efferent neurons after transplantation and inconsistent input from parasympathetic efferent preganglionic neurons. These heterogeneous neuronal inputs are not reflected in heart rate variability or ventricular beta-adrenergic receptor function. Transplanted angiotensin II-sensitive intrinsic cardiac neurons exert greater cardiac control than do nicotine-sensitive ones. The intrinsic cardiac nervous system remodels itself after cardiac transplantation, and this indicates that direct assessment of extracardiac and intrinsic cardiac neuronal behavior is required to fully understand cardiac control after transplantation.

Ion channel modifying agents influence the electrical activity generated by canine intrinsic cardiac neurons in situ.

This study was designed to establish whether agents known to modify neuronal ion channels influence the behavior of mammalian intrinsic cardiac neurons in situ and, if so, in a manner consistent with that found previously in vitro. The activity generated by right atrial neurons was recorded extracellularly in varying numbers of anesthetized dogs before and during continuous local arterial infusion of several neuronal ion channel modifying agents. Veratridine (7.5 microM), the specific modifier of Na+-selective channels, increased neuronal activity (95% above control) in 80% of dogs tested (n = 25). The membrane depolarizing agent potassium chloride (40 mM) reduced neuronal activity (43% below control) in 84% of dogs tested (n = 19). The inhibitor of voltage-sensitive K+ channels, tetraethylammonium (10 mM), decreased neuronal activity (42% below control) in 73% of dogs tested (n = 11). The nonspecific potassium channel inhibitor barium chloride (5 mM) excited neurons (47% above control) in 13 of 19 animals tested. Cadmium chloride (200 microM), which inhibits Ca2+-selective channels and Ca2+-dependent K+ channels, increased neuronal activity (65% above control) in 79% of dogs tested (n = 14). The specific L-type Ca2+ channel blocking agent nifedipine (5 microM) reduced neuronal activity (52% blow control in 72% of 11 dogs tested), as did the nonspecific inhibitor of L-type Ca2+ channels, nickel chloride (5 mM) (36% below control in 69% of 13 dogs tested). Each agent induced either excitatory or inhibitory responses, depending on the agent tested. It is concluded that specific ion channels (I(Na), I(CaL), I(Kv), and I(KCa)) that have been associated with intrinsic cardiac neurons in vitro are involved in their capacity to generate action potentials in situ.

Transmyocardial laser revascularization does not denervate the canine heart.

BACKGROUND: Transmyocardial laser revascularization has been used as an indirect approach to improve myocardial perfusion in patients with refractory angina not amenable to conventional therapy. Three mechanisms have been proposed for its therapeutic effects: direct perfusion of the ischemic myocardium through patent channels; induction of angiogenesis; and regional denervation. We sought to determine whether transmyocardial laser revascularization modifies afferent and efferent axonal function within the affected myocardium. METHODS: Studies were performed in 9 dogs that were artificially ventilated and underwent thoracotomy. Changes in ventricular dynamics and intrinsic cardiac neuronal activity were monitored before and after creating 20 transmural channels in the left ventricular ventral free wall with a holmium:yttrium-aluminum-garnet laser in response to three stimuli: application of veratridine or bradykinin to the epicardial sensory neurites of intrinsic cardiac afferent neurons; sympathetic or parasympathetic efferent neuronal activation either electrically (4 V, 10 Hz, 5 ms) or chemically (nicotine, 5 microg/kg intravenously), and direct cardiomyocyte beta-adrenergic receptor stimulation (isoproterenol hydrochloride, 5 microg intravenously). RESULTS: Sensory neurites of right atrial afferent neurons in the studied epicardial region responded similarly to chemical stimulation before and after transmyocardial laser revascularization. Transmyocardial laser treatment did not reduce local ventricular contractile responses to direct activation of sympathetic or parasympathetic efferent neurons by electrical or chemical means, nor did it affect cardiomyocyte augmentor responses elicited by exogenous beta-adrenergic receptor challenge. CONCLUSIONS: As transmyocardial laser revascularization does not affect afferent or efferent axonal function in the affected ventricle, the efficacy of this form of therapy cannot be ascribed to local denervation.

Neuronally induced augmentation of cardiac output.

