**6.1 Linear Gingival Erythema (LGE)**

**6.1.1 Background** 

This lesion is also known as 'red-band gingivitis' or 'HIV-associated gingivitis'. LGE is commonly seen in immune-compromised individuals and is considered to be a potential precursor for necrotizing ulcerative gingivitis (NUG)/ necrotizing ulcerative periodontitis (NUP). According to the recent classification of periodontal diseases (Armitage, 1999), LGE is classified under 'Gingival diseases of fungal origin.'

#### **6.1.2 Pathogenesis**

There is an increased number of bacteria and *Candida* species in the gingival sulcus associated with LGE. The bacteria seen include those commonly observed in periodontal disease such as *Bacteriodes gingivalis, Bacteriodes intermedius, Actinomyces viscosus, Fusobacterium nucleatum,* and *Aggregatibacter actinomycetemcomitans*.

#### **6.1.3 Clinical features**

The lesions present themselves as 2-3 mm wide red band around the marginal gingival of the teeth. These lesions are not typically painful, but bleed readily.

#### **6.1.4 Treatmen**

Typically, no treatment is needed for this condition. Although LGE is listed under 'Lesions of fungal origin', it is not typically treated with anti-fungal medications. Mechanical removal of plaque and calculus helps reduce inflammation and excessive bleeding. Chlorhexidine gluconate (0.12%) mouth rinses can be used twice daily. If the lesion persists, systemic antibiotics (metronidazole) may be prescribed to reduce the bacterial load.

#### **6.2 Necrotizing Ulcerative Gingivitis and Periodontitis (NUG and NUP) 6.2.1 Background**

NUG is a painful condition of the gingiva characterized by ulcerations, bleeding, and foul breath. It is also called Vincent's infection, Vincent's angina, or trench mouth. When the infection spreads to the alveolar bone, it is called NUP. Prevalence of NUP in HIV-infected individuals has been reported by various researchers. Its prevalence with HIV was reported in 1994 as 6% (Glick, et al., 1994). Over a period of a decade, the incidence of HIV in NUP patients increased to 69.6% (Shangase, et al., 2004). Recent reports suggest 43% of patients with NUP were HIV-seropositive (Phiri, et al.). Studies have shown that HIV-infected individuals with NUP are 20.8% more likely to have a CD4+ count lower than 200 (Glick, et al., 1994).

Individuals with HIV/AIDS: Clinical Manifestations in the Oral Cavity in the Post-HAART Era 91

The clinical characteristics of NUG includes ulcerated and necrotic papillary and marginal gingival covered by a yellowish-white or grayish slough or "pseudomembrane", blunting and cratering of papillae, spontaneous bleeding or bleeding on probing, pain and fetid breath (Barnes, et al., 1973, Falkler, et al., 1987, Horning and Cohen, 1995). It may be accompanied by fever, lymphadenopathy, and malaise. Progression of gingivitis to NUP is

The first treatment for NUG was devised by Dr. S. Schluger in 1949 (Schluger, 1949).Bacterial pathogens were controlled or eliminated by mechanical debridement or use of antibiotics in earlier days (Johnson and Engel, 1986). Aureomycin and penicillin were the first antibiotics considered for treatment of NUG in 1950 (Goldman and Bloom, 1950, Montis, 1950). Mechanical treatment consists of scaling and root planing. In addition to mechanical debridement, antibiotic and antimicrobial therapies are essential for management of NUP. Oxidizing mouthwash such as 3% hydrogen peroxide has also shown

There are three subtypes of on-Hodgkin's lymphoma (NHL): diffuse large B cell lymphoma (DLBCL), Burkitt's lymphoma (BL) and central nervous system lymphoma (CNSL)(Engels,

commonly associated with clinical attachment loss and alveolar bone destruction.

**6.2.3 Clinical features** 

Fig. 10. Necrotizing Ulcerative Periodontitis

**7. Non-Hodgkin lymphoma** 

to have beneficial effects in management of NUG and NUP.

