Bacterial infection increases periodontal bone loss in diabetic rats through enhanced apoptosis

Sandra Pacios, Oelisoa Andriankaja, Jun Kang, Maher Alnammary, Jason Bae, Beatriz De Brito Bezerra, Helen Schreiner, Daniel H. Fine, Dana T. Graves

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Periodontal disease is the most common osteolytic disease in humans and is significantly increased by diabetes mellitus. We tested the hypothesis that bacterial infection induces bone loss in diabetic animals through a mechanism that involves enhanced apoptosis. Type II diabetic rats were inoculated with Aggregatibacter actinomycetemcomitans and treated with a caspase-3 inhibitor, ZDEVD-FMK, or vehicle alone. Apoptotic cells were measured with TUNEL; osteoblasts and bone area were measured in H&E sections. New bone formation was assessed by labeling with fluorescent dyes and by osteocalcin mRNA levels. Osteoclast number, eroded bone surface, and new bone formation were measured by tartrate-resistant acid phosphatase staining. Immunohistochemistry was performed with an antibody against tumor necrosis factor-α. Bacterial infection doubled the number of tumor necrosis factor-α-expressing cells and increased apoptotic cells adjacent to bone 10-fold (P < 0.05). Treatment with caspase inhibitor blocked apoptosis, increased the number of osteoclasts, and eroded bone surface (P < 0.05); yet, inhibition of apoptosis resulted in significantly greater net bone area because of an increase in new bone formation, osteoblast numbers, and an increase in bone coupling. Thus, bacterial infection in diabetic rats stimulates periodontitis, in part through enhanced apoptosis of osteoblastic cells that reduces osseous coupling through a caspase-3-dependent mechanism.

Original languageEnglish (US)
Pages (from-to)1928-1935
Number of pages8
JournalAmerican Journal of Pathology
Volume183
Issue number6
DOIs
StatePublished - Dec 1 2013

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Alveolar Bone Loss
Bacterial Infections
Apoptosis
Bone and Bones
Osteogenesis
Caspase Inhibitors
Osteoclasts
Osteoblasts
Caspase 3
Tumor Necrosis Factor-alpha
Aggregatibacter actinomycetemcomitans
Periodontitis
Osteocalcin
In Situ Nick-End Labeling
Periodontal Diseases
Fluorescent Dyes
Diabetes Mellitus
Immunohistochemistry
Staining and Labeling
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine

Cite this

Pacios, S., Andriankaja, O., Kang, J., Alnammary, M., Bae, J., De Brito Bezerra, B., ... Graves, D. T. (2013). Bacterial infection increases periodontal bone loss in diabetic rats through enhanced apoptosis. American Journal of Pathology, 183(6), 1928-1935. https://doi.org/10.1016/j.ajpath.2013.08.017
Pacios, Sandra ; Andriankaja, Oelisoa ; Kang, Jun ; Alnammary, Maher ; Bae, Jason ; De Brito Bezerra, Beatriz ; Schreiner, Helen ; Fine, Daniel H. ; Graves, Dana T. / Bacterial infection increases periodontal bone loss in diabetic rats through enhanced apoptosis. In: American Journal of Pathology. 2013 ; Vol. 183, No. 6. pp. 1928-1935.
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Pacios, S, Andriankaja, O, Kang, J, Alnammary, M, Bae, J, De Brito Bezerra, B, Schreiner, H, Fine, DH & Graves, DT 2013, 'Bacterial infection increases periodontal bone loss in diabetic rats through enhanced apoptosis', American Journal of Pathology, vol. 183, no. 6, pp. 1928-1935. https://doi.org/10.1016/j.ajpath.2013.08.017

Bacterial infection increases periodontal bone loss in diabetic rats through enhanced apoptosis. / Pacios, Sandra; Andriankaja, Oelisoa; Kang, Jun; Alnammary, Maher; Bae, Jason; De Brito Bezerra, Beatriz; Schreiner, Helen; Fine, Daniel H.; Graves, Dana T.

In: American Journal of Pathology, Vol. 183, No. 6, 01.12.2013, p. 1928-1935.

Research output: Contribution to journalArticle

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AU - Pacios, Sandra

AU - Andriankaja, Oelisoa

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AU - Fine, Daniel H.

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Pacios S, Andriankaja O, Kang J, Alnammary M, Bae J, De Brito Bezerra B et al. Bacterial infection increases periodontal bone loss in diabetic rats through enhanced apoptosis. American Journal of Pathology. 2013 Dec 1;183(6):1928-1935. https://doi.org/10.1016/j.ajpath.2013.08.017