OBJECTIVE: To determine whether cardiac output can be augmented by preferentially activating cardiac adrenergic efferent neurons. DESIGN: Elicited cardiac output responses were compared when cardiac myocytes were directly stimulated by a beta1-adrenoceptor agonist versus when they were indirectly influenced by beta2- adrenergic-sensitive cardiac efferent neurons. ANIMALS AND METHODS: The beta1-adrenoceptor agonist dobutamine or the selective beta2-adrenoceptor agonist terbutaline was continuously infused individually into the systemic circulation of 15 anesthetized pigs for 20 mins in 5 and 15 microgram/kg/min doses. Heart rate, left atrial chamber pressure, regional left ventricular intramyocardial systolic pressure, left ventricular chamber pressure and aortic pressure were monitored. Cardiac output was determined via the thermodilution technique before and at 10 min intervals during drug infusions. Ventricular tissues were removed thereafter and immediately frozen in liquid nitrogen for subsequent cardiac myocyte cell surface beta-adrenoceptor analysis. MAIN RESULTS: Both doses of terbutaline increased heart rate (approximately +18%) and cardiac output (approximately +20%). Heart rate (+12%) and cardiac output (+16%) increased when the high dose of dobutamine was tested. Left ventricular intramyocardial systolic pressure was increased by dobutamine (+15%) but not by terbutaline. Porcine ventricular cardiac myocytes primarily possess cell surface beta1-, rather than beta2-, adrenoceptors, making it unlikely that cardiac myocytes were directly affected by the doses of terbutaline tested. CONCLUSIONS: Beta2-adrenoceptor agonists enhance cardiac output primarily as a result of neuronally induced increases in heart rate in the porcine model. Adrenergic efferent neuronal enhancement of heart rate may be an effective way to increase cardiac output independently of directly augmented ventricular dynamics. Further study is required to determine whether the diseased myocardium can be supported by such neurocardiological means.

Canine intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors.

To determine whether intrinsic cardiac neurons involved in cardiac regulation possess neurokinin (NK) receptor subtypes, we administered selective NK receptor agonists individually (100 microM; 0.1 ml) into the coronary arterial blood supply of right atrial intrinsic cardiac neurons of 18 anesthetized dogs. The selective NK1 receptor agonist [Sar9,Met(O2)11]-substance P depressed the spontaneous activity of right atrial neurons (26.7 +/- 6.7 to 13.0 +/- 4.0 impulses/min; P < 0.05) in 11 dogs and augmented such activity in the other 5 dogs (8.0 +/- 3.1 to 27.8 +/- 8.7 impulses/min; P < 0.05). Local administration of the selective NK2 receptor agonist [beta-Ala8]-NKA-(4-10) depressed right atrial neuronal activity (27.3 +/- 6.4 to 14.7 +/- 3.8 impulses/min; P < 0. 05), whereas the selective NK3 receptor agonist senktide augmented such activity (18.9 +/- 6.4 to 53.1 +/- 12.0 impulses/min; P < 0.05). Left ventricular chamber pressure fell when selective NK1 and NK2 receptor agonists were administered. Increases in heart rate and right ventricular intramyocardial systolic pressure occurred when the selective NK3 receptor agonist was studied. Administration of a selective NK1 or NK2 receptor antagonist altered neuronal activity, with no subsequent change in activity occurring after administration of its respective receptor agonist. Receptor autoradiography demonstrated tachykinin receptors associated with ventral right atrial intrinsic cardiac neurons. It is concluded that intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors and that some intrinsic cardiac neurons receive tonic input via endogenously released NKs.

Sensitivity of canine intrinsic cardiac neurons to H2O2 and hydroxyl radical.

To determine whether intrinsic cardiac neurons are sensitive to oxygen-derived free radicals in situ, studies were performed in 44 open-chest anesthetized dogs. 1) When H2O2 (600 microM) was administered to right atrial neurons of 36 dogs via their local arterial blood supply, neuronal activity either increased (+92% in 16 dogs) or decreased (-61% in 20 dogs), depending on the population of neurons studied. H2O2 (600 microM) administered into the systemic circulation did not affect neuronal activity, measured cardiac indexes, or aortic pressure. 2) The iron-chelating agent deferoxamine (20 mg/kg iv), a chemical that prevents the formation of oxygen-derived free radicals, reduced the activity generated by neurons (-57%) in 8 of 10 dogs. 3) H2O2 did not affect neuronal activity when administered in the presence of deferoxamine in these 10 dogs. 4) When the ATP-sensitive potassium (KATP) channel opener cromakalim (20 microM) was administered to intrinsic cardiac neurons in another 21 animals via their regional arterial blood supply, ongoing neuronal activity in 15 of these dogs decreased by 54%. 5) Neuronal activity was not affected by H2O2 when administered in the presence of cromakalim in 16 dogs. These data indicate that 1) some intrinsic cardiac neurons are sensitive to exogenous H2O2, 2) such neurons are tonically influenced by locally produced oxygen-derived free radicals in situ, and 3) intrinsic cardiac neurons possess KATP channels that are functionally important during oxidative challenge.

