The roles of viruses in periodontal diseases Azodo C C, Erhabor P - J Dent Res Rev
MICROBIAL ETIOLOGY OF PERIODONTAL DISEASE – MINI REVIEW. Ljiljana Kesic1 All bacteria in the periodontal pocket could damage periodontal tissues, and good .. relationship of Treponema denticola to severity of periodontal. Periodontal disease, also known as gum disease, is a set of inflammatory conditions affecting Periodontal disease is generally due to bacteria in the mouth infecting the tissue around Although no causal association was proven, a recent study showed correlation between chronic periodontitis and erectile dysfunction. ETIOLOGY AND PATHOGENESIS OF PERIODONTAL INFECTIONS discovery of the relationships between dental plaque and the host periodontal tissues. . evidence supporting the bacterial etiology of periodontal diseases includes many .
May 8, ; Published date: May 15, Citation: J Interdiscipl Med Dent Sci 2: This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. View PDF Download PDF Abstract The palatal radicular groove is a morphological tooth defect, which act as local predisposing risk factor favoring accumulation of the bacterial plaque, permitting microbial invasion via root groove way, directly into periodontal structures.
A patient diagnosed with palatal radicular groove and a localized periodontal disease was treated by procedures to control bacterial action and procedures to eliminate local predisposing risk factor.
To treat the periodontal bone defect a sequelae of periodontal disease, a guided tissue regeneration technique was applied by using allograft and xenograft materials associated with a resorbable demineralized bovine cortical bone membrane. The objective of surgical regenerative procedure was to recover the periodontal tissues nearly as they were before periodontal disease destruction.
Keywords Bacteria; Etiology; Guided tissue regeneration; Periodontal disease Introduction The etiology of inflammatory periodontal disease is a complex interaction of bacteria, and predisposing risk factors as local factors and systemic factors [ 1 - 6 ]. Bacteria colonizing and growing at the gingival margin may be the main cause of the periodontal tissue inflammation, pocket development, and periodontal tissue destruction [ 7 - 9 ].
However, the role of local predisposing risk factors in the etiology of periodontal disease may be determinant to induce localized destruction of periodontal tissues [ 121011 ]. One of the local predisposing factors may be maxillary incisors radicular grooves.
The radicular grooves may be a morphological defect located in palatal region of the upper incisors teeth, extending beyond the cementoenamel junction, along the root surface [ 12 - 14 ]. Palatal radicular groove has been implicated as the local predisposing risk factor for periodontal disease, due the extreme difficult to maintain the area free of microbial deposits [ 1214 ].
Moreover, such sites have a high frequency of pocket formation due bacteria and microbial products invasion directly via radicular groove way into periodontal tissues [ 13 ]. Consequently to treat a localized periodontal disease which is provoked by bacteria and palatal radicular groove is necessary to establish a plan of treatment that needs to be focused in plaque control and also in elimination of local predisposing risk factor.
After providing a control in all etiologic factors associated with local periodontal disease, the effort to reach health in periodontal tissues was centered in eliminating the anatomic defects produced during periodontal disease activity. Then a regenerative periodontal procedure as guided tissue regeneration and bone graft was applied, attempting to gain new clinical attachment, improve bone level, and minimize postoperative recession [ 15 ].
Clinical examination revealed a localized deep periodontal pocket and a palatal radicular groove in the left upper lateral incisor Figure 1. The radiographic image showed a normal appearance due the periodontal alteration was localized in the lingual side Figure 2.
The therapy of localized periodontal disease was based in plaque control and root groove elimination. To achieve these goals, a full-thickness mucoperiosteal flap was reflected to access diseased root surface and then, all diseased periodontal soft tissue were curetted carefully Figure 3. Subsequently, were applied mechanical and chemical root biomodification to promote favorable characteristics on a pathologically root surface which was inside of the contaminated periodontal pocket.
The mechanical root biomodification was applied by using scaling and root planning, including the use of rotatory instruments Kavo, Joinville, Brazil to remove mainly radicular groove [ 1617 ] Figure 4. The chemical root biomodification was centered in application of acid therapy by using tetracycline hydrochloride mg diluted in 5ml of distilled solution on root surface mechanically treated [ 18 ] Figure 5.
Then regenerative procedures techniques were applied to treat the sequel produced by periodontal disease activity [ 1519 - 21 ]. There is an association between these bacteria and periodontal disease in the Sri Lankan population.
