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Dive into the research topics where Harold V. Jordan is active.

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Featured researches published by Harold V. Jordan.


Archives of Oral Biology | 1964

Periodontal lesions in the Syrian hamster—III

Paul H. Keyes; Harold V. Jordan

Abstract Three strains of hamsters are produced by the NIH Animal Production Center, the golden, the cream, and the albino. An active type of periodontal disease develops in golden and cream animals when they are fed a high carbohydrate diet, but it does not develop in the albino hamster tested under similar conditions. However, the disease can be readily induced in “noninfected” albino animals by an inoculation of scrapings of subgingival plaque from affected animals, and once acquired, either by direct inoculation or other contamination, it can be transmitted from generation to generation. Filamentous bacteria have been recovered from cultures of the plaque material in high numbers. In histological sections filamentous organisms are found deep in the gingival pockets, often surrounded by inflammatory cells. Under certain dietary conditions, the same organisms apparently invade the root surfaces and produce changes which might be classified as root surface caries. If the diet be changed, e.g. to one composed of commercial laboratory chows, the soft subgingival plaque will mineralize and form typical subgingival calculus. Periodontal lesions can be produced separately or together with enamel caries because different bacterial components are apparently associated with the two diseases.


Archives of Oral Biology | 1964

Aerobic, gram-positive, filamentous bacteria as etiologic agents of experimental periodontal disease in hamsters

Harold V. Jordan; Paul H. Keyes

Abstract The bacteriology of a spontaneous periodontal disease of hamsters was investigated. This disease is characterized by a heavy, adherent, subgingival plaque and accompanies the feeding of a high carbohydrate diet. Pure cultures of aerobic branching filaments isolated from the plaque induced the disease when inoculated orally into uninfected albino hamsters. Other plaque organisms including streptococci and various unidentified gram-negative rods did not induce the disease. A filamentous strain “labelled” by making it resistant to terramycin was used to induce the disease and to trace implantation, persistence and transfer of the organism. The “labelled” strain was recovered in high numbers from all hamsters infected with this strain and its transfer from infected mothers to offspring was observed. Simultaneous inoculations with the aerobic filament and a specific streptococcus induced both periodontal disease and caries in the same animal.


Archives of Oral Biology | 1966

In vitro methods for the study of plaque formation and carious lesions

Harold V. Jordan; Paul H. Keyes

Abstract Streptococci known to be caries-conducive in experimental animals formed heavy bacterial plaques on extracted teeth, artificial teeth, stainless-steel wires and other objects. This was accomplished by cyclic exposures to a growth medium for 3 hr, 5% sucrose solution for 1 hr, and synthetic saliva for 3 hr in that order, for a total of 2 weeks. Streptococci known to be caries-inactive in animal tests did not form plaque under these conditions. Sucrose was required for plaque production and could not be replaced by glucose, fructose, galactose, lactose, sorbitol, or a mixture of glucose and fructose. The mucin in the synthetic saliva was found to be essential for plaque production in this test system. Filament-forming actinomycetes isolated from animal periodontal disease also formed a heavy plaque. Plaques were grown on a glass probe electrode using the above mentioned methods in order to obtain an estimate of acidity levels which develop under such deposits. In 5% sucrose the pH dropped to a range where enamel would be decalcified (4.5–5.0). The low pH values persisted under the plaque for 3 hr after the electrode had been subsequently transferred to synthetic saliva. Extracted human teeth were placed in an apparatus in which the various media described above could be automatically metered to an incubation chamber in preselected sequences for varying the time periods. Extensive plaque formation and incipient carious lesions developed within a 3-week period.


Journal of Dental Research | 1974

Characterization of bacteria isolated from human root surface carious lesions.

David L. Sumney; Harold V. Jordan

Carious lesions in the root surfaces of extracted human teeth were sampled qualitatively for the presence of bacterial forms. Streptococcus mutans was a predominant organism from this lesion. The filamentous organisms appeared typical of the genus Actinomyces. Bacterial strains from the advancing front of the lesions were aerobic gram-positive diphtheroids, with the key characteristics of the genus Arthrobacter.


Journal of Dental Research | 1972

Observations on the Implantation and Transmission of Streptococcus mutans in Humans

Harold V. Jordan; Harold R. Englander; W.O. Engler; S. Kulczyk

One parent from each of 26 families was reinfected with a strain of Streptococcus mutans that was isolated from his mouth and made resistant to streptomycin. The person-to-person spread of S mutans in their families was studied. No uniform spread of the organisms occurred.


Archives of Oral Biology | 1966

Dental caries in gnotobiotic rats infected with a variety of Lactobacillus acidophilus

R.J. Fitzgerald; Harold V. Jordan; H.O. Archard

Abstract A Lactobacillus originally isolated from a caries active conventional Sprague-Dawley rat was inoculated orally in two separate groups of weanling germfree rats of the same strain receiving a coarse particle, high sugar diet. All twenty-two of the animals so challenged developed dental caries lesions which were primarily confined to the molar sulci. The active micro-organism appears to be a variety of Lactobacillus acidophilus .


