Periodontal diseases and HIV infection

The workshop considered six related questions about periodontal changes seen in HIV infection. 1) To what extent are specific periodontal changes associated with HIV? 2) Are conventional periodontal diseases modified by HIV infection? The changes associated with HIV appear to be modified presentations of conventional diseases. Research should identify initiation and progression factors for necrotizing diseases. 3) What is the role of geography and transmission groups? These questions cannot be answered without greater standardisation of research methods. 4) Has the epidemiology of these changes changed with the advent of new therapies? The data required to answer this question should be available soon but this question is irrelevant to the vast majority of people with HIV. 5) What pathogens are involved in periodontal changes seen in HIV infection? The role of Candida spp. and other potential pathogens requires further investigation. 6) What management protocols are suitable for the periodontal diseases? The significance of periodontal diseases among people with HIV in developing countries is not known. Further research is needed of the effectiveness of interventions especially necrotizing disease in developing countries. The quality of research of these diseases would be enhanced by standardized approaches. A list of relevant variables might prevent their omission from studies.     

Which periodontal changes are associated with HIV infection?

Abstract. To assess the validity of diagnostic criteria for HIV-associated periodontal diseases, existing sets of criteria were applied post-hoc to cross-sectional data of the periodontal health of men with and without HIV and their ability to predict HIV infection was compared. Criteria for gingival or periodontal ulceration predicted HIV infection to a similar level. Criteria sensitive to erythema of the attached gingiva and interdental craters had high positive predictive values. Distinct gingival red bands did not predict HIV. 3 HIV-associated periodontal changes were recognised: erythema of the attached gingiva; necrotizing periodontal disease and interdental craters. Epidemiological research should also consider conventional gingivitis and lost periodontal attachment. The presence or absence of all 5 conditions should be recorded at each site. Hierarchies of diagnoses with only the most severe condition assigned to each individual swamp valuable information.     

Gingival ulceration in HIV infection

Abstract. All cases of HIV-associated gingival ulceration seen at a dedicated dental clinic in a 5-ycar period were reviewed and compared against other patients attending the clinic. 94 (7.1%) of 1308 patients had 146 episodes of gingival ulceration. 89 patients had 140 episodes similar to acute necrotising ulcerative gingivitis (ANUG) and responded well to conventional treatment for ANUG. The cases were compared with 269 controls in logistic regression. Gingival ulceration was associated with oral candidiasis, lower age and lack of AIDS diagnosis possibly due to a protective effect of co-trimoxazole medication. 5 patients with neutropenia had extensive ulceration without the microflora of ANUG. Histopathology, viral and bacterial culture revealed non-specific changes. The ulcers did not respond to the treatment regimen for ANUG but responded to treatment of their neutropenia. Gingival ulceration is not common in HIV infection. Most cases resemble severe ANUG. It is more frequent in younger people, those with oral candidiasis and without AIDS. Co-trimoxazole may be protective. A minority of cases with ulceration and associated neutropenia resembled the non-specific oral ulceration associated with HIV.     

Is there an association between periodontal condition and HIV infection?

Abstract Individuals in Tanzania who have limited access to medical and dental treatment provide an opportunity to study the natural association between periodontal condition and HIV infection and the stage of infection. 119 HIV infected adult individuals and 73 individuals with AIDS from the AIDS Clinical Trial Clinic at Muhimbili Medical Centre (MMC) in DaresSalaam participated as cases. Mean age was 35.3 and 35.1 years, respectively. 156 individuals with a mean age of 28.3 years, confirmed as HIV seronegative, served as controls. There were no significant differences in bleeding on probing, pocket formation or attachment loss among the HIV seronegative individuals. HIV seropositive and AIDS patients. We applied multiple logistic regression to calculate odds ratios for presence of periodontal conditions adjusting for age, gender and DMFT. Our odds ratios did not reveal any significant associations between bleeding on probing, pocket formation or attachment loss with regard to lymphocyte and CD4+ T cell counts among the HIV infected individuals and AIDS patients. When associations were investigated with regard to HIV serostatus (HIV seronegative. HIV seropositive or AIDS), our adjusted odds ratios were insignificant, too. In fact, most odds ratios were close to 1. Thus, our study supports recent views that the presence, extent and severity of periodontal disease among HIV infected individuals, may be less that hitherto thought.     

