Various studies have shown that both host inflammatory response and bacteria play central roles in the development of the various types of periodontal diseases. Periodontal medical complications are basically mixed infections and various types of bacteria are essential for both the initiation as well as the progression of the condition in susceptible individuals. The identities of these bacteria may vary among patients, among diseases as well as among sites in a given individual. It is worth noting that most of these bacteria are always present in disease free individuals and hence periodontal complications can be taken to be part of the opportunistic infections. Periodontal disease development is closely related to gingival crevice deepening into a periodontal pocket, approximately several millimetres deep and normally bleeds when probed. Jain and Darveau (2000) points out periodontal medical complications are having become common phenomena and that more than fifty percent of adult individuals in the United States have experienced the diseases to some degree. However, the number of individuals with severe forms of the diseases is less than ten percent.
The metabolic activities of initial bacterial colonizers in the gingival crevice change the microenvironment and promote colonization by secondary bacteria or organisms. Unlike their predecessors, the secondary colonizers have been shown to be more pathogenic and when their levels surpass threshold, periodontal diseases develop. However, the presence of periodontal bacteria does not guarantee development of periodontal disease. The combined effort of various factors is required for the initiation of the complication. Some of these factors include, host immune system, bacterial virulence factors and the activity as well as composition of the commensal microbiota (Jain and Darveau , 2000) Some of the main bacteria that have been shown to play a central role in the development of periodontal disease are Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis
Aggregatibacter actinomycetemcomitans is a fairy small, non-motile, gram-negative, saccharolytic, rounded-ended rod. In the last two decades various studies have shown that Aggregatibacter actinomycetemcomitans is one of the major contributors in the development of destructive periodontal disease. According to Jain and Darveau (2000) the species is composed of 6 serotypes denoted (a-f). Both serotype a and c have correlated with periodontal health whereas serotype b has been detected in large quantities in active periodontal lesions. Jain and Darveau , (2000) Points out that serotype are commonly detected in aggressive periodontitis as opposed to chronic periodontitis. Other studies have shown that serotype b is most common in individuals under age of 18 years relative to those above 35 years old. Jain and Darveau (2000) argues that Aggregatibacter actinomycetemcomitants was first discovered as potential pathogen in the development of periodontal disease in 1975 in various studies of localized juvenile periodontitis, currently referred to as localized aggressive perodontitis commonly denoted as (LAP). Numerous studies have shown close relationship between Aggregatibacter actinomycetemcomitans and destructive periodontitis in young children. Earlier types of periodontitis especially prebubertal periodontitis have been shown yield the organism in prevalence above 5o percent. Another periodontal disease that is commonly associated with organism is the localized juvenile periodontitis. Other studies have linked the organism with the development of periodontitis lesions of papillon-Lefevre syndrome patients. These patients are characterised with reduced functions of lymphocytes, monocytes and neutrophils , which may be partially be as a result of cytomegalovirus infection. Most researchers have hypothesized that the defense impairment resulting from viral infection may provide conducive micro-environment for proliferation and hence overgrowth of sub gingival Aggregatibacter actinomycetemcomitans. it has also been shown that approximately 40 percent of adults patients with adult periodontitis test positive for this organism. According to Jain and Darveau (2000) this organism has been detected in higher frequencies in periodontal lesions with angular relative to horizontal alveolar bone loss. A central characteristic of periodontal disease in the decay and eventual loss of the bone supporting the teeth. Numerous studies have that A. Actinomycetemcominants plays a key role in the stimulation of bone resorption through various mechanisms including proteolysis-sensitive factor in microvesicles, lipopolysaccharide and surface associated material. Recent studies have identified the surface associated material as the molecular chaperon, GroEL. This chaperon has been shown to function with most of the major resorbing cell population, the osteoclast in a longitudinal study by Jain and Darveau (2000) aimed at investigating risk factors for the development of the diseases in untreated population concluded that A. Actinomycetemcomitans is one of the major risk factors.
Another important contributor to periodontis is the Porphyromonas gingivalis through its lipopolysaccharride. Reijden et al (2008) points out that the mild antagonistic and agonistic lipid A structures of this organism play a significant role in the disruption of the host’s oral immune homeostasis essential for oral health and hence promote periodontal diseases. The unique lipid A of the organism has been shown to play a central role in the dampening or evading the host immune system hence promoting periodontal disease by the bacteria. According to Reijden et al (2008) tetra-acyl 1-lipd A plays a role in immune suppression whereas tetra-acyl no-lipid A plays a role in immune evasion. It is also worth noting that this organism is part of the periodontal causing ‘red complex’, a complex of major bacteria involved in the development of the periodontal disease.
Periodontal complications can be considered opportunistic infection since the major bacteria responsible for this infection are always present in health individuals. It is also worth noting no single factor is fully responsible for this condition, since for it to develop these factors reinforce one another to complete their ‘task’. Both actinomycetemcomitans and Porphyromonas gingivalis play a central role through the creation of a microenvironment for secondary bacteria.
References
Jain, S & Darveau, R. P. (2000). Contribution of Porphyromonas gingivalis Lipopolysaccharide to periodontitis. Journal of clinical periodontology. (54) 53-70.
Reijden et al (2008). Java project on periodontal disease: serotype distribution of Aggregatibacter actinomycetemcomitans and serotype dynamics over an 8-year period. Journal of clinical periodontology. (35) 487-492.