Dr Mariana Isabel Zamora Aguirre
PERIODONTAL NECROSANTE DISEASE / HIV: REPORT OF A CASE 18 YEARS OF FOLLOW UP
Mariana Isabel Zamora Aguirre*, Johana Salinas**, María Elena Guerra***
(*) Dentist Specialist in Periodontics and Orthodontics UCV
(**) Dentist Magister Scienciarum in Oral Medicine UCV
(***) Dentist Doctor of Sciences Mention Oral Health Mother and Child and Specialist in Children’s Dentistry
SUMMARY:
The human immunodeficiency virus (HIV) produces an immune deterioration that induces the manifestation of opportunistic diseases in the organism and, the oral cavity does not escape from it, having influence at the periodontal level. A patient is presented to the Center for Attention to Patients with Infectiouscontagious Diseases of the Faculty of Dentistry of the Central University of Venezuela (CAPEI / UCV) with a confirmed diagnosis of HIV / AIDS, presenting an advanced stage of Necrotizing Periodontitis (PN), as well as also Kaposi’s sarcoma, leucoplasias, ulcers, hairy leukoplakia and candidiasis. Controlled patient in the CAPEI / UCV and after 18 years of follow-up a healthy mouth is observed with the use of traditional approach techniques to HIV patients, together with treatment, control and interdisciplinary follow-up that includes oral, medical and psychological.
INTRODUCTION:
The PN is an entity that, along with Necrotizing Gingivitis (GN) and Necrotizing Stomatitis (EN), are part of the so-called Necrotizing Periodontal Disease (EPN) (1-4), presenting a higher prevalence of GN among HIV patients. seropositive versus healthy subjects. It is estimated that between 5 and 11% of these patients suffer from GN while PN affects approximately 1% (5). In more than 50% of HIV / AIDS it is possible to find some type of periodontal disease (6).
Periodontal diseases may be the first clinical sign of HIV infection. Immunosuppression and subsequent susceptibility can alter the response of buccal tissues that include the periodontium and buccal microflora and, therefore, modify the periodontal treatment and the results of the therapy. Periodontal disease in seropositive patients commonly includes the presence of less conventional forms of gingivitis and periodontitis and viral, mycotic and bacterial infections (7).
Among the most relevant predisposing factors are: stress, immunosuppression, especially in patients with HIV infection, smoking, food deficit and the existence of gingivitis (1). In recent years, the diagnosis of NPS has become more important, not only because of its contribution to the loss of periodontal insertion, but also because it has been described as a marker of immunological deterioration in patients with HIV infection (1,6 -9).
HIV infection affects the T helper cells of the organism causing a drastic change in the proportion T helper (CD4 +) / suppressor (CD8 +) lymphocytes with a great decrease in host resistance to infection and this correlates closely with the appearance of the GN. The complete absence of T lymphocytes in gingival tissue has been seen in patients infected with HIV, so the lack of an immune effector and regulatory cells in these patients could explain the characteristic and rapidly progressive nature of periodontitis in these patients(1).
During the progression of HIV infection, patients develop a continuous immune deterioration. Severe clinical markers of immune suppression have been documented, including oral candidiasis and hairy leukoplakia. Although the presence of oral manifestations influences the state of the disease due to HIV infection, a small attention has been focused on specific oral lesions as markers of the immune deterioration and the progression of the infection (4).
The decrease in T lymphocyte count seems to correlate closely with the susceptibility for GN infection (8,10). The predictive value ofa CD4 + cell count below 200 cells / mm3 in patients with PN was 95.1%, with cumulative probability of death within 24 months after diagnosis, so it has been suggested that the presence of PN in patients infected with HIV, is a predictive marker of immune deterioration and progression of the disease.