The periodontal health of homosexual men with HIV infection: a controlled study

OBJECTIVE Identify types, prevalence and severity of periodontal changes associated with HIV infection. DESIGN: Cross-sectional controlled blinded study. SETTING: Open access genito-urinary medicine clinic. PARTICIPANTS: Convenience sample of 794 homosexual men aged 18–65.
OUTCOME MEASURES: Prevalence, extent and severity of probing attachment loss (PAL), pocketing, gingival ulceration, gingivitis, bleeding on probing (BOP), gingival red bands and diffuse and punctate erythema of the attached gingiva (selected a priori ).
RESULTS: Prevalences in men with (n = 312) and without HIV (n = 260) were: PAL (≥l site ≥4 mm), 59.6% and 28.5% respectively (P < 0.001. x²); pocketing (≥1 site ≥4 mm) 51.0% and 31.9% (P < 0.001); BOP, 96.5% and 92.3% (P = 0.038); gingival ulceration. 3.2% and 1.0% (P = 0.031), red banding, 12.2% and 10.0% (P = 0.410); diffuse erythema, 12.5% and 3.1% (P < 0.001) and punctate erythema, 9.6% and 1.1% (P < 0.001). Decreased CD4 lymphocyte counts predicted the presence, extent and severity of PAL (P = 0.023, 0.027 and 0.060) but not pocketing. Oral candidiasis predicted the extent and severity of gingivitis and the presence of diffuse and punctate erythema (P = 0.037, 0.011, 0.002 and <0.001).
CONCLUSIONS: Destruction of periodontal attachment is associated with progression of HIV disease whereas pocketing is associated with HIV infection but not disease progression. Gingival ulceration is associated with HIV but gingivitis and erythema of the attached gingiva are most strongly associated with oral candidiasis. Gingival red bands were not associated with HIV infection.     

The microbiology of HIV-associated periodontal lesions

2 intraoral lesions associated with human immunodeficiency virus (HIV) infection have recently been described: an atypical gingivitis and a rapidly progressive periodontitis. The microbiota associated with these gingival and periodontal lesions was investigated. Subgingival plaque samples were taken from 45 HIV-seropositive homosexual men and from 44 HIV-seronegative control subjects. Each sampled site was clinically and radiographically classified as HIV-associated gingivitis, HIV-associated periodontitis, healthy in an HIV-seropositive subject, or healthy, conventional gingivitis or classical periodontitis in a control subject. Plaque samples were examined by indirect immunofluorescence with polyclonal antisera to detect Bacteroides gingivalis, B. intermedius, Fusobacterium nucleatum, and Actinobacillus actinomycetemcomitans. Anaerobic culturing was used to detect black-pigmented Bacteroides species, Fusobacterium species, and A. actinomycetemcomitans to confirm the immunofluorescence findings. We detected B. gingivalis, B. intermedius, F. nucleatum, and A. actinomycetemcomitans in significantly more HIV-periodontitis sites (80, 65, 59 and 61% of sites, respectively) and HIV-gingivitis sites (61, 70, 52 and 52%, respectively) than in HIV-seropositive healthy and control sites (p less than 0.05). The results indicate that the microbiota found in HIV-periodontitis is similar to that of classical periodontitis. In contrast, however, the microbiota associated with HIV-gingivitis is strikingly different from that of conventional gingivitis. The similarity in the prevalence of periodontopathic organisms in both HIV-gingivitis and HIV-periodontitis suggests that the HIV-gingivitis lesion may be a precursor to the tissue destruction observed in HIV-periodontitis. Hence, early detection and treatment of the HIV-gingivitis lesion may prevent the rapid and extensive breakdown of periodontal tissues associated with HIV-periodontitis.     

