Biomedical subjects

Craig S Miller

Publications and source records attributed to Craig S Miller.

18 recordsLinked to original sources

PubMed2006

JC virus detection in bodily fluids: clues to transmission.

JC virus in saliva, oropharyngeal fluid, blood, and urine samples obtained from 58 human immunodeficiency virus-infected persons and 58 matched controls was investigated by performing quantitative polymerase chain reaction. JC virus was rarely present in oropharyngeal fluid and blood samples, even in those obtained from immunosuppressed individuals, but it was commonly detected in urine samples from both groups, suggesting that urine contributes to transmission.

Adult↗

PubMed2006

Cerebral activation during thermal stimulation of patients who have burning mouth disorder: an fMRI study.

The pathophysiology of burning mouth disorder (BMD) is not clearly understood, but central neuropathic mechanisms are thought to be involved. The aim of this study was to gain insight into the pathophysiology associated with BMD by using functional magnetic resonance imaging (fMRI). Areas of brain activation following thermal stimulation of the trigeminal nerve of eight female patients with BMD (mean age 49.1+/-10.1) were mapped using fMRI and compared with those of eight matched pain-free volunteers (mean age 50.3+/-12.3). Qualitative and quantitative differences in brain activation patterns between the two study groups were demonstrated. BMD patients displayed greater fractional signal changes in the right anterior cingulate cortex (BA 32/24) and bilateral precuneus than did controls (p<0.005). The control group showed larger fractional signal changes in the bilateral thalamus, right middle frontal gyrus, right pre-central gyrus, left lingual gyrus, and cerebellum than did the BMD patients (p<0.005). In addition, BMD patients had less volumetric activation throughout the entire brain compared to the control group. Overall, BMD patients displayed brain activation patterns similar to those of patients with other neuropathic pain conditions and appear to process thermal painful stimulation to the trigeminal nerve qualitatively and quantitatively different than pain-free individuals. These findings suggest that brain hypoactivity may be an important feature in the pathophysiology of BMD.

Adult↗

PubMed2006

Reactivation from quiescence does not coincide with a global induction of herpes simplex virus type 1 transactivators.

Herpes simplex virus type 1 (HSV-1) reactivates from a small fraction of latently infected neurons in vivo and neuronally differentiated (ND), quiescently infected (QIF)-PC12 cells in vitro. This may be the result of reactivation initiating in only a few cells, or reactivation followed by premature termination of the productive virus life cycle in many or even a majority of cells. To examine the viral stress response, HSV-1 promoters of representative alpha, beta, and gamma class genes were examined in ND- and QIF-PC12 cells after treatments with agents known to induce reactivation. HSV-1 promoters displayed variable levels of basal gene expression in ND-PC12 cells ranging from 2 to 1,200 times the level of the control vector pGL3-Basic. Expression of the latency associated transcript (LAT) was greatest, with representatives of the alpha class exhibiting greater expression than the beta and gamma classes. The HSV-1 promoters examined did not respond dramatically to stress treatments. The viral gene response was also measured during the initiation of reactivation of a cryptic HSV-1 genome after forskolin treatment, under conditions that restricted DNA replication. During the first 24 h after stress induction the response was limited. By 48 h post-forskolin treatment, only modest increases occurred for ICP0, ICP4, and LAT transcripts, reaching levels of no greater than 2.2 times mock treated levels. In contrast, ICP27, ribonucleotide reductase (RR), and VP16 promoters did not respond. These findings indicate that reactivation from QIF-PC12 cells does not result in a global response of the specific HSV-1 genes tested, when assessed at the population level. These data support the hypothesis that stress-induced reactivation initiates in a minority of cells.

Animals↗

PubMed2006

High prevalence of multiple human herpesviruses in saliva from human immunodeficiency virus-infected persons in the era of highly active antiretroviral therapy.