**6.2.4 Treatment** 

**7.1 Background** 

Fig. 9. Linear Gingival Erythema

#### **6.2.2 Pathogenesis**

NUP is commonly a progression of NUG that demonstrates bone loss and clinical attachment levels (MacCarthy and Claffey, 1991). Both are primarily caused by bacterial infection with microflora consisting of Treponema and Selenomonas species, *Prevotella intermedia, Fusobacterium nucleatum* and *Porphyromonas gingivalis* (Falkler, et al., 1987, Loesche, et al., 1982). Malnutrition, smoking, stress, trauma and preexisting gingivitis are other etiologic factors (Peruzzo, et al., 2007, Taiwo, 1993). Most persons with NUG have alterations in the immune system making them more prone to microbial infections (Cogen, et al., 1983). This immunosuppression is also evident in infection by HIV (Goedert, et al., 1984). *Treponema denticola* (*T. denticola*) is the principal oral helical-shaped anaerobic spirochete that plays an essential role in immunosuppression. The disease process is mediated through adherence to mucosal surfaces, specific cleavage of cell surface receptors, inhibition of host defense mechanisms, penetration in epithelial cells, and induction of gingival inflammation and bone resorption. Proteases such as chymotrypsin, phospholipase C, oligopeptidase and cystalysin play an important role in pathogenicity (Chi, et al., 2003, Ellen and Galimanas, 2005, Fenno and McBride, 1998) and is induced by a range of proinflammatory cytokines such as IL-1α, IL-1β, tumor necrosis factor-α, IL-6 and IL-8 (Gemmell and Seymour, 1998, Nixon, et al., 2000). These cytokines affect connective tissue destruction and alveolar bone desorption (Gemmell and Seymour, 1998). Phosphorylation of intracellular receptors such as Fos-c, MKK1, MAP kinase and nuclear factor κB molecules by *T. denticola* affect these changes (Tanabe, et al., 2008).

### **6.2.3 Clinical features**

90 Global View of HIV Infection

NUP is commonly a progression of NUG that demonstrates bone loss and clinical attachment levels (MacCarthy and Claffey, 1991). Both are primarily caused by bacterial infection with microflora consisting of Treponema and Selenomonas species, *Prevotella intermedia, Fusobacterium nucleatum* and *Porphyromonas gingivalis* (Falkler, et al., 1987, Loesche, et al., 1982). Malnutrition, smoking, stress, trauma and preexisting gingivitis are other etiologic factors (Peruzzo, et al., 2007, Taiwo, 1993). Most persons with NUG have alterations in the immune system making them more prone to microbial infections (Cogen, et al., 1983). This immunosuppression is also evident in infection by HIV (Goedert, et al., 1984). *Treponema denticola* (*T. denticola*) is the principal oral helical-shaped anaerobic spirochete that plays an essential role in immunosuppression. The disease process is mediated through adherence to mucosal surfaces, specific cleavage of cell surface receptors, inhibition of host defense mechanisms, penetration in epithelial cells, and induction of gingival inflammation and bone resorption. Proteases such as chymotrypsin, phospholipase C, oligopeptidase and cystalysin play an important role in pathogenicity (Chi, et al., 2003, Ellen and Galimanas, 2005, Fenno and McBride, 1998) and is induced by a range of proinflammatory cytokines such as IL-1α, IL-1β, tumor necrosis factor-α, IL-6 and IL-8 (Gemmell and Seymour, 1998, Nixon, et al., 2000). These cytokines affect connective tissue destruction and alveolar bone desorption (Gemmell and Seymour, 1998). Phosphorylation of intracellular receptors such as Fos-c, MKK1, MAP kinase and nuclear factor κB molecules by

Fig. 9. Linear Gingival Erythema

*T. denticola* affect these changes (Tanabe, et al., 2008).

**6.2.2 Pathogenesis** 

The clinical characteristics of NUG includes ulcerated and necrotic papillary and marginal gingival covered by a yellowish-white or grayish slough or "pseudomembrane", blunting and cratering of papillae, spontaneous bleeding or bleeding on probing, pain and fetid breath (Barnes, et al., 1973, Falkler, et al., 1987, Horning and Cohen, 1995). It may be accompanied by fever, lymphadenopathy, and malaise. Progression of gingivitis to NUP is commonly associated with clinical attachment loss and alveolar bone destruction.

