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The risk of developing osteochemonecrosis is increased in patients who are taking bisphosphonate drugs and must undergo extractions or other dental surgery. Because of the difficulty in predicting and preventing osteochemonecrosis and in managing patients after it has occurred, avoidance of surgery has been advised. This paper reports on the development of this complication in a patient who received nonsurgical periodontal treatment. Although it is believed that the risk of developing this severely debilitating complication is low when treating patients nonsurgically, practitioners must be able to recognize and understand the presentation and difficulties in managing osteochemonecrosis, even when only nonsurgical therapy is performed.

Background: Gingival crevicular fluid (GCF) biomarkers associated with bone resorption may be useful to determine periodontal disease status and response to therapy. The pyridinoline cross-linked carboxy-terminal telopeptide of type I collagen (ICTP), a bone-specific degradation product, and interleukin 1-beta (IL-1), a potent bone-resorptive cytokine, have both been associated with periodontal disease activity. Minocycline is a tetracycline derivative possessing antimicrobial effects on periodontal pathogens and inhibitory properties on matrix metalloproteinases (MMPs) associated with tissue destruction. The aim of this study was to evaluate the effect of periodontal treatment in the form of scaling and root planing (SRP) and locally administered minocycline microspheres on the GCF levels of ICTP and IL-1., Methods: Forty-eight chronic periodontitis patients were randomly assigned to 2 groups (SRP plus subgingival application of vehicle control [SRP + V], or SRP plus subgingival application of minocycline microspheres [SRP + M]) and monitored at 8 sites per subject at baseline and 1, 3, and 6 months. Four shallow (PD < or = 3 mm) and 4 deep (PD > or = 5 mm) sites were evaluated for both marker levels and for probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BOP). Eight periodontally healthy control subjects with no probing depths >3 mm and no loss of attachment were also monitored at the same time intervals. GCF levels of ICTP and IL-1 were determined using radioimmunoassay and enzyme-linked immunosorbent assay techniques, respectively., Results: Significant differences (P<0.001) in GCF levels of ICTP and IL-1 were found between deep and shallow sites at all time points in both treatment groups. In addition, healthy subjects demonstrated significantly reduced levels of both markers compared to both shallow and deep sites in periodontitis patients (P <0.001). Only the SRP + M treated patients exhibited significant reductions (P <0.05) in both ICTP and IL-1 levels 1 month after treatment. Furthermore, the SRP + M group demonstrated significantly lower IL-1 levels (P <0.02) at 1 month compared to the SRP + V group., Conclusions: Results of this study indicate that GCF levels of ICTP and IL-1 correlate with clinical measures of periodontal disease and may aid in assessing disease status and response to periodontal therapy. Furthermore, local administration of minocycline microspheres led to a potent short-term reduction in GCF IL-1 levels. Additional studies are needed to address whether repeated administration of scaling and root planing along with minocycline microspheres will achieve long-term reductions in GCF ICTP and IL-1 levels.

Background: Biochemical markers harvested from gingival crevicular fluid (GCF) may be useful to identify and predict periodontal disease progression and to monitor the response to treatment. C-telopeptide pyridinoline cross-links (ICTP), a host-derived breakdown product specific for bone, and interleukin-1beta (IL-1), a potent bone-resorptive cytokine, have been associated with periodontal tissue destruction. The aim of this study was to examine the effect of non-surgical periodontal therapy on GCF levels of ICTP and IL-1., Methods: Twenty-five chronic periodontitis subjects were monitored at 8 sites per subject at baseline prior to scaling and root planing and 1, 3, and 6 months after therapy. Four shallow (probing depths < 4 mm) and 4 deep (probing depths > or = 5 mm) sites were monitored for both marker levels and clinical parameters. GCF was collected for 30 seconds on paper strips, and levels of ICTP and IL-1 were determined using radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA) techniques, respectively. Clinical measurements included probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BOP)., Results: Deep sites exhibited significantly (P<0.001) higher ICTP and IL-1 levels compared to shallow sites at all time intervals. ICTP demonstrated a stronger association to clinical parameters than IL-1 including a modest correlation (r = 0.40, P<0.001) between ICTP and attachment loss. Significant improvements in PD, CAL, and BOP were observed at 1, 3, and 6 months in all sites (P<0.01). However, non-surgical mechanical therapy did not significantly reduce ICTP and IL-1 levels over the 6-month period. Further examination of subjects based on smoking status revealed that ICTP levels were significantly reduced at 3 and 6 months and IL-1 levels reduced at 3 months among non-smokers only., Conclusions: A single episode of non-surgical mechanical therapy did not significantly reduce biochemical markers associated with bone resorption in patients exhibiting chronic periodontitis. Future longitudinal studies are warranted to specifically evaluate the relationship between C-telopeptide pyridinoline cross-links and periodontal disease progression.

Two patients were referred to the Graduate Periodontal Clinic, one for placement of dental implants, the other for treatment of advanced periodontal disease. It was determined from an analysis of the Hounsfield scales of bone density from a CT scan that the patient requesting dental implants had severe osteoporotic changes and was, therefore, not a good candidate for the procedure. The second patient's medical history revealed multiple fractures occurring over the years that suggested the presence of osteoporosis. This diagnosis was subsequently confirmed by referral of the patient to an osteoporosis clinic.