Following initial screening, 79 patients years of age, with interproximal CAL 6mm in 2 or more teeth and PD 5mm in one or more sites were included. PI, GI, calculus index, PD and AL were recorded at baseline 3months post- initial exam and were repeated every 3 months for another 9 months total of one year from initial exam.
Full mouth x-rays were taken at baseline and at 12 months. Sub-gingival plaque samples were taken at baseline and at every 3 months. Samples were also drawn at each visit for a quantitative of serum cotinine level. The overall mean attachment loss and bone loss were very close over the year: Average probing depth showed minimal change Smokers showed greater attachment loss and radiographic bone loss than non-smokers. Mean attachment loss was three times greater in smokers compared to non-smokers 0.
Radiographic bone loss was twice as much in smokers compared to non-smokers 0. Plaque, calculus and GI in baseline, showed no correlation with any of the changes in perio parameters at the end of the year. Past severity of periodontal involvement as reflected in baseline measurements showed direct correlation with outcomes of progressive periodontal breakdown. Tf, Pi, and Pg were frequently found in all of these patients, and the patients with higher numbers of these bacteria showed further disease progression.
Subjects with mean baseline PD were at greater risk for future bone loss 1 year later OR 2. Smokers were at SS greater risk for further attachment loss when compared to nonsmokers OR of 5. Subjects that harbored Tf, were at 7X greater risk for increased pocket depth. Past periodontal destruction, smoking habits, Tf, Pg, Pi are prognostic factors for further periodontal breakdown.
To investigate the role of systemic diseases, socio-economic factors, smoking, occupational hazards, and subgingival bacteria as risk indicators for attachment loss. Cross-sectional study of 1, subjects years old residing in Erie County, New York area. Subjects broken into case group with attachment loss and control group no attachment loss.
Statistical analysis conducted to assess associations between the extent of periodontal disease and patient characteristics including age, smoking, systemic diseases, exposure to occupational hazards, and subgingival microbial flora.
Age and smoking amount were further stratified. Control for gender, socioeconomic status, subgingival calculus. Age was the factor most strongly associated with attachment loss, with odds ratios for subjects 35 to 44 years old being 1. Diabetes mellitus was the only systemic disease positively associated with attachment loss with an odds ratio of 2.
Smoking had relative risks ranging from 2.
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The presence of two bacteria, Porphyromonas gingivalis and Bacteroides forsythus now T. Age, smoking, diabetes mellitus, and the presence of subgingival P.
The odds ratio for having attachment loss increased with age and higher rates of smoking. Adult Periodontitis Microbiology Listgarten To review the pathogenesis of periodontitis with an emphasis on the changes in the last decade.
Periodontitis is an inflammatory disease of the periodontium, which is characterized by loss of the tissues supporting the tooth. Its primary etiology is an ill-defined series of microbial infections, which may be composed of more than species currently recognized in the oral cavity. Other factors associated with periodontitis are occlusal trauma, hormonal alterations, and leukocyte dysfunctions.
It may be necessary to differentiate between periodontitis and gingivitis with pre-existing bone loss, since the clinical implications as well as the microbial etiology may differ significantly. Pattern of tissue loss tends to be bilaterally symmetrical. It is possible that the bacteria accumulate symmetrically due to anatomical factors that are present symmetrically in the mouth. Data appears to indicate that breakdown occurs in episodic, random episodes of active disease Socransky.
Transition from health to clinically detectable disease is characterized by prolonged periods of remission and even spontaneous reversals of the disease process Socrasky There is still a lack of clinically useful diagnostic tests to determine disease activity. Clinical findings may reflect the result of previous disease activity, but we still do not know how to determine when active destruction is taking place.
Etiology Local: Microbiology and Periodontal Diseases
It has been suggested that bacterial invasion of the tissues may be the underlying cause of the elusive episodes of disease activity which, through cumulative damage, lead to the progressive destruction of periodontal support no real evidence to support this yet.
To determine the correlations between various clinical assessments of inflammatory periodontal disease and the percentage of motile bacteria in the sub-gingival flora in sites of varying states of periodontal disease.
Two sites from each patient were selected so that 20 sites total can be assigned to each of the 6 categories, ranging from health to advanced periodontitis. The following measurements were recorded for each site: Dark field microscopy was used to determine the percentage of bacteria to three categories: Clinically healthy sites harbored much lower percentages of motile bacteria than did clinically diseased sites.