Fig. 10. Necrotizing Ulcerative Periodontitis

#### **6.2.4 Treatment**

The first treatment for NUG was devised by Dr. S. Schluger in 1949 (Schluger, 1949).Bacterial pathogens were controlled or eliminated by mechanical debridement or use of antibiotics in earlier days (Johnson and Engel, 1986). Aureomycin and penicillin were the first antibiotics considered for treatment of NUG in 1950 (Goldman and Bloom, 1950, Montis, 1950). Mechanical treatment consists of scaling and root planing. In addition to mechanical debridement, antibiotic and antimicrobial therapies are essential for management of NUP. Oxidizing mouthwash such as 3% hydrogen peroxide has also shown to have beneficial effects in management of NUG and NUP.

## **7. Non-Hodgkin lymphoma**

#### **7.1 Background**

There are three subtypes of on-Hodgkin's lymphoma (NHL): diffuse large B cell lymphoma (DLBCL), Burkitt's lymphoma (BL) and central nervous system lymphoma (CNSL)(Engels,

Individuals with HIV/AIDS: Clinical Manifestations in the Oral Cavity in the Post-HAART Era 93

Involvement of two or more lymph node regions on the same side of the diaphragm (II) alone or with localized involvement of an

Involvement of lymph node regions on both sides of the diaphragm (III) alone or with localized involvement of an extralymphatic organ or site (IIIE) or spleen (IIIS) or both (IIISE)

extralymphatic organs with or without associated lymph node

Diffuse or disseminated involvement of one or more

Stage I Involvement of a single lymph node region (I) or a single extralymphatic organ or site (IE)

extralymphatic organ or site (IIE)

Table 3. Ann Arbor Classification of Non-Hodgkin's Lymphomas (Rupniewska, 1979)

Oral NHL lesions are often in disseminated disease states. The most common oral sites of involvement are the palate, tonsil, buccal mucosa, floor of the mouth, and the retromolar region. These lesions are non-tender, diffuse swellings usually involving the gingiva, buccal vestibule and posterior hard palate. Gnathic lesions arise from soft tissue invading the bony skeleton. One third of patients show fever, weight loss, adenopathy, night sweats, or hepatosplenomegaly. Oral lesions are fluctuant swellings showing ulceration, pain, tooth mobility and paresthesia when peripheral nerves are involved (Vega, et al., 2005). Salivary gland lymphomas account for approximately 3% of all salivary gland tumors (Barnes, et al., 1998). About 80% of the cases are reported in parotid gland, 16% in submandibular, 2% in sublingual and 2% in minor salivary glands. Affected bony areas show a "punched out" pattern that is due to multiple areas of destruction with ill defined radiolucent lesion. Involvement of the maxillary sinus will cause opacification with eroded cortical walls and associated sinus mass (Fukuda, et al., 1987). The Ann Arbor staging system, originally

A prognostic index has been developed by the International NHL prognostic factors project based on data from 2,031 patients with aggressive lymphomas treated with regimens containing doxorubicin ("A Predictive Model for Aggressive Non-Hodgkin's Lymphoma," 1993). Analysis of 1274 patients younger than 60 years showed three clinical features independently associated with survival: serum LDL (lactate dehydrogenase) levels, tumor stage, and their performance status ("A Predictive Model for Aggressive Non-Hodgkin's Lymphoma," 1993). Past studies showed the importance of gallium-67 uptake in lymphomas as a useful prognostic indicator (Janicek, et al., 1997). The importance of prognostic index is that good-risk patients can be identified for standard therapy and poor-risk patients can be identified for new research protocols to improve the rate of therapy. With conventional therapy only 25% of patients who were gallium-positive midway through therapy had durable responses , while 70% of those who were gallium-negative remained free of disease (Janicek, et al., 1997). In patients with stage I or II disease, regional therapy leads to longterm control, with relapse rate of 44%-47% at 10 years and survival rates of 75% for patients younger than 60 years (Vaughan Hudson, et al., 1994). Stage III and IV patients can be treated by alkylating agents, combination chemotherapy regimens with 2-4 drugs, and high

involvement

designed for Hodgkin's disease, is used for NHL as evident above.