Human immunodeficiency virus (HIV) infection is associated with an increased risk for human herpesviruses (HHVs) and their related diseases. Methods for limiting the transmission of HHVs require a better understanding of the prevalence and infectiousness of oral HHVs in HIV-infected patients. We performed quantitative PCR to investigate the prevalence, quantity, risk, and correlates of salivary HHVs from 58 HIV-seropositive individuals in a case control study. HHVs were significantly more prevalent in the salivas of HIV-seropositive persons than in those of the controls (odds ratios [ORs], 4.2 to 26.2; P<or=0.008). In HIV-infected patients, Epstein-Barr virus (EBV), human herpesvirus 8 (HHV-8), cytomegalovirus (CMV), and herpes simplex virus type 1 (HSV-1) were detected in 90%, 57%, 31% and 16% of samples, respectively, compared with 48%, 24%, 2%, and 2%, respectively, of samples from controls. Multiple HHVs were observed in 71% of HIV-seropositive persons and only 16% of controls (OR, 13.0; 95% confidence interval, 5.29 to 32.56). HIV-positive patients had significantly higher EBV loads than HIV-negative persons (P<0.0001). HIV-infected patients with CD4 counts above 200 cells/microl had increased probability for having HHV-8 in saliva (P=0.009) compared with patients whose counts were less than 200. In contrast, HSV-1, EBV, and CMV were detected more often when CD4 counts were low. High salivary HHV loads were detected for those (n=7) with oral lesions. These findings suggest that saliva is a potential risk factor for the acquisition of multiple HHVs, and several host factors may function to accelerate HHV reactivation or replication in patients with HIV infection.

Adult↗

PubMed2006

ICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.

Viral genes sufficient and required for herpes simplex virus type 1 (HSV-1) reactivation were identified using neuronally differentiated PC12 cells (ND-PC12 cells) in which quiescent infections with wild-type and recombinant strains were established. In this model, the expression of ICP0, VP16, and ICP4 from adenovirus vectors was sufficient to reactivate strains 17+ and KOS. The transactivators induced similar levels of reactivation with KOS; however, 17+ responded more efficiently to ICP0. To identify viral transactivators required for reactivation, we examined quiescently infected PC12 cell cultures (QIF-PC12 cell cultures) established with HSV-1 deletion mutants R7910 (deltaICP0), KD6 (deltaICP4), and in1814, a virus containing an insertion mutation in VP16. Although growth of these mutant viruses was impaired in ND-PC12 cells, R7910 and in1814 reactivated at levels equivalent to or better than their respective parental controls following stress (i.e., heat or forskolin) treatment. After treatment with trichostatin A, in1814 and 17+ reactivated efficiently, whereas the F strain and R7910 reactivated inefficiently. In contrast, KD6 failed to reactivate. In experiments with the recombinant KM100, which contains the in1814 mutation in VP16 and the n212 mutation in ICP0, spontaneous and stress-induced reactivation was observed. However, two strains, V422 and KM110, which lack the acidic activation domain of VP16, did not reactivate above low spontaneous levels after stress. These results demonstrate that in QIF-PC12 cells ICP0 is not required for efficient reactivation of HSV-1, the acidic activation domain of VP16 is essential for stress-induced HSV-1 reactivation, and HSV-1 reactivation is modulated uniquely by different treatment constraints and phenotypes.

Acyclovir↗

PubMed2006

Salivary biomarkers of existing periodontal disease: a cross-sectional study.

BACKGROUND: The authors conducted a study to determine if salivary biomarkers specific for three aspects of periodontitis--inflammation, collagen degradation and bone turnover--correlate with clinica features of periodontal disease. METHODS: The relationship between periodontal disease and the levels of interleukin-1 beta (IL-1beta), matrix metalloproteinase (MMP)-8, and osteoprotegerin (OPG) in whole saliva of 57 adults (28 "case" subjects with moderate-to-severe periodontal disease and 29 healthy control subjects) was examined in a case-control trial. RESULTS: Mean levels of IL-1beta and MMP-8 in saliva were significantly higher in case subjects than in controls. Both analytes correlated with periodontal indexes, whereas, after adjustment for confounders, OPG did not. Elevated salivary levels of MMP-8 or IL-1beta (more than two standard deviations above the mean of the controls) significantly increased the risk of periodontal disease (odds ratios in the 11.3-15.4 range). Combined elevated salivary levels of MMP-8 and IL-1beta increased the risk of experiencing periodontal disease 45-fold, and elevations in all three biomarkers correlated with individual clinical parameters indicative of periodontal disease. CONCLUSION: Salivary levels of MMP-8 and IL-1beta appear to serve as biomarkers of periodontitis. CLINICAL IMPLICATIONS: Qualitative changes in the composition of salivary biomarkers could have significance in the diagnosis and treatment of periodontal disease.

