Periodontitis, A True Infection

Sir, Periodontal infection is initiated by specific invasive oral pathogens that colonize dental plaque biofilms on tooth surface, and host immune response to inflammation plays a central role in disease pathogenesis. Periodontal diseases are recognized as infectious processes that require bacterial presence and a host response and are further affected and modified by other local, environmental and genetic factors. Association of periodontal infection with organ systems like cardiovascular system, endocrine system, reproductive system and respiratory system makes periodontal infection a complex multiphase disease.


Periodontitis, A True Infection
DOI: **** Sir, Periodontal infection is initiated by specific invasive oral pathogens that colonize dental plaque biofilms on tooth surface, and host immune response to inflammation plays a central role in disease pathogenesis. Periodontal diseases are recognized as infectious processes that require bacterial presence and a host response and are further affected and modified by other local, environmental and genetic factors. Association of periodontal infection with organ systems like cardiovascular system, endocrine system, reproductive system and respiratory system makes periodontal infection a complex multiphase disease.
Periodontitis is defined as an inflammatory disease of supporting tissues of teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with periodontal pocket formation, gingival recession or both. [1] Periodontal disease is a complex infectious disease resulting from interplay of bacterial infection and host response to bacterial challenge, and the disease is modified by environmental, acquired risk factors and genetic susceptibility. Dental plaque represents a classic example of both a biofilm and a micro bial community, in that it displays emer gent properties, i.e., plaque displays properties that are more than the sum of its constituent members, [2] and microbial communities are ubiquitous in nature and usually exist attached to a surface as a spatially organized biofilm. Recent studies suggest that the environmental heterogeneity generated within biofilms promotes accelerated genotypic and phenotypic diversity that provides a form of "biological insurance" that can safeguard the "microbial community" in the face of adverse conditions, such as those faced by pathogens in the host. [2] The diversity of bacterial species in the periodontal flora, the variation in composition of floras from individual to individual and the variation in host response to bacterial species are some of the major reasons that the specific etiology of periodontal disease has not been clearly established. [3,4] Bacteria are the primary etiological agent in periodontal disease, and it is estimated that more than 500 different bacterial species are capable of colonizing the adult mouth. [5] Some of the most common organisms associated with periodontal diseases are Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus, Campylobacter

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rectus and Actinobacillus actinomycetemcomitans, as well as the treponemes. [6] A variety of techniques for analyzing the plaque samples have been developed. These include microscopy, bacterial culture, enzymatic assays, immunoassays, nucleic acid probes and polymerase chain reaction assays, [7] and yet more advanced methods should be explored for more accurate detection of pattern of microbial diversity within the oral cavity.
Recent evidence suggests that periodontal infection may significantly enhance the risk for certain systemic diseases or alter the natural course of systemic conditions; and conditions in which influences of periodontal infection are documented include coronary heart diseases (CHD) and CHD-related events such as angina and infarction, atherosclerosis, stroke, diabetes mellitus; preterm labor, low-birth-weight delivery; and respiratory conditions such as chronic obstructive pulmonary diseases. [1,8] This affiliation does not affect all but definitely affects several. Periodontitis initiates systemic inflammation and can be monitored by inflammatory markers like C-reactive protein or fibrinogen levels.
Periodontitis and periodontal diseases are true infections of the oral cavity. There is an equilibrium that exists between microbial challenge and host's immune response; any alteration to that with addition of other modifying factors is responsible for clinical manifestation of periodontal disease. Pathogens of the subgingival microbiota can interact with host tissues even without direct tissue penetration, and the subgingival microbiota accumulate on the oral cavity to form an adherent layer of plaque with the characteristics of a biofilm. The oral cavity works as a continuous source of infectious agents, and its condition often reflects progression of systemic pathologies. Periodontal infection happens to serve as a bacterial reservoir that may exacerbate systemic diseases. He consumed 75 mg cyclosporine (in a low dose because of chronic allograft nephropathy), one gram mycophenolate mofetil, five mg prednisolone, and antihypertensive drugs. On physical examination, normal body temperature, pallor, left flank tenderness, diminished left side breath sounds and normal transplanted kidney were found. Because of low back pain radiating to lower limb associated with flank tenderness; absence of native kidneys, fever and urinary symptoms accompanied with normal transplanted kidney; the patient had been worked up by a neurologist for spinal nerve compression. Plain radiography of vertebral column showed extensive degenerative joint disease. However, neurologic exams were normal. If the patient had native kidneys, following diagnoses became propounded: nephrolithiasis, urinary tract obstruction and infection, lumbar disc disease and spondylosis, splenic and abdominal abscesses.

Urinary Tract Abscess in Nephrectomized Renal Transplant Recipient
Laboratory investigations revealed elevated serum creatinine and erythrocyte sedimentation rate (ESR),; abnormal urine with many granular casts, protein and positive colony count for pseudomonas aeroginosa, susceptible only to piperacillin; and negativeblood culture. Ultrasonography showed a 75-mm heterogeneous cyst in previous left kidney site confirmed by spiral computed tomography (CT) scan [ Figure 1, arrow]. The presence of such cysts in imaging studies is a typical feature of renal abscess. However, the patient had been nephrectomized and this abscess was accompanied with positive urine culture for P. aeroginosa which indicates left kidney remnant or retroperitoneal abscess penetration into native urinary tract. Incidence of infection is significantly higher in renal transplant recipients than general population.Although, among solid-organ transplants, kidney transplantation is associated with the lowest rates of infections, in part because of the elective or semielective nature of kidney transplantation These patients have multiple risk factors for infection including defect in immune system that result in decreased host resistance to infection. [1] Urinary tract infection is traditionally the most common bacterial infection occurring in the renal transplant recipient, particularly in the first few months post transplant; [2,3] . After posttransplant month 6, patients generally can be categorized as those with successful graft outcome, those with poor graft function because of chronic rejection and those chronically infected with immunomodulating viruses such as cytomegalovirus. Infections in patients with longterm successful allografts are typically similar to those that develop in persons in the community, while the latter two patient groups are at ongoing risk of opportunistic infections. [2][3][4][5] However, bacterial infections are common in the late posttransplant period but native urinary tract infection occurs rarely, particularly in a nephrectomized patient and this may mislead the physician because of