This study, indicating significant correlations between body composition and periodontal disease (with WHR being the most significant, followed by BMI, FFM, and S), showed similarities to those observed in other obesity-related health problems. This strengthened arguments that periodontal disease and certain obesity-related systemic illnesses are related, with abnormal fat metabolism possibly being an important factor.

Gingival concentrations of IL-11 and IL-17 are different in diseased gingiva adjacent to 3, 4 to 5, and > or = 6 mm pockets, suggesting that their concentrations change as a consequence of the progression of gingivitis to periodontitis and that both cytokines could have a significant role in this progression. These data may be useful for the design of procedures for prevention of periodontal disease.

Fibrous dysplasia has been regarded as a developmental skeletal disorder characterized by replacement of normal bone with benign cellular fibrous connective tissue. It has now become evident that fibrous dysplasia is a genetic disease caused by somatic activating mutation of the Gsα subunit of G protein-coupled receptor resulting in upregulation of cAMP. This leads to defects in differentiation of osteoblasts with subsequent production of abnormal bone in an abundant fibrous stroma. In addition there is an increased production of IL-6 by mutated stromal fibrous dysplastic cells that induce osteoclastic bone resorption.

Human papillomavirus (HPV) is widespread and can cause latent infection in basal cells, with low HPV DNA copy-number insufficient for transmission of infection; can cause subclinical infection that is active but without clinical signs; or can cause clinical infection leading to benign, potentially malignant or malignant lesions. The HPV cycle is influenced by the stage of maturation of the infected keratinocytes, and the production of virions is restricted to the post-mitotic suprabasal epithelial cells where all the virus genes are expressed.Low-risk HPV genotypes are associated with the development of benign oral lesions, whereas high-risk HPV genotypes are implicated in the development of malignant epithelial neoplasms. The rôle of high-risk HPV as a causative agent in epithelial malignancy is different at different anatomical sites: it is almost invariably implicated in squamous cell carcinoma of the uterine cervix, fairly frequently implicated in squamous cell carcinoma of the oropharynx, and it is seldom implicated in squamous cell carcinoma of the mouth.

Human papillomavirus (HPV) infection of the mouth and oropharynx can be acquired by a variety of sexual and social forms of transmission. HPV-16 genotype is present in many oral and oropharyngeal squamous cell carcinomata. It has an essential aetiologic role in the development of oropharyngeal squamous cell carcinoma in a subset of subjects who are typically younger, are more engaged with high-risk sexual behaviour, have higher HPV-16 serum antibody titer, use less tobacco and have better survival rates than in subjects with HPV-cytonegative oropharyngeal squamous cell carcinoma. In this subset of subjects the HPV-cytopositive carcinomatous cells have a distinct molecular profile.In contrast to HPV-cytopositive oropharyngeal squamous cell carcinoma, the causal association between HPV-16 and other high-risk HPV genotypes and squamous cell carcinoma of the oral mucosa is weak, and the nature of the association is unclear.It is likely that routine administration of HPV vaccination against high-risk HPV genotypes before the start of sexual activity will bring about a reduction in the incidence of HPV-mediated oral and oropharyngeal squamous cell carcinoma.This article focuses on aspects of HPV infection of the mouth and the oropharynx with emphasis on the link between HPV and squamous cell carcinoma, and on the limitations of the available diagnostic tests in identifying a cause-and-effect relationship of HPV with squamous cell carcinoma of the mouth and oropharynx.