Stage II

Stage III

Stage IV

**7.3 Clinical features** 

**7.4 Treatment** 

et al., 2006). An increase in occurrence of DLBCL (10.2%), BL (27.8%) and CNSL (48.3%) was seen in individuals with AIDS during 1990-1995 (Shiels, et al., 2011). The 5-year survival rate improved from 1960 to the mid 1970s, but not much after that in the USA (Shiels, et al., 2011). NHL relates to congenital and acquired immunodeficiency diseases (Filipovich, et al., 1992). The relative risk of NHL in individuals with AIDS is about 150-250 in Western countries and over 1000 in children (Goedert, 2000).

### **7.2 Pathogenesis**

The head and neck regions are the most common sites for NHL, showing in 30-40% of cases (Economopoulos, et al., 1996). The neoplastic cells express CD20, CD79, BCL-2 and BCL-6, most of which are B-cell antigens (Hoefnagel, et al., 2003). The hallmark of B-cell malignancies is chromosomal translocation involving the immunoglobulin heavy chain (IGH) gene at band 14q32.33 with specific oncogene loci, referred to as the 14q32 translocation. Among these specific 14q32 translocations, *de novo* acute leukemia/lymphoma with c-MYC and/or BCL6 abnormalities in addition to t(14;18) was characterized by an extremely aggressive clinical course with nodal and/or extranodal involvement, and massive bone marrow infiltration(Kramer, et al., 1991). Incidence of IGH translocation on Bcell NHL has been reported in previous studies (Kramer, et al., 1998). Thus multiple involvement of the IGH gene in chromosomal rearrangements is associated with the pathogenesis and the progression of NHL.

Fig. 11. Histology of NUP lesion- Infiltration of Spirochetes into the Connective Tissue


Table 3. Ann Arbor Classification of Non-Hodgkin's Lymphomas (Rupniewska, 1979)

#### **7.3 Clinical features**

92 Global View of HIV Infection

et al., 2006). An increase in occurrence of DLBCL (10.2%), BL (27.8%) and CNSL (48.3%) was seen in individuals with AIDS during 1990-1995 (Shiels, et al., 2011). The 5-year survival rate improved from 1960 to the mid 1970s, but not much after that in the USA (Shiels, et al., 2011). NHL relates to congenital and acquired immunodeficiency diseases (Filipovich, et al., 1992). The relative risk of NHL in individuals with AIDS is about 150-250 in Western

The head and neck regions are the most common sites for NHL, showing in 30-40% of cases (Economopoulos, et al., 1996). The neoplastic cells express CD20, CD79, BCL-2 and BCL-6, most of which are B-cell antigens (Hoefnagel, et al., 2003). The hallmark of B-cell malignancies is chromosomal translocation involving the immunoglobulin heavy chain (IGH) gene at band 14q32.33 with specific oncogene loci, referred to as the 14q32 translocation. Among these specific 14q32 translocations, *de novo* acute leukemia/lymphoma with c-MYC and/or BCL6 abnormalities in addition to t(14;18) was characterized by an extremely aggressive clinical course with nodal and/or extranodal involvement, and massive bone marrow infiltration(Kramer, et al., 1991). Incidence of IGH translocation on Bcell NHL has been reported in previous studies (Kramer, et al., 1998). Thus multiple involvement of the IGH gene in chromosomal rearrangements is associated with the

Fig. 11. Histology of NUP lesion- Infiltration of Spirochetes into the Connective Tissue

countries and over 1000 in children (Goedert, 2000).

pathogenesis and the progression of NHL.

**7.2 Pathogenesis** 

Oral NHL lesions are often in disseminated disease states. The most common oral sites of involvement are the palate, tonsil, buccal mucosa, floor of the mouth, and the retromolar region. These lesions are non-tender, diffuse swellings usually involving the gingiva, buccal vestibule and posterior hard palate. Gnathic lesions arise from soft tissue invading the bony skeleton. One third of patients show fever, weight loss, adenopathy, night sweats, or hepatosplenomegaly. Oral lesions are fluctuant swellings showing ulceration, pain, tooth mobility and paresthesia when peripheral nerves are involved (Vega, et al., 2005). Salivary gland lymphomas account for approximately 3% of all salivary gland tumors (Barnes, et al., 1998). About 80% of the cases are reported in parotid gland, 16% in submandibular, 2% in sublingual and 2% in minor salivary glands. Affected bony areas show a "punched out" pattern that is due to multiple areas of destruction with ill defined radiolucent lesion. Involvement of the maxillary sinus will cause opacification with eroded cortical walls and associated sinus mass (Fukuda, et al., 1987). The Ann Arbor staging system, originally designed for Hodgkin's disease, is used for NHL as evident above.

