A. D. Haffajee

Bio: A. D. Haffajee is an academic researcher from The Forsyth Institute. The author has contributed to research in topics: Clinical attachment loss & Bleeding on probing. The author has an hindex of 41, co-authored 54 publications receiving 8524 citations.

The bacterial etiology of destructive periodontal disease: current concepts.

Abstract: The interpretation of diagnostic tests for the detection of subgingival bacterial species is dependent on knowledge of the microbial etiology of destructive periodontal diseases. Specific etiologic agents of these diseases have been sought for over 100 years; however, the complexity of the microbiota, an incomplete understanding of the biology of periodontal diseases, and technical problems have handicapped this search. Nonetheless, a number of possible pathogens have been suggested on the basis of their association with disease, animal pathogenicity, and virulence factors. The immunological response of the host to a species and the relation of successful therapy to the elimination of the species have also been used to support or refute suspected periodontal pathogens. Current data suggest that pathogens are necessary but not sufficient for disease activity to occur. Factors which influence activity include susceptibility of the individual host and the presence of interacting bacterial species which facilitate or impede disease progression. Recent studies have attempted to distinguish virulent and avirulent clonal types of suspected pathogenic species and seek transmission of genetic elements needed for pathogenic species to cause disease. Finally, the local environment of the periodontal pocket may be important in the regulation of expression of virulence factors by pathogenic species. Thus, in order that disease result from a pathogen, 1) it must be a virulent clonal type; 2) it must possess the chromosomal and extra-chromosomal genetic factors to initiate disease; 3) the host must be susceptible to this pathogen; 4) the pathogen must be in numbers sufficient to exceed the threshold for that host; 5) it must be located at the right place; 6) other bacterial species must foster, or at least not inhibit, the process; and 7) the local environment must be one which is conducive to the expression of the species' virulence properties.

New concepts of destructive periodontal disease.

Abstract: The most common forms of destructive periodontal disease have been thought to slowly and continuously progress until treatment or tooth loss. Recently, data have become available which are inconsistent with this "continuous disease" hypothesis. Data from longitudinal monitoring of periodontal attachment levels and alveolar bone in humans and in animals suggest that periodontal disease progresses by recurrent acute episodes. In addition, rates of attachment loss have been measured in individual sites which are faster than those consistent with the continuous disease hypothesis or slower than those expected from estimates of prior loss rates. To account for these observations, a model of destructive periodontal disease is described in which bursts of activity occur for short periods of time in individual sites. These bursts appear to occur randomly at periodontal sites throughout the mouth. Some sites demonstrate a brief active burst of destructive periodontal disease (which could take a few days to a few months) before going into a period of remission. Other sites appear to be free of destructive periodontal disease throughout the individual's life. The sites which demonstrate destructive periodontal activity may show no further activity or could be subject to one or more bursts of activity at later time periods. Comparison of monitored loss rates for a year with mean loss rates prior to monitoring suggested that there may be relatively short periods in an individual's life in which many sites undergo periodontal destruction followed by periods of extended remission. An extension of the random disease model is also suggested in which bursts of destructive periodontal disease activity occur with higher frequency during certain periods of an individual's life.

Patterns of progression and regression of advanced destructive periodontal disease.

Abstract: Attachment level at two sites on each tooth in 22 untreated subjects with existing periodontal pockets was measured every month for 1 year. Regression analysis was then applied to the data from each periodontal site to determine if statistically significant trends in attachment level change could be detected. 82.8% of the sites monitored did not significantly change during the year. 5.7% of the sites became significantly deeper and 11.5% of the sites became significantly shallower (P less than 0.01) during the period. Among those sites in which pocket depth increased, approximately half exhibited a cyclic deepening followed by spontaneous recovery to their original depth. In 15 of the subjects, sites were found which became significantly deeper while other sites within the same subject became significantly shallower. In six subjects, who might be considered to have an arrested form of periodontal disease, virtually no sites became deeper during the monitoring period whereas 11-36% of their sites became significantly shallower. The results of this investigation suggest that a dynamic condition of disease exacerbation and remission as well as periods of inactivity may be characteristic of periodontal disease.