Adult↗

PubMed2005

NF-kappaB dependent cytokine levels in saliva of patients with oral preneoplastic lesions and oral squamous cell carcinoma.

Previous investigations in our laboratory and others (Chen et al., 1998) have shown that the levels of certain inflammatory, proangiogenic cytokines in saliva and tissue specimens of patients with oral premalignant lesions (OPML) are elevated. We have also shown that these cytokines are elevated in tissue culture of oral squamous cell carcinoma (OSCC) cell lines. The purpose of this pilot study was to determine the level of several inflammatory, NF-kappaB-dependent cytokines in whole unstimulated saliva (WUS), in subjects with OPML as compared to those with diagnosed OSCC. Subjects (n=13) with OMPL, OSCC (n=13), and age-sex matched controls without oral lesions (C) (n=13) were enrolled. The mean age was 58.7 years. WUS was collected by standard techniques for 5 min (Navazesh, 1993). WUS samples were centrifuged and the cytokine analysis was performed on the supernatants by ELISA as previously described by Ondrey et al. (1991). The cytokines analyzed were: TNF-alpha, interleukin-1, interleukin-6, and interleukin-8 (TNF-alpha, IL-1, IL-6, and IL-8). The results as analyzed by Pairwise t-tests revealed significant differences in the salivary levels of: (1) TNF-alpha: (mean+/-S.E.M.: TNF-alpha-OSSC=28.9+/-14.6* pcg/ml versus OPML=10.5+/-7.4* pcg/ml versus controls=3.0+/-1.0 pcg/ml; *p<0.01); (2) IL-1: (IL-1-OSSC=454.4+/-215.8* pcg/ml versus OPML=255.1+/-124.8* pcg/ml versus controls=173.2+/-66.9 pcg/ml; *p<0.01); (3) IL-6: (mean+/-S.E.M.: IL-6-OSSC=88.2+/-43.2* pcg/ml versus OPML=70.8+/-24.3* pcg/ml versus controls=1.4+/-1.0 pcg/ml; *p<0.001) and (4) IL-8 in saliva: (mean+/-S.E.M.: IL-8-OSSC=3154.1+/-1023.2* pcg/ml versus OPML=1918.2+/-899.1* pcg/ml versus controls=1580.7+/-789.0 pcg/ml; *p<0.001). There was a significant increase in the levels of all cytokines in the saliva of the OPML as compared to controls, and a significant difference in the cytokines of OSSC saliva compared to the OPML and controls. These results suggest that these proangiogenic, proinflammatory cytokines are elevated in the saliva of patients with OSSC and OPML as compared to controls, which may have diagnostic and/or prognostic significance.

Adult↗

PubMed2005

Application of microchip assay system for the measurement of C-reactive protein in human saliva.

In the last decade, saliva has been advocated as a non-invasive alternative to blood as a diagnostic fluid. However, use of saliva has been hindered by the inadequate sensitivity of current methods to detect the lower salivary concentrations of many constituents compared to serum. Furthermore, developments in the areas related to lab-on-a-chip systems for saliva-based point of care diagnostics are complicated by the high viscosity and heterogeneous properties associated with this diagnostic fluid. The biomarker C-reactive protein (CRP) is an acute phase reactant and a well-accepted indicator of inflammation. Numerous clinical studies have established elevated serum CRP as a strong, independent risk factor for the development of cardiovascular disease (CVD). CVD has also been associated with oral infections (i.e. periodontal diseases) and there is evidence that systemic CRP may be a link between the two. Clinical measurements of CRP in serum are currently performed with "high sensitivity" CRP (hsCRP) enzyme-linked immunosorbent assay (ELISA) tests that lack the sensitivity for the detection of this important biomarker in saliva. Because measurement of salivary CRP may represent a novel approach for diagnosing and monitoring chronic inflammatory disease, including CVD and periodontal diseases, the objective of this study was to apply an ultra-sensitive microchip assay system for the measurement of CRP in human saliva. Here, we describe this novel lab-on-a-chip system in its first application for the measurement of CRP in saliva and demonstrate its advantages over the traditional ELISA method. The increased sensitivity of the microchip system (10 pg ml(-1) of CRP with 1000-fold dilution of saliva sample) is attributed to its inherent increased signal to noise ratio, resulting from the higher bead surface area available for antigen/antibody interactions and the high stringency washes associated with this approach. Finally, the microchip assay system was utilized in this study to provide direct experimental evidence that chronic periodontal disease may be associated with higher levels of salivary CRP.