Periodontal health and HIV infection

Despite a large amount of research of periodontal health seen in HIV infection, much remains to be learned. Very few large controlled studies of infected people at settings not self-selected for oral disease have been reported, and few have investigated the necrotising periodontal diseases described in HIV infection. In this paper we present a brief review of three approaches to identify periodontal changes associated with HIV infection and identify possible aetiological factors for them. First, we summarise the methods and findings of a controlled blinded study of the periodontal health of homosexual men attending a genito-urinary medicine clinic. Second, we précis a case-control study of gingival ulceration among patients at a dedicated dental clinic. Finally, we outline how the validity of diagnostic criteria for HIV-associated periodontal changes were tested against the data collected in the controlled study.     

Classifications of oral lesions in HIV infection

BACKGROUND: Manifestations of immunosuppression may take the form of opportunistic infection, and neoplasia. While this paper has focused on gingival and periodontal manifestations. these tissues cannot be evaluated in isolation. The presence of involvement of other oral tissues such as the cheek or tongue with manifestations associated with HIV such as hairy leukoplakia, Kaposi's sarcoma at these sites, and candidiasis in addition to periodontal manifestations may further increase the clincal suspicion of underlying immunosuppression and/or progression of the immunosuppressive state. DISCUSSION: The periodontist plays an essential r le in identifying the periodontal status of an individual and has an important r le to play in early recognition of signs and symptoms of HIV disease or progression of the medical condition. CONCLUSION: Only through such recognition can appropriate definitive diagnostic testing be conducted, and appropriate therapeutic intervention for the oral condition and the systemic condition be considered.     

HIV infection and the dentist. 2. The diagnosis and management of gingivitis and periodontitis

In HIV infected patients, a distinct form of gingivitis and periodontitis was reported recently. This paper reviews the clinical and microbiological features of these lesions and makes recommendations regarding their clinical management. The need for early treatment and control of periodontitis in HIV seropositive patients is emphasized.     

Mouthrinses and periodontal disease

It is known that mouthwashes can influence gingivitis; however, their role in the three different kinds of periodontitis is unclear. Some solutions have demonstrated some effect on necrotising periodontitis, yet none have been shown to influence early onset periodontitis. The literature provides us with a wide range of in vitro concentrations of substances used pure or in various mixtures in mouthwashes. Although only a few solutions can be used in a curative approach, most mouthwashes represent an essential tool in prophylaxis and thus also in post-periodontal treatment (maintenance phase). However, severe qualitative differences exist between the diverse families of mouthwashes. Many studies have shown that the use of a mouthwash associated with regular tooth cleaning was more beneficial than the utilisation of mouthrinse alone.     

Classification and diagnostic criteria for oral lesions in HIV infection

A consensus has been reached on the classification of the oral manifestations of HIV infection and their diagnostic criteria, based on presumptive and definitive criteria. The former relate to the initial clinical appearance of the lesion and the latter are often the result of special investigations. Candidiasis, hairy leukoplakia, specific forms of periodontal disease [linear gingival erythema, necrotising-(ulcerative) gingivitis and necrotising(ulcerative) periodontitis], Kaposi's sarcoma and non-Hodgkin's lymphoma are strongly associated with HIV infection. Lesions less commonly associated with HIV infection and lesions seen in HIV infection, but not indicative of the disease, are also listed.     

Management of the oral mucosal lesions seen in association with HIV infection

Oral lesions cause considerable morbidity in association with HIV infection. Their successful management depends upon accurate diagnosis and the use of appropriate therapy. Various treatment approaches are described for some of the common oral lesions including Kaposi's sarcoma, oral candidiasis, hairy leukoplakia and recurrent oral ulcers associated with HIV disease. This paper will discuss the therapies available in the USA and UK. In other countries some of the drugs discussed will be available in different doses and preparations. In addition other drugs may be available in other parts of the world that are not licensed for use in the USA or UK, and their availability may vary.     