The ability of both human and hen egg white lysozymes to lyse Actinobacillus actinomycetemcomitans Y4 was investigated. Lysis was followed optically at 540 nm by measuring the percent reduction in turbidity of freshly harvested log-phase cells suspended in Tris-maleate buffers within a wide range of pH (5.2 to 8.5) and molarity (0.01 to 0.2 M) and containing various amounts of enzyme and EDTA. In several instances, treated microorganisms were subsequently examined in thin sections by electron microscopy. Reductions in turbidity and clearing of suspensions occurred with small amounts of lysozyme (less than 1 microgram) under relatively alkaline conditions and at low ionic strength and in the presence of small amounts of EDTA (greater than 0.01 mM). Under the most alkaline conditions, EDTA alone effected turbidity reductions similar to those observed in the presence of lysozyme, which suggested that EDTA not only increased outer membrane permeability but also caused cell lysis. Ultrastructural analysis did not always correspond to turbidimetric observations. Cell lysis was virtually complete in suspensions containing both lysozyme and EDTA. However, in contrast to turbidimetric findings, a significant percentage of cells (greater than 25%) was lysed in the presence of lysozyme alone. Furthermore, significant damage occurred in the presence of EDTA alone. Spheroplast-like cell ghosts were present which surrounded condensed cytoplasm or relatively clear spaces. These findings further support the concept of the requirement for electron microscopy to assess lytic damage in addition to turbidimetric and biochemical methods. Our results are the first to demonstrate the remarkable sensitivity of A. actinomycetemcomitans Y4 to lysozyme and to show that EDTA not only affects outer membrane permeability but effects cell lysis, possibly through activation of autolytic enzymes at the cytoplasmic membrane. The exquisite sensitivity of A. actinomycetemcomitans Y4 to lysis could be an important mechanism by which lysozyme participates in the regulation of this suspected periodontal pathogen.

Howard H Wang, 1 Hsi-Ming Lee, 2 Veena Raja, 2 Wei Hou, 3 Vincent J Iacono, 4 Joseph Scaduto, 5 Francis Johnson, 6,7 Lorne M Golub, 2 Ying Gu 8 1Department of Periodontology and Endodontology, School of Dental Medicine, State University of New York at Buffalo, Buffalo, NY, USA; 2Department of Oral Biology and Pathology, School of Dental Medicine, Stony Brook University, Stony Brook, NY, USA; 3Department of Preventive Medicine, School of Medicine, Stony Brook University, Stony Brook, NY, USA; 4Department of Periodontology, School of Dental Medicine, Stony Brook University, Stony Brook, NY, USA; 5Traverse Biosciences Inc., Stony Brook, NY, USA; 6Department of Chemistry, Stony Brook University, Stony Brook, NY, USA; 7Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, USA; 8Department of General Dentistry, School of Dental Medicine, Stony Brook University, Stony Brook, NY, USA Introduction: Dental microbial biofilm initiates gingival inflammation, and its suppression is the current dominant strategy for treating periodontitis. However, the host response to the biofilm is largely responsible for the connective tissue breakdown including alveolar bone loss, which is mediated by proinflammatory cytokines and matrix metalloproteinases (MMPs). Methods: The current study compared the efficacy of a novel host-modulation compound, a chemically modified curcumin (CMC 2.24), to that of its parent compound (natural curcumin), in both lipopolysaccharide (LPS) (a bacterial endotoxin)-induced cell culture and in vivo models of periodontitis. Results: In cell culture, both CMC 2.24 and curcumin appeared similarly effective in suppressing LPS-induced cytokine (IL-1β and TNF-α) secretion by mononuclear inflammatory cells; however, CMC 2.24 significantly reduced MMP-9 secretion by 78% (P< 0.05) whereas curcumin was ineffective. In vivo, CMC 2.24 administration was more effective than curcumin in suppressing (a) IL-1β in gingival tissue and (b) MMP-9 in both gingiva and plasma, the latter indicating a reduced severity of systemic inflammation. The difference in primary clinical outcome between the two treatments was that CMC 2.24 reduced the pathologically excessive alveolar bone loss, assessed morphometrically at multiple sites, by 80%– 90% (P< 0.01), whereas curcumin, surprisingly, either increased (P< 0.05) or had no effect on alveolar bone loss at these sites. Conclusion: These data, plus that from previous studies, support the therapeutic potential of CMC 2.24 in the management of inflammatory periodontal disease and its ability to reduce the risk of associated systemic diseases. The current study also indicates that the MMP-9 inhibitor efficacy is associated with the ability of CMC 2.24 (but not curcumin) to inhibit alveolar bone loss in this rat model of periodontitis. Keywords: chemically modified curcumin, cytokines, matrix metalloproteinases, MMPs, periodontitis, ratsCorrigendum for this paper has been published

Wang HH, Lee HM, Raja V, et al. J Exp Pharmacol. 2019;11:1–14.On page 13 the disclosure section should be presented as follows:DisclosureLMG is listed as an inventor on several related patents and these have been fully assigned to his institution, Stony Brook University, The State University of New York (SUNY). FJ is also listed as an inventor on several related patents which have been fully assigned to Stony Brook University and to Chem-Master Int. Inc. on a shared basis. In addition, both LMG and FJ are minor shareholders in Traverse BioSciences, Inc., and JS is president and major shareholder in Traverse. All other authors declare that there are no conflicts of interest regarding the publication of this paper.Read the original article