The patientl iving with HIV can be classified, according to the WHO based on the criteria dictated by the Center for Disease Control in Atlanta(CDC), within the following categories according to their clinical stage,depending on the clinical and immunological criteria (Table 1).Clinical category A comprises three situations (in the absence of criteria for B or C):
a)Primary infection orHIVprimaryinfection syndrome,b)Persistent generalized lymphadenopathy, and c) Asymptomatic HIV infection.CategoryBappliesto HIV-infected persons not includedd in category C, where the patient has a secondary infection within an open list(such as oral candidiasis, oral hairy leukoplakia, etc.) attributable to infection by the patient. HIV and that are sometimes indicative of cellular immunity deficit and progression to AIDS. Category C contains 26 clinical processes (closed list)defining AIDS(8), among which pulmonary tuberculosis, Pneumocystiscarinni pneumonia, esophageal candidiasis and neoplasms such as Kaposi’s sarcoma and non-Hodgkin’slymphoma among others(5)
OBJECTIVE:
Share our experience with a case where the cause-effect relationship between the immune deterioration of an HIV / AIDS patient is shown, the importance of patient management within the interdisciplinary team of all the health personnel involved, where the role of the dentist is fundamental and the evolution and stability over time of the patient’s immune system to maintain the periodontal tissues and, in general, oral health condition, improving the quality of life of these patients.
DESCRIPTION AND FOLLOW-UP OF THE CASE:
A 32-year-old male patient was presented to CAPEI / UCV at the time of the initial evaluation, who was diagnosed with HIV infection in February 1992, who was not receiving systemic treatment with antiretrovirals (ARVs) and since then referred alterations. systemic symptoms such as fever, vomiting, recurrent diarrhea, rashes, sexually transmitted diseases such as syphilis and gonorrhea, tuberculosis diagnosed in 1995; for the year 1997 his clinical history indicates other complications such as diarrhea, fever, scabies, amoebiasis, proctitis in the anus that required the hospitalization of the patient.
In November 1999 he was referred by the infectious medicine doctor and came to CAPEI / UCV, for presenting a violaceous macule on the hard palate and white lesions on the lateral border of the tongue, being evaluated by the oral doctors of the service. (Fig. 1 and 2)
Fig. 1: Violet color macule on the palate in Nov 1999.
Fig. 2: White lesions on lateral edge of the tongue in Nov 1999.
In January 2000 he returned to CAPEI / UCV again, this time referring pain throughout the mouth; On clinical examination, multiple oral lesions compatible with Kaposi’s Sarcoma were observed on the palate, already with an elevated form and upper vestibular gingiva, ulcerated lesions on the lower lip, lingual leukoplakia, hairy leukoplakia on the tongue and PN. The oral doctors of the CAPEI / UCV performed a biopsy of the palate and tongue lesion, which yielded a histopathological diagnosis of Kaposi’s Sarcoma and Hairy leukoplakia respectively (Figs 3-13).
The laboratory tests corresponding to the immunological tests showed low values of CD4 + of 131 cells / mm3 (normal values 1400 ± 512) and CD4 + / CD8 + index of 0.02 (normal values 1.95 ± 0.44). According to the parameters dictated by the Center for the Control of Atlanta Diseases presented in Table 1, this patient was classified as a category C3 patient and according to the immunological and clinical criteria was located in stage AIDS.
Fig. 3: High violaceous lesion on the palate in January 2000.
Fig. 4: White lesion on the lateral border of the tongue in January 2000.
Fig. 5: Ulcerated lesions in the lower lip in January 2000.
Fig. 6: High violaceous lesion on the attached gingiva at the level of 1.4 in January 2000.
Fig. 7: Histopathological results of palate and tongue injuries in January 2000.
Fig. 8, 9 y 10: Lesions at the level of gingival papillae in the form of bite-shaped, necrotic with pseudomembrane throughout the upper arch in January 2000.
Fig. 11, 12 y 13: Lesions at the level of gingival papillae in the shape of a bite, necrotic with pseudomembrane throughout the lower arch along with white lesions at the level of the lingual gingiva in January 2000.
The periapical radiographic examination shows the loss of the continuity of the alveolar ridge cortex and in some areas it is observed in the form of a characteristic bite of the PN. (Figs 14-16)
Fig. 14, 15 y 16: Radiographic appearance showing the activity of bone loss in anterior and posterior areas in January 2000.