Bradycardia induced by intravascular versus direct stimulation of the vagus nerve.

BACKGROUND: Electrical stimulation of the parasympathetic nervous system results in slowing of the heart. We sought to determine whether cardiac vagal efferent axons can be stimulated adequately to induce bradycardia without disturbing the integrity of the thorax. METHODS: Cardiodepressor effects elicited by direct stimulation of a vagus nerve in anesthetized dogs and pigs were compared with those generated when the same nerve was stimulated indirectly through bipolar electrodes placed in the adjacent superior vena cava. RESULTS: The heart rate of dogs decreased by about 80% when electrical stimuli were delivered to the right thoracic vagus at the level of the thoracic outlet through bipolar electrodes placed either in the adjacent superior vena cava (intravascular method) or directly on the nerve (direct method). Maximal responses were achieved with 10-V, 5-ms, and 20-Hz stimuli. In anesthetized pigs, similar bradycardia occurred when the right cervical vagus or the right cranial thoracic vagus was stimulated either directly or indirectly through the intravascular method. Atrial dysrhythmias occurred when the stimulating electrodes were placed by either method within 1 cm of the right atrium in both animal models. CONCLUSIONS: Controlled bradycardia can be induced during operation without the risk of generating cardiac dysrhythmias using electrical stimuli (10 V, 5 ms, and 10 to 20 Hz) delivered to the right cervical vagus nerve or the right cranial thoracic vagus nerve through adjacent intravascular electrodes.

The impact of the demographics of aging and the edentulous condition on dental care services.

Over the next 20 years, the number of people aged 65 years and older is expected to increase substantially in both Canada and the United States. Moreover, advances in dental treatment are resulting in reduced levels of the edentulous condition, such that there will be more people in need of various dental services. The purpose of this study was to determine what effect the increase in the overall population of the United States and Canada, and specific cohorts such as the senior citizen population, would have on the decrease in the levels of the edentulous condition. Through the use of population data obtained through Statistics Canada and the U.S. Census Bureau, it was determined that there will be 25.2% more Americans and 36.5% Canadians who are 65 years of age and over. Furthermore, an algorithm was developed using the United States national tooth loss data, which determined the percentage of people who would be edentulous at 75 years of age and older. The tooth retention rate improves with the younger age cohorts. The 50- to 54-year age group in the year 2000 will, on average, have 6.6 more teeth than the current elderly when they are 75 years of age and older. The percentage of the edentulous condition for the 75-plus age group will decrease by about 50% over the 35-year period from 1990 to 2025. The clinical significance of this trend means that there will be more people with more teeth in need of various dental treatments.

Awareness of periodontal disease in a group of northern Canadian children.

Periodontal disease destroys the supporting structures of the teeth. The clinical signs start early in childhood as inflammation of the gingival tissues; if uncontrolled, it becomes the major cause of loss of teeth in adult life. The purpose of this survey was to determine the understanding that a group of 10- to 15-year-olds living in the Inuvialuit, Gwich'in, and Sahtu Districts of the Northwest Territories have regarding the recognition and prevention of periodontal-gingival disease. A total of 953 students, with a median age of 12.5 years, completed the survey. The data, which included rural and urban centers as well as rural and remote regions, were analyzed using the chi-square method. Ethnic and gender differences are reported. Results indicate that girls have a better awareness of good oral health. Non-Native children have a somewhat better understanding regarding the recognition and prevention of periodontal disease. Both Native and non-Native groups share uncertainties with respect to the rationale and reasons behind the disease process. Educators of oral health prevention should incorporate into their programs preventive measures that take into consideration Native culture and traditions.

Dental caries knowledge in a group of Northwest Territories children.