#### **7.4 Treatment**

A prognostic index has been developed by the International NHL prognostic factors project based on data from 2,031 patients with aggressive lymphomas treated with regimens containing doxorubicin ("A Predictive Model for Aggressive Non-Hodgkin's Lymphoma," 1993). Analysis of 1274 patients younger than 60 years showed three clinical features independently associated with survival: serum LDL (lactate dehydrogenase) levels, tumor stage, and their performance status ("A Predictive Model for Aggressive Non-Hodgkin's Lymphoma," 1993). Past studies showed the importance of gallium-67 uptake in lymphomas as a useful prognostic indicator (Janicek, et al., 1997). The importance of prognostic index is that good-risk patients can be identified for standard therapy and poor-risk patients can be identified for new research protocols to improve the rate of therapy. With conventional therapy only 25% of patients who were gallium-positive midway through therapy had durable responses , while 70% of those who were gallium-negative remained free of disease (Janicek, et al., 1997). In patients with stage I or II disease, regional therapy leads to longterm control, with relapse rate of 44%-47% at 10 years and survival rates of 75% for patients younger than 60 years (Vaughan Hudson, et al., 1994). Stage III and IV patients can be treated by alkylating agents, combination chemotherapy regimens with 2-4 drugs, and high

Individuals with HIV/AIDS: Clinical Manifestations in the Oral Cavity in the Post-HAART Era 95

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#### **8. Conclusions**

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**6** 

**Epidemiology and Treatment of Kaposi's** 

**Sarcoma in HIV-1 Infected Individuals in a** 

*1Departments of Surgery, HIV Control Programme Ahmadu Bello University* 

*2Haematology and Blood Transfusion, HIV Control Programme Ahmadu Bello University* 

Kaposi's sarcoma was first described in 1872 by Moritz Kaposi, a Vienna-based Hungarian dermatologist, as a rare multifocal angioproliferative tumour involving blood and lymphatic vessels in elderly men of Jewish origin (Kaposi, 1872). Before the AIDS epidemic three clinico-epidemiological forms with similar histological features have been described. The classic Kaposi's sarcoma (KS) originally described by Kaposi is primarily a skin disease with a chronic indolent course that can sometimes regress spontaneously (Kaposi, 1872). Most of the cases occurred in elderly men of Mediterranean and Jewish origin. The African-endemic KS is seen in the indigenous population of sub-Saharan Africa (Franceschi & Geddes, 1995). It is also seen more commonly among male patients, but differs from the classic form in that it may affect a younger population and is more likely to spread to visceral organs and lymphatics. In addition, it has a variable clinical presentation ranging from a benign disease with few skin lesions to a widely disseminated disease associated with high morbidity and mortality (Franceschi & Geddes, 1995; Taylor et al 1971). Kaposi's sarcoma seen in patients as a result of immunosuppression complicating organ transplantation may have chronic or progressive course and spontaneous remission after discontinuation of immunosuppressive

The first description of AIDS-associated Kaposi's sarcoma (AAKS) was in 1981, when Friedman-Kien et al (1981) reported some previously healthy young homosexual men with Kaposi's sarcoma involving lymph nodes, viscera, and mucosa as well as skin. This was associated with life-threatening opportunistic infections and a profound defect in cellmediated immunity. This aggressive and frequently fatal form of Kaposi's sarcoma is the most common cancer in patients with HIV infection (Schwartz, 2004). Before the discovery and widespread use of highly active antiretroviral therapy (HAART) KS was over 20,000 times more common in AIDS patients than the general population (Engels et al 2006). However, several studies showed that HAART reduced the incidence of KS in high income countries (.Franceschi et al, 2008; Pipkin et al, 2011; Simard et al, 2011). The cumulative incidence of Kaposi sarcoma declined from 14.3% during 1980 to 1989, to 6.7% during 1990

therapy is observed in the majority of patients (Penn, 1979).

**1. Introduction** 

**Poor Resource Setting** 

Ahmed A.1 and Muktar H.M.2

*Teaching Hospital Zaria*

*Teaching Hospital Zaria* 

*Nigeria* 

