In the present study, we investigated the association between periodontitis and sarcopenia indicators (cHGS and SMMI), without using tooth loss as a proxy and taking common risk factors and demographic characteristics into consideration. The results indicated that both non-severe and severe periodontitis were significantly associated with cHGS but not with SMMI in adults below 60 years of age, after adjusting for covariates that were associates of muscle function and muscle metabolism as well as common risk factors of sarcopenia and periodontitis, such as diabetes mellitus, BMI, and smoking [41, 42].
A possible explanation of the association between the cHGS and periodontitis could be the reduced oral function and worsened nutrition as a result of tooth loss [43]. Although the reasons of tooth loss are often unspecified in most studies in the literature, periodontitis is a leading cause of tooth loss in adults [44]. Adults with tooth loss are at greater risk of malnutrition [45], a significant risk factor for sarcopenia and frailty [46].
Tooth mobility in periodontitis patients has been associated with a reduced bite force [47]. The reduced mechanoreceptive activity in the periodontal ligament can result in reduced periodontal support, which impairs the regulation of masticatory forces [48]. Function is an important predictor of muscle strength and skeletal and masticatory muscle endurance capacity [49]. Thus, reduced masticatory function due to periodontitis can contribute to oral hypofunction and sarcopenia [50]. A recent study reported that oral hypofunction was significantly associated with frailty [51]. In a study of a nationally representative cohort, participants with fewer than nine teeth showed significant associations with lower hand-grip strength in Korean men (OR: 1.39, 95% CI 1.03–1.88, mean age 72.9 ± 0.1) after adjusting for covariates [52]. In a study of 2,089 adult men and women between the ages of 30 and 90 in northern Germany, higher CAL was associated with lower handgrip strength [53]. In sarcopenic Korean adults, periodontitis prevalence was significantly higher compared to non-sarcopenic adults (30.3% vs. 18.3% in males, 45.9% vs. 17.4% in females, p < 0.001) [54]. The same study reported that having fewer than 20 teeth was associated with a higher incidence of sarcopenia in adults aged 65 years and older (OR 1.92 95% CI, 1.49–2.66 in men and OR 2.63 95% CI, 2.25–3.64 in women) [54].
Not only epidemiological studies but also in vivo experiments suggest that periodontitis may possibly be associated with muscle strength and mass. In an experimental ligature-induced periodontitis model, reduced strength, a reduced number of capillaries, and an increased number of inflammatory cells and fibroblasts in skeletal striated muscles were detected in immobilised Wistar rats with periodontitis compared to those without periodontitis, suggesting that periodontitis could possibly contribute to muscle atrophy [55]. In mice, the injection of the lipopolysaccharide of Porphyromonas (P.) gingivalis, a major periodontal pathogen, into the masseter and tibialis anterior muscles decreased muscle weight and increased fibrotic area and myocyte apoptosis eight-fold in the masseter muscle, mediated in part by the activation of the toll-like receptor 4 (TLR4)/extracellular signal-regulated kinase (ERK) pathway [56]. Oral administration of P. gingivalis also altered glucose uptake signalling and gene expression in soleus muscle tissue in mice, resulting in increased mRNA expression of tumour necrosis factor alpha (Tnfa), interleukin-6 (Il6), C-C motif chemokine 2 (Ccl2), and myogenin (Myog) compared to administration of saline [57]. Approximately 79% of periodontitis patients may harbour P. gingivalis [58], a highly virulent pathogen that can also invade peripheral tissues [59, 60], e.g., atherosclerotic plaques [61] and synovial fluids [62], and contribute to the pathogenesis of cardiovascular and rheumatic diseases [61, 63, 64].
The present study has several limitations. Firstly, there were relatively fewer participants in the severe periodontitis group compared to the non-severe periodontitis group, which may have influenced the results [65]. Secondly, a causal relationship between periodontitis and cHGS should not be inferred from this cross-sectional study design. Our cohort lacked participants with low SSMI or low cHGS, because the study population included only dentate U.S. adults below 60 years of age who underwent both a clinical periodontal examination and a whole-body DXA scan. Therefore, our results are only representative for the studied sub-cohort (n = 1,912), but not for the entire NHANES 2013–2014 cohort (n = 10,683). This affects the generalisation of the results and introduces selection bias. Despite these limitations, our results align with previous studies conducted in different populations and age groups that investigated the association between periodontitis proxies, i.e., tooth loss, and sarcopenia indicators.