Treatment of HIV-associated periodontal diseases

Three presentations of periodontal disease are associated with HIV infection: necrotising periodontal disease; forms of atypical gingivitis and exacerbated attachment loss. Necrotising disease resembling aggressive acute necrotising ulcerative gingivitis and is the most acute and painful of these. Response to treatment by debridement of lesions, irrigation with aqueous chlorhexidine solution and oral metronidazole 200 mg, tds is almost diagnostic of the condition. Affected individuals are prone to relapse. Prevention by meticulous home care and frequent hygiene recalls is advised. The forms of atypical gingivitis are classically not plaque related. This means that persistence of gingivitis in the absence of plaque is required to establish the diagnosis. There is a consensus that these diseases are related to candidiasis. Treatment with antifungals may be contraindicated due to the emergence of resistant strains of Candida spp. Exacerbated attachment loss may be the legacy of repeated episodes of necrotic disease or may be due to accelerated periodontitis. In either event the principles of treatment are to encourage and facilitate plaque removal.     

Association between asthma and periodontal disease: A systematic review and meta‐analysis

1 Background

The aim of this systematic review (SR) is to evaluate the association between asthma and periodontal disease.

2 Methods

An electronic search without date or language restrictions was carried out in PubMed/MEDLINE, Cochrane Central Register of Controlled Trials, Web of Science, and LILACS until May 2016. In addition, manual searches and searches of the gray literature were conducted. The search process, data analysis, and quality assessment were performed by two independent reviewing authors. Eligibility criteria included prospective and retrospective cohort studies, case‐controls, and randomized clinical trials.

3 Results

The search and selection process yielded 21 studies, published between 1979 and 2017. The meta‐analysis showed a statistically significant difference for the parameters of gingival bleeding, plaque index, and gingival index for participants with asthma (P < 0.001).

4 Conclusion

Data from this SR strongly suggest the association of asthma with periodontal disease.     

Candidal infection of the gingiva in HIV-infected persons

Gingival biopsies were taken from 27 HIV (human immunodeficiency virus)-seropositive persons with gingivitis or periodontitis and 16 HIV-seronegative persons with periodontitis. Sections were stained with hematoxylin and eosin or periodic acid-Schiff. Candidal hyphae and pseudohyphae were found in the para-keratinized oral epithelium in 7 specimens from the HIV-infected patient group and in the connective tissue close to the bottom of the gingival pocket in one such specimen. No fungal invasion was found in any of the biopsies from the HIV-seronegative persons. Candidal invasion was significantly more frequent ( P <0.05) in patients with a confirmed history of necrotizing periodontal diseases (5/9) than in patients without known episodes of such diseases (3/18). The most prominent histopathologic changes observed in connection with candidal invasion comprised polymorphonuclear leucocyte infiltration of the oral gingival epithelium and numerous mitoses, some of which were located suprabasally. It is suggested that Candida albicans may contribute to the development of necrotizing periodontal diseases in HIV-infected persons.     

Diagnosis and classification of periodontal disease

Periodontal diseases have been recognized and treated for at least 5000 years. Clinicians have recognized for many years that there are apparent differences in the presentation of periodontal diseases and have attempted to classify these diseases. Systems of classifications of disease have arisen allowing clinicians to develop structures which can be used to identify diseases in relation to aetiology, pathogenesis and treatment. It allows us to organize effective treatment of our patients' diseases. Once a disease has been diagnosed and classified, the aetiology of the condition and appropriate evidence-based treatment is suggested to the clinician. Common systems of classification also allow effective communication between health care professionals using a common language. Early attempts at classification were made on the basis of the clinical characteristics of the diseases or on theories of their aetiology. These attempts were unsupported by any evidence base. As scientific knowledge expanded, conventional pathology formed the basis of classification. More recently, this has been followed by systems of classification based upon our knowledge of the various periodontal infections and the host response to them. Classification of periodontal diseases has, however, proved problematic. Over much of the last century clinicians and researchers have grappled with the problem and have assembled periodically to review or develop the classification of the various forms of periodontal disease as research has expanded our knowledge of these diseases. This has resulted in frequent revisions and changes. A classification, however, should not be regarded as a permanent structure. It must be adaptable to change and evolve with the development of new knowledge. It is expected that systems of classification will change over time. This review examines the past and present classifications of the periodontal diseases.     

