The control of potentially periodontopathic microorganisms by host neutrophils is crucial to periodontal health. Neutrophils may use oxidative or nonoxidative mechanisms and either kill bacteria, influence bacterial growth, or modify bacterial colonization in the periodontium. Delivery of antimicrobial substances by neutrophils involves respiratory burst activity, phagocytosis, secretion, or cytolysis/apoptosis. Neutrophils contain a number of antimicrobial components including calprotectin complex, lysozyme, defensins, cofactor‐binding proteins, neutral serine proteases, bactericidal/ permeability increasing protein, myeloperoxidase, and a NADPH oxidase system. Many of these components are multifunctional and exhibit several mechanisms of antimicrobial activity. When comparisons are made among periodontal bacteria, differences in sensitivity to different components are observed. A hypothesis of specific defense is presented: That specific periodontal diseases can result from the failure of specific aspects of the host immune system (the neutrophil, in particular) in its interaction with specific periodontal pathogens. Failure may be due to phenotypic variation (pleomorphism) within the host or bacterial evasive strategies. J Periodontol 1991; 62:761–774.

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Previous reports have demonstrated that oral mucosa and periodontal lesions occur in patients suffering from inflammatory bowel disease (Crohn's disease [CD] and ulcerative colitis [UC]). It is unknown whether periodontal disease is an occasional or regular finding in these patients. The purpose of this study was to assess the prevalence and severity of periodontal disease in patients with inflammatory bowel disease (IBD). The periodontal status of 107 consecutive patients seeking treatment for inflammatory bowel disease was assessed. Examination of the mid- and mesiobuccal aspects of one quadrant on one jaw and the contralateral quadrant of the opposite jaw revealed the 93.5% of the CD patients and 95.1% of UC patients had at least one site with probing attachment loss of 2 mm or greater, and a mean probing attachment loss 1.4 +/- 0.9 mm and 1.5 +/- 1.0 mm, respectively. We found that 28.3% of CD patients and 29.5% of UC patients possessed at least 1 site with a pocket probing depth of 4 mm or greater; the mean pocket probing depth in these patients was 2.4 +/- 0.2 mm and 2.3 +/- 0.2 mm, respectively. Compared with the assessment of Oral Health of United States Adults, IBD patients revealed a 11.9% higher prevalence (P less than or equal to 0.01) but 0.6 mm lower severity (P less than or equal to 0.01) of periodontal disease. The magnitudes of these differences suggest no clinical implications for the management of periodontal disease in IBD subjects.

Calprotectin is a complex of two anionic proteins found in abundance in the cytosol of neutrophils, certain macrophages, and oral epithelial keratinocytes. Bacteria of the genus Capnocytophaga are pathogens of periodontal origin which can cause systemic infection in neutropenic subjects. Recently, it has been observed that Capnocytophaga may be internalized by neutrophils within the cytosol rather than within a membrane-delimited phagosome. The purpose of this study was to test the in vitro antibacterial effect of the cytosolic complex, calprotectin, against Capnocytophaga sputigena. Calprotectin was purified from the cytosol of human neutrophils by gel filtration and anion exchange FPLC, and it exerted potent in vitro antimicrobial effects against C. sputigena. Net bacteriostatic activity was exerted up to 18 h, after which bactericidal effects were observed. Both net bacteriostatic and bactericidal activity occurred at concentrations above 20 micrograms/mL and exhibited identical dose-response characteristics. Particle counts increased in the presence of calprotectin, despite net bacteriostasis as assessed by changes in colony-forming units (CFU). Dose-response characteristics and direct particle counts suggested that net bacteriostatic effects were the result of balanced cell division and death, rather than suspension of cell division. We conclude that calprotectin can be a significant contributor to host defense against infection by Capnocytophaga.

The bactericidal activity of synthetic LL-37, a cathelicidin, was assessed against Actinobacillus actinomycetemcomitans (three strains) and Capnocytophaga spp. (three strains). All strains were sensitive to LL-37, and exhibited 99% effective dose of 7.5-to-11.6 micrograms/ml. An amidated form of LL-37, pentamide-37, killed with about the same efficacy as LL-37. Partial inhibition of killing was noted at physiologic concentrations of NaCl, and complete inhibition was observed at 400 mM NaCl. At approximately the 99% effective dose--i.e., 10 micrograms/ml--LL-37 also lost activity against A. actinomycetemcomitans in the presence of native or heat-inactivated 10-15% normal human AB serum. Pentamide-37 was less sensitive to serum inhibition than LL-37. In conclusion, certain oral, gram-negative bacteria are sensitive to the bactericidal activity of LL-37 at low concentrations of serum and salt, a condition likely to be found within the membrane-delimited phagolysosome. Modified forms of LL-37, such as pentamide-37, may be more suitable for future therapeutic application in the presence of serum.