Journal of Dental Research | 1972

Relation Between Streptococcus mutans and Smooth Surface Caries in the Deciduous Dentition

Harold R. Englander; Harold V. Jordan

Streptococci with a caries-inducing potential of the type described in Streptococcus mutans have been found with greater frequency in the dental plaque of populations with a high prevalence of dental caries than in populations with a low prevalence (B. KRASSE, H. V. JORDAN, S. EDWARDSSON, I. SVENSSON, and L. TRELL, Arch Oral Biol 13:911-918, 1968; H. V. JORDAN, H. R. ENGLANDER, and S. LIM, JADA 78:1331-1335, 1969; J. D. DE STOPPELAAR, J. VAN HOUTE, and 0. BACKER-DIRKS, Caries Res 3:190-199, 1969). The following data are from a survey of the presence of S muitans in plaque and dental caries experience on smooth surfaces of the deciduous teeth of a group of 93 Caucasian pre-school children, aged 19 to 54 months, who were dependents of US Coast Guard personnel living on Governors Island, NY. The children had been exposed to fluoridated water either partially or continuously from birth. Ages were computed to the nearest birthday and the children were distributed uniformly over the age range; about 42% were females. Each child was considered to have experienced dental caries that had been initiated on a smooth surface, if he showed one tooth or more with a discrete lesion or a restoration on any smooth area of the facial, lingual, or proximal surfaces. The mean age of the 15 children with such caries experience was 45 months, ranging from 37 to 54. None of the children had any molars missing. Bitewing radiographs for diagnosis were used for only the older children whose proximal surfaces could not be clearly observed clinically. To identify children harboring S mutans, plaque samples were collected from all accessible tooth surfaces with a cleoid carver and were cultured on Mitis-Salivarius agar. Isolates were identified by methods described previously


Annals of the New York Academy of Sciences | 1965

BACTERIOLOGICAL ASPECTS OF EXPERIMENTAL DENTAL CARIES

Harold V. Jordan

Certain reports appearing in the literature within the last 10 years have tended to modify the long-held view that dental caries results from the activity of a wide spectrum of acidogenic bacteria in the oral cavity. The possibility is now being considered that there is a degree of specificity in the microbiological component associated with this disease. As far back as 1954 Orland’ showed that germ-free rats living in the absence of bacteria remained free of dental caries regardless of the dietary challenge. Monoinfection with a proteolytic streptococcus was sufficient to induce significant caries activity.2 This work was confirmed and extended by Fitzgerald and associates3 using a different experimental diet and a nonproteolytic streptococcus. Thus, the etiologic role of certain streptococci in experimental dental caries was established. Since that time other workers have confirmed the caries producing activity of these strains in gnotobiotic4 and conventional rats.* In 1960 Keyes5 reported that an infectious and transmissible factor was associated with experimental caries in hamsters. This finding was demonstrated in a group of hamsters which remained caries-free because the cariogenic flora had been suppressed in the mother animals with antibiotics. However, these animals readily developed caries when they were caged with caries-active hamsters or were infected with fecal material from other infected animals. In the same year Fitzgerald and Keyes6 found that the disease could be induced by pure cultures of a specific type of streptococcus isolated from carious plaque. Lactobacilli, diphtheroids, and other streptococci tested were not pathogenic. Since these were conventional animals with an otherwise normal complement of oral bacteria, the implantation, proliferation and subsequent recovery of the specific streptococcal strains had to be demonstrated by using micro-organisms which had been made resistant to streptomycin, i.e. “tagged” mutants. Again, a causal relationship between streptococci and caries was established, although in a different species and by methods that were not so refined as the gnotobiotic technics. Thus, demonstration of specific streptococci as prime etiologic agents of dental caries in hamsters and gnotobiotic rats has now made it possible to think of this disease as a specific infectious process. Whether or not acidogenic bacteria other than the streptococci will eventually be found to possess comparable pathogenicity in dental caries is open to speculation. Fitzgerald’ has reported that several different species of lactobacilli tested in gnotobiotic rats did not induce caries. Minor cariogenic activity by a lactobacillus strain was reported by Luckey.* An oral report by Orlandt has indicated that minimal cariogenic activity by a lactobacillus was increased in successive generations of gnotobiotic rats. The lactobacilli have not been extensively tested in either the hamster experimental model or in gnotobiotic rats. Thus the possibility exists that


Journal of Dental Research | 1969

Plaque Formation and Implantation of Odontomyces viscosus in Hamsters Fed Different Carbohydrates

Harold V. Jordan; Paul H. Keyes; Sandra Lim

A sucrose diet supported implantation of Odontomyces viscosus and a caries-inducing streptococcus in albino hamsters. Caries and periodontal disease occurred simultaneously when both types of bacteria were implanted. Odontomyces, but not the streptococcus, became implanted in albino hamsters on a starch diet. Glucose and fructose diets also supported implantation of odontomyces and development of periodontal disease in golden hamsters. Caries development was minimal.


Journal of Dental Research | 1974

Effect of a Topically Applied 3 % Vancomycin Gel on Streptococcus mutans on Different Tooth Surfaces

Harold V. Jordan; Paul F. De Paola

A 3% vancomycin gel was applied for ten minutes to the teeth of 10- to 12-year-old children using custom-fitted trays. Treatment was once a day for five consecutive days. Significant suppression of Streptococcus mutans was found in sound and carious fissures one week after treatment, with a decline in the oral hygiene index. Response to treatment was the same in subjects with and without large, open, carious lesions.

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R.J. Fitzgerald

National Institutes of Health

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Paul H. Keyes

National Institutes of Health

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N.D. Berger

National Institutes of Health

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A.E. Bowler

National Institutes of Health

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S. Bellack

National Institutes of Health

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Sandra Lim

National Institutes of Health

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