C-Reactive Protein↗

PubMed2005

Pleiotropic mechanisms of virus survival and persistence.

Viruses are enormously efficient infectious agents that have been implicated in causing human disease for centuries. Transmission of these pathogens continues to be from one life form to another in the form of isolated cases, epidemics, and pandemics. Each infection requires entry into a susceptible host, replication, and evasion of the immune system. Viruses are successful pathogens because they target specific cells for their attack, exploit the cellular machinery, and are efficient in circumventing and/or inhibiting key cellular events required of survival. This article reviews some of the advances that have taken place in human virology in the past 50 years, emphasizing mechanisms that contribute to, and are involved with, virus survival and persistence.

Apoptosis↗

PubMed2005

Histone deacetylase inhibitors induce reactivation of herpes simplex virus type 1 in a latency-associated transcript-independent manner in neuronal cells.

Histone acetylation is implicated in the regulation of herpes simplex virus type 1 (HSV-1) latency. However, the role of histone acetylation in HSV-1 reactivation is less clear. In this study, the well-established model system, quiescently infected, neuronally differentiated PC12 (QIF-PC12) cells, was used to address the participation of histone acetylation in HSV-1 reactivation. In this model, sodium butyrate and trichostatin A (TSA), two histone deacetylase inhibitors, stimulated production of infectious HSV-1 progeny from a quiescent state. To identify viral genes responsive to TSA, the authors analyzed representative alpha, beta, and gamma viral genes using quantitative real-time polymerase chain reaction. Only the latency-associated transcript (LAT) accumulated in response to TSA treatment, under culture conditions that restricted virus replication and spread. This led the authors to evaluate the importance of LAT expression on TSA-induced reactivation. In QIF-PC12 cells, the LAT deletion mutant virus dLAT2903 reactivated equivalently with its wild-type parental strain (McKrae) after TSA treatment, as well as forskolin and heat stress treatment. Both viruses also reactivated equivalently from latently infected trigeminal ganglia explants from rabbits. In contrast, there was a marked reduction in the recovery of dLAT2903, as compared to wild-type virus, from the eyes of latently infected rabbits following epinephrine iontophoresis. These combined in vitro, ex vivo, and in vivo data suggest that LAT is not required for reactivation from latently infected neuronal cells per se, but may enhance processes that allow for the arrival of virus at, or close to, the site of original inoculation (i.e., recrudescence).

Animals↗

PubMed2005

Effect of prophylactic valacyclovir on the presence of human herpesvirus DNA in saliva of healthy individuals after dental treatment.

Human herpesviruses (HHVs) are ubiquitous pathogens that intermittently reactivate from latency. Transmission is believed to be facilitated by their frequent appearance in saliva. This study sought to understand the factors that influence the appearance of these viruses in saliva by examining the prevalence, pattern, and quantity of all eight HHVs in saliva of immunocompetent adults with a history of recurrent oral herpes simplex virus (HSV) infections following dental treatment and antiviral therapy. Valacyclovir or matched placebo was given (2 g twice on the day of treatment and 1 g twice the following day) to 125 patients in a randomized, double-blind controlled trial. Saliva, collected on the day of dental treatment and 3 and 7 days later, was analyzed using real-time quantitative PCR. At all visits, HHVs coinfected saliva. Over the course of the week, the DNAs of HHV-6 and HHV-7 were detected significantly more often (97% to 99% of patients) than Epstein-Barr virus (EBV; 64.8%), HSV-1 (13.0%), HHV-8 (3.2%), cytomegalovirus (2.4%), HSV-2 (0%), and varicella-zoster virus (0%), irrespective of drug treatment (P < 0.002). Mean genome copy numbers were highest for HSV-1 and HHV-6. Dental treatment did not influence asymptomatic viral shedding patterns. However, valacyclovir treatment resulted in significantly fewer patients shedding EBV at both postoperative visits compared with placebo (P < 0.008). These results suggest that HHVs are simultaneously present in the saliva of healthy adults at levels that could facilitate transmission, and valacyclovir therapy decreases the prevalence of EBV in saliva but has little effect on HHV-6 and HHV-7.