Most of the observed variation in the percentage of motile bacteria could be accounted for by variations in the percentage of spirochetes.
Relationship of bacteria to the etiology of periodontal disease.
The mean percentage of spirochetes was 2 to 3 times higher at sites exhibiting bleeding than at sites that did not bled. Significant associations were found between commonly used clinical parameters of periodontal disease and the percentage of motile bacteria at subgingival sites.
BOP showed a particularly strong association. If the presence of motile bacteria is really a valid indication of disease activity, then commonly used clinical parameters of periodontal disease may provide a more time-effective and site-specific means of detecting disease.
To examine a large number of subgingival plaques removed from untrated and successfully treated periodontal patients, to determine wheter characteristic bacterial profile could be identified and relate it to clinical appearance. Plaque was sampled from most severely involved tooth in each quadrant of sampled sites were molars.
Discussion Findings suggest the hypothesis that a succession of pathogenic microbes may exist as B. This study indicates that the various periodontal diseases are specific anaerobic infections involving spirochetes. Direct role in periodontal disease etiology Herpes simplex virus infection Herpes simplex virus, which are of two types: Herpes simplex virus-1 infections occur in the oral cavity while HSV-2 infections occur in the genital area.
However, they can occur in either area and at other sites in the body. These viruses can be carried in body fluids or in fluid from herpes lesions. For an infection to occur, the viruses must gain entry into the body of the uninfected persons through their skin or mucous membrane in the intraoral or genital area. Once the virus has contact with the cells of the mucous membranes or skin tissue, it tries to replicate in the cell nuclei. This can result in symptoms following multiplication and destruction of the vulnerable cells of the skin and mucus membrane in previously uninfected individuals with inflammation and appearance of vesicles.
After this initial infection, the virus is transported through the nerve cell to their sensory dorsal root ganglion where it becomes latent for a period of time. Autoinoculation, which is process by which infected individuals infect other parts of their own bodies, may occur.
However, this is uncommon because of the development of protective antibodies against this problem among affected individuals. The primary oral infection causes symptoms, which can be very painful, particularly in young children. This primary lesion is called primary herpetic gingivostomatitis, which is characterized by the formation of vesicles on the gingival, lips, tongue and buccal mucosa.
The rupture of the vesicles results in painful erosion and ulceration with yellowish membrane development before healing, but disappears within days.
There is also associated increased salivation and bad breath. Rarely, chills, myalgia, dysphagia, or hearing loss may occur.
It is usually caused by the reactivation of the latent virus. Following the primary HSV infection, virions travel from the initial site of infection on the skin or mucosa to the sensory dorsal root ganglion, where latency is established. When the dormant virus in the ganglion is activated, it begins to multiply again and moves down the trigeminal nerve usually to the site of initial inoculation and infect the epithelial cells causing a recurrent infection.
The other, the skin trigger theory proposed by Hill and Blyth, holds that virus is continuously shed from neuronal endings and lesions develop when the susceptibility of the skin is sufficiently permissive for the development of a clinically apparent infection.
Trigger of latent virus within about 3 days of intense dental work like root canal treatment or tooth extraction have been reported. Recurrence can occur as herpes zoster often after many decades. The virus is presumed to spread through air droplets or direct contact with an active lesion. The periodontal lesion is indistinguishable from HSV except that the lesion of chicken pox tends to be relatively painless. Herpes zoster is characterized by pain and rash in one dermatome.
Pain that persists long after the rash has healed is recognized as postherpetic neuralgia. Different clinical patterns of Kaposi's sarcoma have been described: Oral lesions are frequently seen in the immunodeficiency state than in other forms of Kaposi sarcoma. Kaposi's sarcoma has been described in most oral regions, although the palate, gingiva, and tongue seem to be the most commonly affected sites.
It is similar to other HHV that is, after infection, latency is established and reactivation is possible after conditions favorable to the virus. This infection is often subclinical and usually occurs in young children but may also be seen in adolescents and adult. It is common in the developing world especially among the low socioeconomic group. In infants, the virus is contracted through the placenta, during delivery or during breast feeding.
Transmission occurs during adolescence during sexual activity. Transmission has also been documented during blood transfusion and organ transplantation.