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Oral malodor or halitosis is a condition characterized by unpleasant odors emanating from the oral cavity. The aim of the present review is to classify and explain the etiology and pathogenesis of oral malodor. Volatile sulfur compounds (VSCs) that result from bacterial breakdown of protein are considered to be the main culprits for this foul odor. The etiology of oral malodor can be attributed to both systemic and oral conditions. However, nearly 85% of the cases originate from mouth due to tongue coating (especially posterior third of the dorsal surface), periodontal disease, poor oral hygiene, infections, ulcerations, food debris, dry mouth and faulty restorations. Bad breath can be caused by systemic disorders such as upper and lower respiratory tract infections; hepatic, pancreatic, and nephritic insufficiencies; trimethylaminuria and some medications. In addition, there are very few instances where patients suffer from pseudohalitosis or halitophobia.

Introduction: The usage of Calcium hydroxide (CaOH2) has wide applications due to the property of osteo-inductive, protective, and antibacterial actions. However, it is not used in primary teeth, as it fails to form reparative dentin and the exact mechanism has not been explained. The hypothesis: The authors propose an explanation that lack of dentin bridge formation in response to (CaOH2) in primary teeth could be multifactorial: inability of the deciduous stem cells to generate complete dentin-pulp-like tissue; the absence of calcium-magnesium-dependent adenosine triphosphatase (Ca-Mg ATPase) in the odontoblasts; the pre-existing predilection of deciduous dentine pulp to form odontoclasts; the solubility of (CaOH2). Evaluation of the hypothesis: The hypothesis discusses the innate traits of the deciduous stem cells that lack the ability to form the dentin bridge, the absence of Ca-Mg ATPase enzyme and increased solubility of (CaOH2) together fail to stimulate the odontoblasts. Alternatively, pre-existing progenitor cells with proclivity to change into odontoclasts may cause internal resorption and hamper formation of reparative dentin.

The dental clinician frequently comes across lesions that involve the hard and soft tissues of the oral cavity. Most of these conditions do not pose a diagnostic problem for the dental surgeon. However, the clinical dentist is sometimes accosted with a lesion, the diagnosis of which is not only challenging, but influencing the choice of treatment. This review article provides a systematic and logical approach for diagnosing common lesions encountered in the dental practice.

Introduction: Calcium hydroxide (CaH) is customarily used for permanent teeth but not for deciduous dentition because it is known to cause internal resorption in the latter. Though this has been attributed to chronic inflammation and odontoclasts, the exact mechanism has not been elucidated. The Hypothesis: The authors propose an explanation that CaH-induced odontoclastogenesis could be multifactorial. Odontoclasts may result from fusion of cells of monocyte/macrophage series either due to inflammatory mediators or through stimulation by stromal odontoblasts /fibroblasts. Pre-existing progenitor cells of primary tooth pulp because of their inherent propensity may transform into odontoclasts. Evaluation of the Hypothesis: The hypothesis discusses the role of various inflammatory cytokines that may be responsible for CaH-induced transformation of pre-odontoclasts to odontoclasts. Alternatively, pre-existing progenitor cells with proclivity to change into odontoclasts may cause internal resorption. The loss of protective layer of predentin over mineralized dentin may also make the primary tooth more susceptible to resorption.

Background. Sebaceous carcinoma (SC) is an uncommon cutaneous malignancy, usually occurring predominantly in the eyelids and only occasionally involving the oral cavity. Sebaceous carcinoma (SC) is a rare malignancy. Only 10 cases of sebaceous carcinoma of the oral cavity have been reported so far. Case Presentation. A 40-year-old female presented with a mass on the left side of the middle third of the face. Radiographic findings were inconclusive. Resection of the mass was consistent with the diagnosis of primary sebaceous carcinoma. Conclusion. Intraoral sebaceous carcinoma is uncommon. Due to its varied clinical appearance and presence of a diverse histopathologic appearance, the diagnosis is quite often confounding and elusive. Hence, it is imperative to familiarize oneself about various aspects of this rare tumor for earlier diagnosis, to improve the chances of patient’s survival.