Acyclovir↗

PubMed2004

The efficacy of valacyclovir in preventing recurrent herpes simplex virus infections associated with dental procedures.

BACKGROUND: Oral herpes simplex virus, or HSV, infections recur after trauma and stress. The prevalence of these infections after dental procedures is not known. Also, it is unclear whether antiviral agents are effective in preventing dental procedure-induced HSV recurrences. This study determined the efficacy and safety of oral valacyclovir in suppressing dentally related cold sore outbreak and HSV shedding. METHODS: The authors enrolled 125 otherwise healthy HSV-seropositive adults who reported having recurrent herpes labialis (more than one episode per year and at least one episode in the previous year) in a randomized, double-blind, placebo-controlled study and gave them valacyclovir prophylactically (2 grams taken twice on the day of dental treatment and 1 g taken twice the next day) or a matching placebo. To detect the presence of the virus, the authors used clinical examinations, viral cultures and real-time polymerase chain reaction analysis of saliva. RESULTS: During the one-week observation period after treatment, there were more clinical lesions (20.6 percent versus 11.3 percent), more HSV-1-positive culture specimens (7.9 percent versus 1.6 percent) and more HSV-1-positive saliva specimens (7.9 percent versus 4.0 percent) in placebo than in valacyclovir-treated patients, respectively. The percentage of patients who developed recurrences and shed HSV-1 in saliva 72 hours after dental procedures was significantly smaller in the valacyclovir group than in the placebo group (11.3 percent versus 27 percent; P = .026). The mean time to pain cessation was significantly less in the valacyclovir group (3.2 days) than in the placebo group (6.2 days) (P = .006). CONCLUSION: HSV recrudescence after routine dental treatment is suppressed by valacyclovir prophylaxis. CLINICAL IMPLICATIONS: HSV recrudescence is common after routine dental treatment. Clinicians should consider antiviral therapy for patients at risk of experiencing a recurrence, as well as to minimize transmission of the disease.

Acyclovir↗

PubMed2003

Disparities in risk of and survival from oropharyngeal squamous cell carcinoma.

BACKGROUND: Oropharyngeal cancer has a low 5-year survival rate in the United States, indicating that much remains to be learned about risk and survival factors. The purpose of this research was to identify factors that contribute to risk of and survival from this disease in a region associated with high tobacco use. METHODS: A retrospective chart review of 221 subjects with diagnosis of head and neck cancer at a regional University Medical Center during a 10-year period (1986 to 1995) was performed to identify relationships between risk and survival factors of oropharyngeal squamous cell carcinoma (OSCC). Data from 92 records met the inclusion criteria and were analyzed with the chi(2) test of association, the Fisher exact test, and the log-rank test for comparison of survival distributions. The software used was SAS for Windows, release 8.2. RESULTS: Most study subjects were white men between the ages of 50 and 75 years who chronically used tobacco and alcohol. The overall median survival period of the group was 18.1 months. The percentage of subjects surviving to 3 years was 35.6%. Disparities were identified in risk and survival by sex, race, age, dwelling, anatomic site, and exposure to carcinogenic substances. In particular, the disease more adversely affected minorities and those who chronically used tobacco or alcohol. CONCLUSIONS: Our results show that, in the examined regional population, a high prevalence of tobacco use correlated with alcohol use and a lower rate of survival from OSCC than the national rate. Also, risk of and survival from OSCC are affected by demographic, geographic, and behavioral factors. This information is useful for the design and implementation of more effective preventive and intervention strategies.

Adult↗

PubMed2003

Herpesvirus quiescence in neuronal cells. V: forskolin-responsiveness of the herpes simplex virus type 1 alpha0 promoter and contribution of the putative cAMP response element.

