The effect of subclinical ascorbate deficiency on periodontal health in nonhuman primates

Alvares, Olav; Altman, Leonard C.; Springmeyer, Steven C.; Ensign, Wayne; Jacobson, Kerry L.

doi:10.1111/j.1600-0765.1981.tb01001.x

Cited by 32 publications

(18 citation statements)

References 21 publications

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“…PMN chemotaxis in monkeys was not monitored and whether defective PMN chemotaxis could influence the onset of disease in these animals is unknown at the present time. Periodontal destruction in scorbutic monkeys may, at least in part, be due to this complication (Alvares et al, 1981). The third possible explanation is that A. actinomycetemcomitans can initiate periodontal problems, but tissue destruction is minimized because monkeys develop an effective antibody response to such challenge and thereby limit the chance of developing clinically-significant lesions.…”

Section: Discussionmentioning

confidence: 99%

Cytopathic effects of Actinobacillus actinomycetemcomitans on monkey blood leukocytes

Taichman

Shenker

Tsai

et al. 1984

J of Periodontal Research

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The suitability of cynomolgus monkeys (Macaca fascicularis) for studies concerned with the biologic properties of Actinobacillus actinomycetemcomitans is the subject of the present investigation. We found that normal monkeys harbored leukotoxic strains of A. actinomycetemcomitans in subgingival plaque samples. Monkey peripheral blood PMNs and monocytes were killed following in vitro exposure to sonic extracts of leukotoxic strains of A. actinomycetemcomitans. Monkey sera were capable of inhibiting the leukotoxic properties of A. actinomycetemcomitans sonic extracts due to the presence of IgG antibodies which neutralized the leukotoxin. Similarly, sera from patients with juvenile periodontitis (but not normal human sera) abolished leukotoxin‐mediated killing of monkey PMNs. Monkey peripheral blood lymphoid cells were not killed by A. actinomycetemcomitans but demonstrated depressed responses to mitogens following pre‐incubation with A. actinomycetemcomitans sonicates prepared from either leukotoxic or “non‐leukotoxic” human strains. These studies suggest that cynomolgus monkeys may serve as a suitable in vitro and in vivo model for delineating more about host‐A. actinomycetemcomitans interrelationships in the etiology of human periodontal disease.

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Section: Discussionmentioning

confidence: 99%

Cytopathic effects of Actinobacillus actinomycetemcomitans on monkey blood leukocytes

Taichman

Shenker

Tsai

et al. 1984

J of Periodontal Research

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“…However, contemporary studies suggest that the various forms of gingivitis and periodontitis result mainly from the activities of certain oral micro-organisms that colonize the teeth and adjacent periodontal tissues (Socransky, 1977;Page and Schroeder, 1982;Williams, 1990). A secondary role in the infectious process has been postulated for ascorbic acid deficiency (Dreizenet al, 1969;Alvares et al, 1981), but most of the epidemiological and experimental evidence accumulated in the last several decades has failed to demonstrate any significant etiological relationship between ascorbic acid deficiency and the periodontal diseases (Russell, 1963;Enwonwu and Edozien, 1970;Robinson, 1977;Woolfe et al, 1980;Ismail et al, 1983;Vogel et al, 1986).…”

Section: Introductionmentioning

confidence: 97%

Effects of Ascorbic Acid Depletion and Supplementation on Periodontal Health and Subgingival Microflora in Humans

et al. 1991

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This study describes the relationship between varying ascorbate intake, periodontal status, and subgingival microflora as part of a multidisciplinary investigation of ascorbic acid (AA) metabolism in young men housed for 13 weeks in a nutrition suite that provided controlled periods of ascorbic acid depletion and repletion. Twelve medically healthy non-smoking men, aged 25 to 43 years, ate a rotating four-day diet adequate in all nutrients except ascorbic acid. Following an initial baseline period during which the subjects received 250 mg AA/day, the subjects received 5 mg AA/day for a 32-day depletion period. Eight of the 12 subjects participated in a subsequent 56-day repletion period designed to replace the reduced body AA pool slowly. Plasma and leukocyte ascorbate levels, Plaque Index, Gingival Index, probing depths, and attachment level were monitored at the beginning and end of the depletion and repletion periods. Subgingival plaque samples were obtained and examined for selected organisms by indirect immunofluorescence microscopy. A uniform oral hygiene program was reinforced after each examination. Ascorbate concentrations in plasma and leukocytes responded rapidly to changes in vitamin C intake. There were no significant changes in plaque accumulation, probing pocket depth, or attachment level during the study. In contrast, gingival bleeding increased significantly after the period of AA depletion and returned to baseline values after the period of AA repletion. However, no relationship could be demonstrated between either the presence or proportion of target periodontal micro-organisms and measures of bleeding or ascorbate levels.

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“…Alvares et al [ 5 ] evaluated the effects of chronic subclinical ascorbic acid defi ciency on periodontal health in a monkey model and found that gingival index (GI) [ 46 ] score and PPD were signifi cantly greater in the ascorbate defi cient animals than in the controls. Recent animal studies indicated the effi cacy of vitamin C in improving periodontal disease.…”

Section: Animal Studies On the Effects Of Vitamin C On Periodontal Dimentioning

confidence: 98%

Role of Vitamin C and Vitamin E in Periodontal Disease

Nagata

2013

Studies on Periodontal Disease

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Vitamin C is a water-soluble organic substance that cannot be synthesized by the body; therefore, it must be obtained from an individual's daily diet. Also known as ascorbic acid, it is involved in wound healing and collagen production by preventing iron-dependent oxidation of lysyl and prolyl hydroxylase. In human and animal studies on vitamin C defi ciency, ascorbate supplementation increased collagen synthesis and decreased polymorphonuclear neutrophil (PMN) chemotaxis [ 4 , 5 , 9 ]. High vitamin C levels are accumulated in granulocytes, mononuclear leucocytes, and platelets [ 28 ], and neutrophil polymorphonuclear leucocytes and macrophages contain an intracellular ascorbate concentration that is 10-40 times higher than that in the plasma [ 58 ]. Chapple and Matthews [ 19 ] summarized the following functions of vitamin C: (1) scavenging water-soluble peroxyl radicals; (2) scavenging superoxide and perhydroxyl radicals; (3) preventing damage mediated by hydroxyl radicals on uric acid; (4) scavenging hypochlorous acid; (5) decreasing heme breakdown and subsequent Fe 2+ release, thereby preventing Fenton reactions; (6) scavenging single oxygen and hydroxyl radicals; (7) re-forming α-tocopherol from its radical; (8) protecting against reactive oxygen species (ROS) released from cigarette smoke; (9) reducing C-reactive protein-mediated expression of monocyte adhesion molecules; (10) decreasing pro-infl ammatory gene expression through effects on the nuclear factor-κB transcription factor.Vitamin E, which comprises related compounds named tocopherols or tocotrienols, is a fat-soluble vitamin with primary function of antioxidation. It is essential for maintaining cell membrane integrity against lipid peroxidation by peroxyl

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The effect of subclinical ascorbate deficiency on periodontal health in nonhuman primates

Cited by 32 publications

References 21 publications

Cytopathic effects of Actinobacillus actinomycetemcomitans on monkey blood leukocytes

Cytopathic effects of Actinobacillus actinomycetemcomitans on monkey blood leukocytes

Effects of Ascorbic Acid Depletion and Supplementation on Periodontal Health and Subgingival Microflora in Humans

Role of Vitamin C and Vitamin E in Periodontal Disease

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