Antibiotic prophylaxis for dentoalveolar surgery: is it indicated?

Usually dentists in Australia give patients oral antibiotics after dentoalveolar surgery as a prophylaxis against wound infection. When this practice is compared to the principle of antibiotic prophylaxis in major surgery it is found to be at variance in a number of ways. In major surgery, the risk of infection should be high, and the consequences of infection severe or catastrophic, before antibiotic prophylaxis is ordered. If it is provided then a high dose of an appropriate spectrum antibiotic must be present in the blood prior to the first incision. Other factors which need to be considered are the degree of tissue trauma, the extent of host compromise, other medical comorbidities and length of hospitalization. Standardized protocols of administration have been determined and evaluated for most major surgical procedures. Dentoalveolar surgery is undoubtedly a skilled and technically challenging procedure. However, in contrast to major surgical procedures, it has a less than five per cent infection rate and rarely has severe adverse consequences. Dentoalveolar surgery should be of short duration with minimal tissue damage and performed in the dental chair under local anaesthesia. Controlled studies for both mandibular third molar surgery and placement of dental implants show little or no evidence of benefit from antibiotic prophylaxis and there is an adverse risk from the antibiotic. This review concludes that there is no case for antibiotic prophylaxis for most dentoalveolar surgery in fit patients. In the few cases where it can be considered, a single high pre-operative dose should be given.     

The effect of public or private management on patients with temporomandibular joint pain dysfunction

Australians may receive free dental treatment via the public sector if they have a health care card but otherwise must seek treatment via the private sector. These two modes of dental delivery have different objectives, facilities, and patient populations. Two groups of patients, one public and one private, who presented to the same clinicians with temporomandibular joint dysfunction were studied. There were differences in age, numbers of natural teeth and some psychological features. However, the outcome to simple non-surgical management resulted in similar levels of successful treatment.     

Bisphosphonates and glucocorticoid osteoporosis in men: results of a randomized controlled trial comparing zoledronic acid with risedronate

Background

We studied 265 men (mean age 56.4 years; range 18-83 years), among patients enrolled in two arms of a double-blind, 1-year study comparing the effects of zoledronic acid (ZOL) with risedronate (RIS) in patients either commencing (prednisolone 7.5 mg/day or equivalent) (prevention arm, n = 88) or continuing glucocorticoid therapy (treatment arm, n = 177).

Methods

Patients received either a single ZOL 5 mg infusion or RIS 5 mg oral daily at randomization, along with calcium (1000 mg) and vitamin D (400-1200 IU). Primary endpoint: difference in percentage change from baseline in bone mineral density (BMD) at the lumbar spine (LS) at 12 months. Secondary endpoints: percentage changes in BMD at total hip (TH) and femoral neck (FN), relative changes in bone turnover markers (β-CTx and P1NP), and overall safety.

Findings

In the treatment subpopulation, ZOL increased LS BMD by 4.7% vs. 3.3% for RIS and at TH the percentage changes were 1.8% vs. 0.2%, respectively. In the prevention subpopulation, bone loss was prevented by both treatments. At LS the percentage changes were 2.5% vs. − 0.2% for ZOL vs. RIS and at TH the percentage changes were 1.1% vs. − 0.4%, respectively. ZOL significantly increased lumbar spine BMD more than RIS at Month 12 in both the prevention population (p = 0.0024) and the treatment subpopulation (p = 0.0232) in men. In the treatment subpopulation, ZOL demonstrated a significantly greater reduction in serum β-CTx and P1NP relative to RIS at all time-points. In the prevention subpopulation, ZOL significantly reduced β-CTx? at all time-points, and P1NP at Month 3 (p = 0.0297) only. Both treatments were well tolerated in men, albeit with a higher incidence of influenza-like illness and pyrexia events post-infusion with ZOL.

Interpretation

Once-yearly ZOL preserves or increases BMD within 1 year to a greater extent than daily RIS in men receiving glucocorticoid therapy.     

Effect of co-morbidities on fracture risk: findings from the Global Longitudinal Study of Osteoporosis in Women (GLOW)

IntroductionGreater awareness of the relationship between co-morbidities and fracture risk may improve fracture-prediction algorithms such as FRAX.Materials and methodsWe used a large, multinational cohort study (GLOW) to investigate the effect of co-morbidities on fracture risk. Women completed a baseline questionnaire detailing past medical history, including co-morbidity history and fracture. They were re-contacted annually to determine incident clinical fractures. A co-morbidity index, defined as number of baseline co-morbidities, was derived. The effect of adding the co-morbidity index to FRAX risk factors on fracture prevention was examined using chi-squared tests, the May–Hosmer test, c index and comparison of predicted versus observed fracture rates.ResultsOf 52,960 women with follow-up data, enrolled between October 2006 and February 2008, 3224 (6.1%) sustained an incident fracture over 2 years. All recorded co-morbidities were significantly associated with fracture, except for high cholesterol, hypertension, celiac disease, and cancer. The strongest association was seen with Parkinson's disease (age-adjusted hazard ratio [HR]: 2.2; 95% CI: 1.6–3.1; P < 0.001). Co-morbidities that contributed most to fracture prediction in a Cox regression model with FRAX risk factors as additional predictors were: Parkinson's disease, multiple sclerosis, chronic obstructive pulmonary disease, osteoarthritis, and heart disease.ConclusionCo-morbidities, as captured in a co-morbidity index, contributed significantly to fracture risk in this study population. Parkinson's disease carried a particularly high risk of fracture; and increasing co-morbidity index was associated with increasing fracture risk. Addition of co-morbidity index to FRAX risk factors improved fracture prediction.     

Who will benefit from treatment with selective estrogen receptor modulators (SERMs)?

Clinical trials have demonstrated that the selective estrogen receptor modulator raloxifene can reduce the risk of vertebral fracture, but have not unequivocally demonstrated an effect on non-vertebral fracture. Consequently it is recommended that raloxifene be used mainly in postmenopausal women with milder osteoporosis as a preventive measure or for treatment in those with predominantly spinal osteoporosis. Since the effects of raloxifene on bone mineral density and bone turnover may reverse soon after cessation, it is recommended that raloxifene be used as long-term therapy for 5-10 years. Because of its quicker offset, use of raloxifene may have advantages over potent bisphosphonates if use of anabolic agents are contemplated in an individual patient.     

Muckle–Wells syndrome in an Indian family associated with NLRP3 mutation

Muckle — Wells syndrome (MWS) is a rare autosomal dominant disease that belongs to a group of hereditary periodic fever syndromes. It is part of the wider spectrum of the cryopyrin-associated periodic syndrome (CAPS) which has only rarely been described in non-Caucasian individuals. It is characterized by recurrent self-limiting episodes of fever, urticaria, arthralgia, myalgia and conjunctivitis from childhood. Progressive sensorineural hearing loss and amyloidosis are two late complications. MWS is caused by gain of function mutations in the NLRP3 gene, which encodes cryopyrin, a protein involved in regulating the production of proinflammatory cytokines. We report two patients with MWS in an Indian family associated with the p.D303N mutation in the NLRP3 gene. These findings promote awareness of these hereditary periodic fever syndromes as a cause for recurrent fevers from childhood in the Indian population.KEY WORDS: Hereditary periodic fever, D303N mutation, Indian family, Muckle—Wells syndrome, p.D303N mutation