Periodontitis arises from imbalanced host–microbe interactions, leading to dysbiosis and destructive inflammation. The host's innate and adaptive immune responses produce pro-inflammatory mediators that stimulate destructive events, which cause loss of alveolar bone and connective tissue attachment. There is no consensus on the factors that lead to a conversion from gingivitis to periodontitis, but one possibility is the proximity of the inflammation to the bone, which promotes bone resorption and inhibits subsequent bone formation during coupled bone formation. Conversely, orthodontic tooth movement is triggered by the mechanical force applied to the tooth, resulting in bone resorption on the compression side and new bone formation on the tension side. However, the environment around orthodontic brackets readily retains dental plaque and may contribute to inflammation and bone remodeling. The immune, epithelial, stromal, endothelial and bone cells of the host play an important role in setting the stage for bone remodeling that occurs in both periodontitis and orthodontic tooth movement. Recent advancements in single-cell RNA sequencing have provided new insights into the roles and interactions of different cell types in response to challenges. In this review, we meticulously examine the functions of key cell types such as keratinocytes, leukocytes, stromal cells, osteocytes, osteoblasts, and osteoclasts involved in inflammation- and mechanical force-driven bone remodeling. Moreover, we explore the combined effects of these two conditions: mechanical force-induced bone remodeling combined with periodontal disease (chronic inflammation) and periodontally accelerated osteogenic orthodontics (acute transient inflammation). This comprehensive review enhances our understanding of inflammation- and mechanical force-induced bone remodeling. © 2024 The Author(s). Periodontology 2000 published by John Wiley & Sons Ltd.