Periodontal diseases and HIV infection

Abstract There have been many references in the literature to HIV-related periodontal diseases, which although poorly substantiated, seem to have established them as part of the expected range of HIV-associated conditions. The original studies have produced conflicting reports which may stem from shortcomings in design. Consequently, the picture remains confused with respect to the classification, epidemiology, microbiology, natural history and management of H1V-related periodontal diseases. Future studies should give greater attention to sampling methods, the use of control groups and defining criteria. This will allow comparison of data between centres and facilitate study of what may be an uncommon disease.     

Salivary IgA responses to bacteria in dental plaque as related to periodontal and HIV infection status

Levels of total IgA and specific IgA reactive with Streptococcus mutans, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens and Fusobacterium nucleatum were measured by ELISA in parotid saliva from HIV⁺ and HIV⁻ persons with healthy gingiva (HG), chronic gingivitis, chronic marginal periodontitis (CMP), or neerotizing ulcerative periodontitis (NUP). When the HIV+ group was compared with the HIV⁻ group regardless of periodontal status, total salivary IgA concentration was higher in HTV⁺ patients, but no such difference was observed for total IgA output. HIV⁺ CMP displayed higher total IgA concentration as compared with HIV⁻ CMP. No significant differences in specific IgA outputs and ratios were detected between HTV⁺ and HIV⁻ subgroups with similar periodontal status. HIV⁻ NUP displayed increased specific IgA output towards S. mutans and increased specific IgA ratio values towards S. mutans, P. gingivalis and P. nigrescens as compared with HIV⁺ CMP, and increased specific IgA ratio values towards S. mutans and P. nigrescens as compared with HIV⁺ HG. No such differences were observed between the HIV⁻ subgroups. In sum. salivary IgA responses to bacteria in dental plaque seem not to be related to chronic periodontal disease and HIV infection, but are possibly influenced by acute periodontal infection.     

Immunohistochemical study of linear gingival erythema from HIV-positive patients

Severe forms of periodontal disease are frequent in patients with acquired immunodeficiency syndrome (AIDS). Linear gingival erythema (LGE) is a progressive disease described in HIV-positive patients and is considered to be an early stage of necrotizing periodontitis. Although clinical and microbiological differences are reported in LGE and non-specific gingivitis (NSG), a comparative immunopathological approach of both has not been performed yet. The purpose of this study was to compare relative populations of T-lymphocytes, B-lymphocytes, neutrophils, macrophages and IgG bearing plasma cells in gingival biopsies from sites exhibiting LGE and from sites exhibiting NSG. A biotin-streptavidin amplified system was used for identification of the following antigens: CD3 (T-lymphocytes), CD20 (B-lymphocytes), elastase (neutrophils), CD68 (macrophages) and IgG (plasma cell's secretors of IgG). The results have demonstrated decrease proportions of T-lymphocytes, macrophages and high percentage of neutrophils and IgG bearing plasma cells in LGE. In contrast with NSG, many neutrophils cells in LGE were found inside oral gingival epithelium. Our results highlight the idea that progressive periodontal disease is not only characterized by increased tissue inflammation, but, in addition, by significant changes in the proportion of specific inflammatory cells. The high number of neutrophils along the gingival epithelium is probably associated with the severe gingival necrosis reported in AIDS patients.