The herpes simplex virus (HSV)-1 alpha0 promoter contains a putative cAMP response element (CRE) located at positions -68 to -60 with respect to the initiation of transcription. In this report, the authors examined the functionality of this element using (1) luciferase reporter gene assays in nerve growth factor-differentiated (ND)-PC12 cells and (2) virus-induced activation from quiescently infected (QIF)-PC12 cells. The putative alpha0 CRE was completely eliminated by digestion with the restriction enzyme Tsp45I followed by mung bean nuclease treatment. The mutated region was verified by DNA sequencing and was inserted into the alpha0-luciferase reporter plasmid (pRDalpha0-LUC) creating (pRDalpha0deltaCRE-LUC), and into the HSV-1 genome of strain 17(+)(alpha0deltaCRE). Insertion into both copies of the alpha0 promoter was verified by Southern blot analysis. ND-PC12 cells transfected with pRDalpha0-LUC and pRDalpha0deltaCRE-LUC plasmids responded similarly to forskolin (50 microM), with approximately 250% increases in luciferase activity compared to mock-treated cultures as measured 3 days following treatment. When QIF-PC12 cultures established with HSV-1 strain 17(+) and alpha0deltaCRE were treated with forskolin (50 microM) 17 days post infection, virus was detected in 9/24 (37.5%) and 13/24 (54.2%) of induced cultures by day 8 post treatment, respectively. In contrast, virus was detected in 0/23 and 1/24 (4.2%) of mock-treated cultures by day 8 post treatment for wild-type and mutant viruses, respectively. These findings indicate that the alpha0 promoter is forskolin responsive, the purported CRE of the alpha0 promoter does not confer forskolin responsiveness in ND-PC12 cells, and this element is not required for reactivation of HSV-1 from QIF-PC12 cells.

Animals↗

PubMed2003

Burning mouth (syndrome) disorder.

Burning mouth disorder (BMD) is a chronic, oral pain condition associated with burning sensations of the tongue, lips, and mucosal regions of the mouth. Diagnosis of the condition is complicated by the fact that a variety of systemic and local factors can be contributory. Treatment goals are to reduce symptoms by eliminating identifiable abnormalities. Secondary lines of therapy include pharmacotherapeutic approaches that target neuropathologic mechanisms that appear to be active.

Burning Mouth Syndrome↗

PubMed2002

Antithrombotic agents: implications in dentistry.

Thrombosis and the complicating emboli that can result are important causes of illness and death. Thrombosis is of greater overall clinical importance in terms of morbidity and mortality than all of the hemorrhagic disorders combined. Agents such as heparin, low-molecular weight heparin, warfarin, aspirin, ticlopidine, clopidogrel, and tirofiban are used to prevent venous or arterial thrombosis. Patients taking these antithrombotic agents may be at risk for excessive bleeding after invasive dental procedures. The current antithrombotic agents used in medicine are reviewed, and the dental management of patients taking these agents is discussed.

Anticoagulants↗

PubMed2002

Valproate-associated stomatitis.

The purpose of this article is to report a case of severe stomatitis in a patient with pediatric epilepsy taking divalproex sodium. The case was reviewed with detailed oral examinations. This 5-year-old child developed severe stomatitis 18 months after institution of divalproex sodium. Cessation of the medication was associated with resolution of the stomatitis. A review of the pertinent literature is also provided. Stomatitis is a rare but potentially serious adverse effect of divalproex sodium administration.

Anticonvulsants↗

PubMed2002

Impact of criteria-based diagnosis of burning mouth syndrome on treatment outcome.

AIMS: Burning mouth syndrome (BMS) primarily affects postmenopausal women and is often difficult to treat successfully. Treatment outcomes have been problematic because of failure to distinguish between patients with BMS and patients presenting with oral burning (OB) resulting from other clinical abnormalities. The purpose of this study was to determine characteristics that might uniquely identify BMS patients from patients with OB and to determine whether proper classification influences treatment outcome. METHODS: The clinical sample consisted of 69 patients (83% female) with an average age of 62 years, pain duration of 2.45 years, and visual analog scale pain rating of 49 mm (rated from 0 to 100 mm). All patients underwent a clinical exam and completed the Multidimensional Pain Inventory and Symptom Checklist 90-Revised. RESULTS: There were no differences between the BMS and OB groups with respect to age, pain duration, pain intensity, life interference, and levels of psychologic distress. Patients with OB demonstrated more clinical abnormalities than BMS patients. Hyposalivation and greater use of prescription medications, most notably hormone replacement therapy, were more common in the OB group compared with the BMS group. When treatment was provided that corrected an identifiable abnormality, significantly more OB than BMS patients reported greater than 50% relief from baseline pain rating. CONCLUSION: These data indicate that while BMS and OB groups may initially present with similar clinical and psychosocial features, they are distinguishable with careful diagnosis that often enables successful management of symptoms for each group.

Adult↗