J Periodontal Res. 2010 Jul 21.

[Epub ahead of print]

Fusobacterium nucleatum regulation of neutrophil

transcription.
Wright HJ, Chapple IL, Matthews JB, Cooper PR.
Periodontal Research Group, School of Dentistry, University of Birmingham,
Birmingham, UK.

Abstract
Wright HJ, Chapple ILC, Matthews JB, Cooper PR. Fusobacterium nucleatum
regulation of neutrophil transcription. J Periodont Res 2010; doi: 10.1111/j.1600-
0765.2010.01299.x. (c) 2010 John Wiley & Sons A/S Background and Objective:
Abnormal neutrophil responses have been observed in periodontitis patients,
including hyper-reactivity in terms of production of reactive oxygen species
(ROS) following exposure to the key quorum-sensing plaque bacterium,
Fusobacterium nucleatum. This study was designed to characterize the
transcriptional response of neutrophils to F. nucleatum. Material and Methods:
Peripheral blood neutrophils were exposed to F. nucleatum, and gene expression
was analysed using high-throughput transcriptomics. Results: Microarray
technology demonstrated differential expression of 208 genes (163 increased
and 43 decreased relative to control genes), which identified regulation of several
ontological classes, including signal transduction (13%), transcription regulation
(7%) and ROS response (14%). Individual gene expression analysis of selected
transcripts, including CSF, CXCL3, FOS, HMOX1, HSP40, SOD2, NFKB2 and
GP91, in individual and pooled RNA samples from control and F. nucleatum-
exposed neutrophils corroborated microarray data. Analysis of ROS generation,
combined with transcript analysis, in response to a panel of proinflammatory
stimuli (F. nucleatum, Porphyromonas gingivalis, Escherichia coli
lipopolysaccharide and opsonized Staphylococcus aureus) identified significant
differences in ROS and transcript regulatory control. Further analyses of
neutrophils from periodontitis patients and periodontally healthy control subjects
stimulated with F. nucleatum indicated significant differential induction of several
ROS response-related transcripts. Conclusion: These data demonstrate that
neutrophils are transcriptionally active in response to the periodontal pathogen F.
nucleatum and that these changes in gene expression are likely to affect
neutrophil function. The differential response of neutrophils to a range of stimuli
combined with data demonstrating differences between patient and control
neutrophils indicate the importance of this cell and its interaction with the local
tissue environment in the pathogenesis of periodontitis.
J Periodontal Res. 2010 Oct;45(5):681-7. Epub 2010 Jun 20.

Relationship between oral malodor and the menstrual

cycle.
Kawamoto A, Sugano N, Motohashi M, Matsumoto S, Ito K.
Dental Hygienist Section, Nihon University Dental Hospital, Tokyo, Japan.
imanaga@dent.nihon-u.ac.jp

Abstract
BACKGROUND AND OBJECTIVE: Sex hormones have been suggested to be
important modifying factors that may influence the pathogenesis of periodontal
disease. This study examined changes in volatile sulfur compounds (VSC) levels,
clinical parameters and bacterial levels during the menstrual cycle.
MATERIAL AND METHODS: The study group consisted of 10 female subjects
with periodontitis and 12 periodontally healthy female subjects. Clinical and
bacterial measurements were performed for all subjects during the ovulation and
follicular phases of the menstrual cycle.
RESULTS: Bleeding on probing (BOP) was significantly increased in the
ovulation phase in periodontitis subjects but not in healthy subjects. The VSC
levels in subjects with periodontitis increased 2.2-fold in the ovulation phase
compared with the follicular phase. In the ovulation phase, VSC levels and BOP
were significantly higher in subjects with periodontitis than in healthy subjects.
The number, and salivary levels, of Prevotella intermedia in subjects with
periodontitis were significantly higher in the ovulation phase than in the follicular
phase.
CONCLUSION: The present study indicated changes in VSC, BOP and P.
intermedia during the menstrual cycles of women with periodontitis.
(c) 2010 John Wiley & Sons A/S.
J Periodontal Res. 2010 Oct;45(5):626-34. Epub 2010 Jun 10.
Butyrate, a bacterial metabolite, induces apoptosis and
autophagic cell death in gingival epithelial cells.
Tsuda H, Ochiai K, Suzuki N, Otsuka K.
Department of Biochemistry, Nihon University School of Dentistry, Tokyo, Japan. tsuda-
h@dent.nihon-u.ac.jp

Abstract
BACKGROUND AND OBJECTIVE: Butyrate is produced by some types of
anaerobic periodontal bacteria. Millimolar concentrations of butyrate are found in
mature dental plaque from periodontitis patients. Although butyrate reportedly
has a variety of effects in many mammalian cells, its effect on gingival epithelial
cells is not well known. In this study, we investigated the effect of butyrate on
gingival epithelial Ca9-22 cell death.
MATERIAL AND METHODS: Death of Ca9-22 cells was assessed after treating
the cells with or without butyrate. A SYTOX Green dye, which exhibits strong
green fluorescence once it enters dead cells through ruptured cell membranes,
was used for cell death detection. Phosphatidylserine redistribution was
measured using fluorescein isothiocyanate-labeled annexin V. The activity of
caspase-3 was measured as the amount of cleaved substrate peptide. Anti-
apoptotic bcl-2 mRNA expression was measured using real-time RT-PCR.
Western blotting and fluoromicroscopic analysis with anti-microtubule-associated
protein 1 light chain 3 (LC3) antibodies were performed for detection of
autophagy.
RESULTS: Stimulation with millimolar concentrations of butyrate for 48 h
induced Ca9-22 cell death. The stimulation also caused increased caspase-3
activity, phosphatidylserine redistribution and bcl-2 down-regulation, suggesting
butyrate-induced apoptosis. However, the pan-caspase inhibitor, Z-VAD-FMK,
did not inhibit cell death completely. This implies the existence of other types of
cell death. In addition, markers of autophagy, namely, the conversion of LC3-I to
LC3-II and increased LC3 accumulation, were observed. Moreover, inhibition of
autophagy by 3-methyladenine suppressed the butyrate-induced cell death,
suggesting that butyrate could induce cell death through autophagy.
CONCLUSION: These data suggest that butyrate induces apoptosis and
autophagic cell death.
J Periodontal Res. 2010 Aug;45(4):557-63. Epub 2010 Jun 10.