Gram negative species associated with active destructive periodontal lesions

Abstract: Apical subgingival plaque samples were taken from 19 subjects exhibiting active destructive periodontal disease. The predominant cultivable Gram negative species from 50 active sites were compared to 69 inactive sites of comparable pocket depth and attachment level loss. Active disease sites were chosen which showed a significant loss of attachment within a two-month interval. Proportions of Gram negative rods were higher in active periodontal disease sites than in inactive sites. Species which were found to be significantly elevated only in active sites were Bacteroides intermedius, "fusiform" Bacteroides, Actinobacillus actinomycetemcomitans and Wolinella recta. Fusobacterium nucleatum, Capnocytophaga gingivalis and Eikenella corrodens were found in significantly increased proportions in active sites of some subjects and inactive sites of others.

Identification of early microbial colonizers in human dental biofilm

Abstract: J. LI, E.J. HELMERHORST, C.W. LEONE, R.F. TROXLER, T. YASKELL, A.D. HAFFAJEE, S.S. SOCRANSKY AND F.G. OPPENHEIM. 2004. Aims: To elucidate the first colonizers within in vivo dental biofilm and to establish potential population shifts that occur during the early phases of biofilm formation. Methods and Results: AcheckerboardDNA-DNA hybridization assay was employed to identify 40 different bacterial strains. Dental biofilm samples were collected from 15 healthy subjects, 0, 2, 4 and 6 h after tooth cleaning and the composition of these samples was compared with that of whole saliva collected from the same individuals. The bacterial distribution in biofilm samples was distinct from that in saliva, confirming the selectivity of the adhesion process. In the very early stages, the predominant tooth colonizers were found to be Actinomyces species. The relative proportion of streptococci, in particular Streptococcus mitis and S. oralis, increased at the expense of Actinomyces species between 2 and 6 h while the absolute level of Actinomyces remained unaltered. Periodontal pathogens such as Tannerella forsythensis (Bacteroides forsythus), Porphyromonas gingivalis and Treponema denticola as well as Actinobacillus actinomycetemcomitans were present in extremely low levels at all the examined time intervals in this healthy group of subjects. Conclusion: The data provide a detailed insight into the bacterial population shifts occurring within the first few hours of biofilm formation and show that the early colonizers of the tooth surface predominantly consist of beneficial micro-organisms. Significance and Impact of the Study: The early colonizers of dental plaque are of great importance in the succession stages of biofilm formation and its overall effect on the oral health of the host.

Biofilms: Survival Mechanisms of Clinically Relevant Microorganisms

Abstract: Though biofilms were first described by Antonie van Leeuwenhoek, the theory describing the biofilm process was not developed until 1978. We now understand that biofilms are universal, occurring in aquatic and industrial water systems as well as a large number of environments and medical devices relevant for public health. Using tools such as the scanning electron microscope and, more recently, the confocal laser scanning microscope, biofilm researchers now understand that biofilms are not unstructured, homogeneous deposits of cells and accumulated slime, but complex communities of surface-associated cells enclosed in a polymer matrix containing open water channels. Further studies have shown that the biofilm phenotype can be described in terms of the genes expressed by biofilm-associated cells. Microorganisms growing in a biofilm are highly resistant to antimicrobial agents by one or more mechanisms. Biofilm-associated microorganisms have been shown to be associated with several human diseases, such as native valve endocarditis and cystic fibrosis, and to colonize a wide variety of medical devices. Though epidemiologic evidence points to biofilms as a source of several infectious diseases, the exact mechanisms by which biofilm-associated microorganisms elicit disease are poorly understood. Detachment of cells or cell aggregates, production of endotoxin, increased resistance to the host immune system, and provision of a niche for the generation of resistant organisms are all biofilm processes which could initiate the disease process. Effective strategies to prevent or control biofilms on medical devices must take into consideration the unique and tenacious nature of biofilms. Current intervention strategies are designed to prevent initial device colonization, minimize microbial cell attachment to the device, penetrate the biofilm matrix and kill the associated cells, or remove the device from the patient. In the future, treatments may be based on inhibition of genes involved in cell attachment and biofilm formation.