The periodontal treatment was performed in the first week of February 2000 and consisted of ultrasonic tartrectomy, scaling and root planing by quadrants and rinses twice a day with 0.12% chlorhexidine gluconate undiluted, in addition to the oral care training at home using a proper brushing technique 3 times a day. It is also indicated to make an interconsultation with the treating infectious doctor to suggest starting treatment with antiretroviral therapy. The interdisciplinary team was included to a psychologist to work the emotional part that in this patient was affected.
By March of that same year, the patient was hospitalized for presenting a decompensation of his immune system and that is when he began his treatment with antiretrovirals. In July 2000, the patient again attended the CAPEI / UCV for control and a reduction of the oral and skin lesions was observed. This indicates a relationship between the stability of the immune system and the periodontal condition and other obvious opportunistic lesions in AIDS. The psychological aspect of the patient was in treatment and clinically stable and improving (Figs 17-25)
Fig. 17: Palate with violaceous appearance hardly noticeable for July 2000.
Fig. 18: Tongue, lateral border where the white lesions have practically disappeared for July 2000.
Fig. 19: Lateral view in the area where Kaposi’s sarcoma was initially attached to the gum, and the lesion has disappeared by July 2000.
Fig. 20, 21 y 22: Palatal view of the area where there were lesions in the gingival papillae where a clear improvement is observed with persistence of lesions of some small areas of the upper arch for July 2000.
Fig. 23, 24 y 25: Lingual view of the area where the lesions were in the gingival papillae and areas of the white lesions where the lesions have disappeared by July 2000.
The patient attended again the CAPEI / UCV in March 2001, for evaluation and periodontal maintenance and to control the areas where the other lesions were initially, finding stability in the soft and hard oral tissues compatible with good oral health. (Figs 26-35)
Fig. 26, 27 y 28: March 2001: All lesions on the hard palate, tongue and lower lip have subsided and the patient has progressed satisfactorily.
Fig. 29: March 2001: Lesion in vestibular gingiva completely absent.
Fig. 30, 31 y 32: March 2001: Periodontally stable patient in the upper arch.
ig. 33, 34 y 35: March 2001: Periodontally stable patient in lower arch.
For the period 2001-2007, the patient attends periodic check-ups and refers to maintaining his medical and dental indications with no significant alterations since his last evaluation in 2001.
In 2007 the patient was referred for the performance of a periodontal surgery to increase clinical crown in 1.6 to then place a large resin with a mesial drawer whose floor was subgingival. The surgical procedure and the resin restoration are performed with a satisfactory evolution. (Figs 36 and 37)
Fig. 36 y 37: The patient goes to a private practice referred for a preprosthetic periodontal surgery in the 1.6 and placement of resin reconstruction for the year 2007.
In 2009, the patient with 10 years of periodic periodontal control, clinically and radiographically, showed stability in the tissues. Routine periodontal maintenance is performed as any patient in control. (Figs 38-40).
Fig. 38 y 39: Complete view of upper and lower arches 10 years after diagnosis where the patient has maintained oral health, but above all, periodontal health for the year 2009.
Fig. 40: Detailed view of the upper and lower anterior sector showing periodontal health for the year 2009.
In February 2018, the patient is scheduled for periodontal and photographic control, the clinical examination shows optimal oral health conditions, continuing in control with the treating infectious disease specialist and eventual appointments with the psychologist, maintaining their serological values within normal ranges. No radiographic monitoring is performed for economic reasons of the patient for the time of evaluation. (Figs 41-50)
Fig. 41, 42 y 43: Clinical appearance of the palate, tongue and lower lip. Stable tissues are observed in time at 18 years of initial treatment. February 2018.
Fig. 44: Clinical appearance of vestibular gingiva, stable in time at 18 years of initial treatment. February 2018.
Fig. 45, 46 y 47: Detailed clinical appearance of upper arch. Stable tissues are observed in time at 18 years of initial treatment. February 2018.
Fig. 48, 49 y 50: Detailed clinical appearance of the lower arch. Stable tissues are observed in time at 18 years of initial treatment. February 2018.