Antibiotic resistance of subgingival species in chronic

periodontitis patients.
Ardila CM, Granada MI, Guzmán IC.
Epidemiology Group, University of Antioquia, Medellín, Colombia.
martinardila@gmail.com

Abstract
BACKGROUND AND OBJECTIVE: The increasing rate of resistance of
microorganisms to penicillin and other antibiotics has generated concern among
health authorities in Latin America. The present investigation determined the in
vitro susceptibility of Porphyromonas gingivalis, Fusobacterium nucleatum, black-
pigmented Prevotella spp. and Aggregatibacter actinomycetemcomitans to
metronidazole, amoxicillin, amoxicillin/clavulanic acid, clindamycin and
moxifloxacin in patients with chronic periodontitis.
MATERIAL AND METHODS: Subgingival plaque samples from patients with
periodontitis were collected and cultured on selective and nonselective culture
media. The antimicrobial susceptibility of periodontopathogenic isolates was
studied in chronic periodontitis patients in Colombia. Metronidazole, amoxicillin,
amoxicillin/clavulanic acid, clindamycin and moxifloxacin were tested on all
bacterial isolates and the percentage of resistant strains was calculated.
RESULTS: Of the 150 bacteria identified, 51 were P. gingivalis, 45 were black-
pigmented Prevotella spp., 36 were F. nucleatum and 18 were A.
actinomycetemcomitans. All the isolates were sensitive to amoxicillin/clavulanic
acid and to moxifloxacin, but exhibited variable susceptibility patterns to the other
antimicrobial agents tested.
CONCLUSION: The results of the present study suggest that periodontal
microorganisms in patients with chronic periodontitis can be resistant to the
antimicrobial agents commonly used in anti-infective periodontal therapy. We
suggest that the indiscriminate use of antimicrobials could result in the
appearance of more highly antibiotic-resistant strains of bacteria associated with
periodontal diseases in our population compared with the populations of other
countries.
J Oral Maxillofac Surg. 2010 Jul;68(7):1656-61.

Use of ultrasound-activated resorbable poly-D-L-lactide pins (SonicPins)

and foil panels (Resorb-X) for horizontal bone augmentation of the
maxillary and mandibular alveolar ridges.
Burger BW.

Dulles Institute for Oral, Maxillofacial and Implant Surgery, Suite 205, Sterling, VA 20165, USA.
drburger@dullesoms.com

Abstract
Horizontal bone augmentation of the maxillary and mandibular alveolar ridges has been conventionally
performed using mini titanium alloy screws. The titanium alloy screws are used to fixate corticocancellous
block grafts to the recipient site or for tenting the mucoperiosteum to retain particulate bone grafts.
Nonresorbable guided tissue regenerative membranes reinforced with titanium have also been developed to
use with particulate bone grafts to augment alveolar ridge defects. This report demonstrates the use of
resorbable ultrasound-activated pins and resorbable foil panels developed by KLS Martin for augmenting the
alveolar ridges with particulate bone grafts.

Indian J Dent Res. 2010 Jul-Sep;21(3):364-8.

ABO blood groups and Rhesus factor: an exploring link

to periodontal diseases.
Koregol AC, Raghavendra M, Nainegali S, Kalburgi N, Varma S.
Department of Periodontics, PMNM Dental College and Hospital, Bagalkot, Karnataka,
India. aratikperio@yahoo.co.in

Abstract
BACKGROUND: The presence or absence of blood group antigens has been
associated with various diseases, with antigens also acting as receptors for
infectious agents. Scanty literature is available in assessing the relative liability of
blood group phenotypes to periodontal diseases. This research was conducted to
determine the association of the ABO blood group and Rhesus (Rh) factor to
periodontal diseases to assess whether they could be the predictors of
periodontal diseases.
MATERIALS AND METHODS: A total of 1,220 subjects aged between 20 and
55 years were selected on a random basis. The study populations were
segregated into three groups according to Ramfjord's periodontal disease index:
Healthy, Gingivitis and Periodontitis. Blood samples were collected to identify the
ABO blood groups and the Rh factor by the slide method.
RESULTS: Blood group A showed a significantly higher percentage in the
gingivitis group and blood group O showed a higher percentage in the
periodontitis group. The blood group AB showed the least percentage of
periodontal diseases. The distribution of Rh factor in all groups showed a
significantly higher distribution of Rh-positive.
CONCLUSION: The genetic factors may alter the oral ecology and the process
of periodontal disease. These data are suggestive of a broad correlation between
periodontal diseases and blood groups, which may act as risk predictors for
periodontal diseases. This will make it possible to better-understand the risk
factors of diseases of the periodontal tissues and to predict the effective methods
of prevention and treatment of periodontal diseases.