Development of a Classification System for Periodontal Diseases and Conditions

Abstract: Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classi- fication system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics.1 Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology.2 These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings including: 1) considerable overlap in disease categories, 2) absence of a gingival disease component, 3) inappropriate emphasis on age of onset of disease and rates of progression, and 4) inadequate or unclear classification criteria. The 1993 Europea...

The Human Oral Microbiome

Abstract: The human oral cavity contains a number of different habitats, including the teeth, gingival sulcus, tongue, cheeks, hard and soft palates, and tonsils, which are colonized by bacteria. The oral microbiome is comprised of over 600 prevalent taxa at the species level, with distinct subsets predominating at different habitats. The oral microbiome has been extensively characterized by cultivation and culture-independent molecular methods such as 16S rRNA cloning. Unfortunately, the vast majority of unnamed oral taxa are referenced by clone numbers or 16S rRNA GenBank accession numbers, often without taxonomic anchors. The first aim of this research was to collect 16S rRNA gene sequences into a curated phylogeny-based database, the Human Oral Microbiome Database (HOMD), and make it web accessible (www.homd.org). The HOMD includes 619 taxa in 13 phyla, as follows: Actinobacteria, Bacteroidetes, Chlamydiae, Chloroflexi, Euryarchaeota, Firmicutes, Fusobacteria, Proteobacteria, Spirochaetes, SR1, Synergistetes, Tenericutes, and TM7. The second aim was to analyze 36,043 16S rRNA gene clones isolated from studies of the oral microbiota to determine the relative abundance of taxa and identify novel candidate taxa. The analysis identified 1,179 taxa, of which 24% were named, 8% were cultivated but unnamed, and 68% were uncultivated phylotypes. Upon validation, 434 novel, nonsingleton taxa will be added to the HOMD. The number of taxa needed to account for 90%, 95%, or 99% of the clones examined is 259, 413, and 875, respectively. The HOMD is the first curated description of a human-associated microbiome and provides tools for use in understanding the role of the microbiome in health and disease.

Prevention of Infective Endocarditis Guidelines From the American Heart Association: A Guideline From the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group

Abstract: Background— The purpose of this statement is to update the recommendations by the American Heart Association (AHA) for the prevention of infective endocarditis that were last published in 1997. Met...

The microbiota associated with successful or failing osseointegrated titanium implants.

Abstract: In this study the microbiota associated with oral endosteal titanium hollow cylinder implants (ITI) was studied using microscopic, immunochemical and cultural methods. Samples from 5 edentulous patients with successfully incorporated implants serving as abutments for overdentures for more than one year were compared with samples from 7 patients with clinically failing implants. Unsuccessful sites were characterized by pocket probing depths of 6 mm or more, suppuration and visible loss of alveolar bone around the implant as visualized on radiographs. These sites harbored a complex microbiota with a large proportion of Gram-negative anaerobic rods. Black-pigmented Bacteroides and Fusobacterium spp. were regularly found. Spirochetes, fusiform bacteria as well as motile and curved rods were a common feature in the darkfield microscopic specimens of these sites. Control sites in the same patients harbored small amounts of bacteria. The predominant morphotype was coccoid cells. Spirochetes were not present, fusiform bacteria, motile and curved rods were found infrequently and in low numbers. The microbiota in control sites in unsuccessful patients and in site in successful patients were very similar. On the basis of these results, it is suggested that “periimplantitis” be regarded as a site specific infection which yields many features in common with chronic adult periodontitis.