A total of 953 children in schools in communities in the Northwest Territories was surveyed to determine their attitudes and knowledge about dental decay. A questionnaire was answered by these Native and non-Native children in the Northwest Territories. The median age of the children was 12.5 years. The girls tended to brush their teeth more frequently and consumed less sugared sweets between meals. More of the girls and in particular the Native girls knew about "nursing" caries. The Native students more often than not went for dental treatment when it was necessary. The Native students brushed their teeth less frequently and often learned to brush their teeth on their own. The consumption of sugared sweets between meals was greater in the Native sample. The knowledge level of the factors that affect dental decay rates was lower in the Native group, but was not extremely high in either group. These children should receive more information on oral health practices and be given an opportunity to improve their oral health knowledge.

A comparison of moderate and high users of Alberta's universal dental plan for the elderly.

The characteristics and service utilization of 2,071 high and 2,337 moderate users of Alberta's dental plan from 1978-79 to 1990-91 are reported. High users are those who used the plan for 14 consecutive years; moderate users are those who used the plan in seven of the 14 years. Both groups were over 74 years of age in 1991-92. Compared to high users, moderate users lived in less urbanized regions, visited denturists more often and received far more complete dentures and fewer partial dentures. As a percentage of their total annual plan expenditures, moderate users spent less on diagnostic, preventive, periodontal and restorative services and much more on removable prosthodontic and denturists' services. However, during the study period, the moderate users increased their annual relative expenditures for diagnostic, preventive and, especially, periodontal services, and decreased them for prosthodontic services. With respect to specific preventive and periodontal services, the percentage of total annual expenditures for dental prophylaxis, topical fluoride applications, periodontal scaling, gingival curettage, and combinations of these, was much higher for the high user group. Despite these differences favoring the high user group, during the 14 year period, the moderate user group considerably increased its relative expenditures for dental prophylaxis, topical fluoride and periodontal scaling services. While the observed differences in service expenditures between high and moderate users were anticipated, the shift over time to using more preventive and periodontal services by both groups was an encouraging harbinger of the "new elderly" dental patients.

Alberta's universal dental plan for the elderly: differences in use over 6 years by two cohorts.

OBJECTIVES: Dental services use by two cohorts under the universal dental plan for the elderly in Alberta, Canada, was examined. METHODS: Two birth cohorts 65 to 69 years old at entry who used the plan from 1978 to 1979 (n = 17,816) or from 1985 to 1986 (n = 27,474) were analyzed over 6 successive years for differences in dental services use and costs. RESULTS: The 1985/86 cohort received 24% more visits per patient than the 1978/79 cohort. Their inflation-adjusted expenditures increased by 19% mainly as a result of increases in denturists' expenditures (33%) (dentists' expenditures increased just 4% because of lower plan fee increases). The 1985/86 cohort received relatively many more periodontal and fewer denture services. Annual attendance over 6 consecutive years was high, especially for the 1985/86 cohort and dentists' patients; 55% of the 1985/86 cohort who used dentists did so in 5 or all 6 years. CONCLUSIONS: Differences in plan expenditures per patient between the birth cohorts and dentists and denturists, along with the high continuity of care for dentists' patients, have important implications for planning and administering dental plans for the elderly. The large expenditure decreases for removable dentures and the large increases for periodontal services to the 1985/86 cohort are noteworthy.

Denture replacement during a 14-year period in Alberta's universal dental plan for the elderly.

Since 1973 Alberta's dental plan for the elderly has made government-sponsored, premium-free, comprehensive dental care available from both dentists and denturists in private practice to all residents older than 64 years. This article is based on an analysis that covered 260,000 patients from 1978 to 1992. It presents the frequency, nature, and cost of denture replacements to patients and pays particular attention to replacements administered within the allowable 5-year time limit stated by the plan for complete and removable partial dentures. During the 14-year period, about 55,000 dentures were replaced; 47% of these were replaced in the year after the individual's 5-year time limit had expired. Within the 5-year limit 1974 dentures were replaced at a nominal cost of +1.09 million, with nearly one half of these costs being attributed to denturists. Relative to the total number of dentures provided during the 14-year period, the denture replacement rate for dentists was 7% to 8%, and for denturists it was nearly three times greater at 21% to 22%. The replacement process included many crossovers by patients between dentists and denturists; for example, nearly one quarter of the 190 complete dentures initially provided by dentists were replaced by denturists within 5 years.