Apoptosis is a highly-regulated, active process of cell death involved in development, homeostasis and aging. Dysregulation of apoptosis leads to pathological states, such as cancer, developmental anomalies and degenerative diseases. Osteoarthritis (OA), the most common chronic joint disease in the elderly population, is characterized by progressive destruction of articular cartilage, resulting in significant disability. Because articular cartilage depends solely on its resident cells, the chondrocytes, for the maintenance of extracellular matrix, the compromising of chondrocyte function and survival would lead to the failure of the articular cartilage. The role of subchondral bone in the maintenance of proper cartilage matrix has been suggested as well, and it has been proposed that both articular cartilage and subchondral bone interact with each other in the maintenance of articular integrity and physiology. Some investigators include both articular cartilage and subchondral bone as targets for repairing joint degeneration. In late-stage OA, the cartilage becomes hypocellular, often accompanied by lacunar emptying, which has been considered as evidence that chondrocyte death is a central feature in OA progression. Apoptosis clearly occurs in osteoarthritic cartilage; however, the relative contribution of chondrocyte apoptosis in the pathogenesis of OA is difficult to evaluate, and contradictory reports exist on the rate of apoptotic chondrocytes in osteoarthritic cartilage. It is not clear whether chondrocyte apoptosis is the inducer of cartilage degeneration or a byproduct of cartilage destruction. Chondrocyte death and matrix loss may form a vicious cycle, with the progression of one aggravating the other, and the literature reveals that there is a definite correlation between the degree of cartilage damage and chondrocyte apoptosis. Because current treatments for OA act only on symptoms and do not prevent or cure OA, chondrocyte apoptosis would be a valid target to modulate cartilage degeneration.

Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis

Summary During chewing, food is reduced in size, while saliva moistens the food and binds the masticated food into a bolus that can be easily swallowed. Characteristics of the oral system, like number of teeth, bite force and salivary flow, will influence the masticatory process. Masticatory function of healthy persons has been studied extensively the last decades. These results were used as a comparison for outcomes of various patient groups. In this review, findings from literature on masticatory function for both healthy persons and patient groups are presented. Masticatory function of patients with compromised dentition appeared to be significantly reduced when compared with the function of healthy controls. The influence of oral rehabilitation, e.g. dental restorations, implant treatment and temporomandibular disorder treatment, on masticatory function will be discussed. For instance, implant treatment was shown to have a significant positive effect on both bite force and masticatory performance. Also, patient satisfaction with an implant-retained prosthesis was high in comparison with the situation before implant treatment. The article also reviews the neuromuscular control of chewing. The jaw muscle activity needed to break solid food is largely reflexly induced. Immediate muscle response is necessary to maintain a constant chewing rhythm under varying food resistance conditions. Finally, the influence of food characteristics on the masticatory process is discussed. Dry and hard products require more chewing cycles before swallowing than moist and soft foods. More time is needed to break the food and to add enough saliva to form a cohesive bolus suitable for swallowing.

Assessment of mastication with implications for oral rehabilitation: a review

Osteoarthritis is a common disease that can cause severe pain and dysfunction in any joint, including the temporomandibular joint (TMJ). TMJ osteoarthritis (TMJOA) is an important subtype in the classification of temporomandibular disorders. TMJOA pathology is characterized by progressive cartilage degradation, subchondral bone remodeling, and chronic inflammation in the synovial tissue. However, the exact pathogenesis and process of TMJOA remain to be understood. An increasing number of studies have recently focused on inflammation and remodeling of subchondral bone during the early stage of TMJOA, which may elucidate the possible mechanism of initiation and progression of TMJOA. The treatment strategy for TMJOA aims at relieving pain, preventing the progression of cartilage and subchondral bone destruction, and restoring joint function. Conservative therapy with nonsteroidal anti-inflammatory drugs, splint, and physical therapy, such as low-energy laser and arthrocentesis, are the most common treatments for TMJOA. These therapies are effective in most cases in relieving the signs and symptoms, but their long-term therapeutic effect on the pathologic articular structure is unsatisfactory. A treatment that can reverse the damage of TMJOA remains unavailable to date. Treatments that prevent the progression of cartilage degradation and subchondral bone damage should be explored, and regeneration for the TMJ may provide the ideal long-term solution. This review summarizes the current understanding of mechanisms underlying the pathogenesis and treatment of TMJOA.

Current Understanding of Pathogenesis and Treatment of TMJ Osteoarthritis

Osteoarthritis (OA) is a joint pathology characterized by progressive cartilage degradation. Medical care is mainly based on alleviating pain symptoms. Compelling studies report the presence of empty lacunae and hypocellularity in cartilage with aging and OA progression, suggesting that chondrocyte cell death occurs and participates to OA development. However, the relative contribution of apoptosis per se in OA pathogenesis appears complex to evaluate. Indeed, depending on technical approaches, OA stages, cartilage layers, animal models, as well as in vivo or in vitro experiments, the percentage of apoptosis and cell death types can vary. Apoptosis, chondroptosis, necrosis, and autophagic cell death are described in this review. The question of cell death causality in OA progression is also addressed, as well as the molecular pathways leading to cell death in response to the following inducers: Fas, Interleukin-1β (IL-1β), Tumor Necrosis factor-α (TNF-α), leptin, nitric oxide (NO) donors, and mechanical stresses. Furthermore, the protective role of autophagy in chondrocytes is highlighted, as well as its decline during OA progression, enhancing chondrocyte cell death; the transition being mainly controlled by HIF-1α/HIF-2α imbalance. Finally, we have considered whether interfering in chondrocyte apoptosis or promoting autophagy could constitute therapeutic strategies to impede OA progression.

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Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis.

Tissue-resident macrophages display varying phenotypic and functional properties that are largely specified by their local environment. One of these functions, phagocytosis, mediates the natural disposal of billions of cells, but its mechanisms and consequences within living tissues are poorly defined. Using a parabiosis-based strategy, we identified and isolated macrophages from multiple tissues as they phagocytosed blood-borne cellular material. Phagocytosis was circadianally regulated and mediated by distinct repertoires of receptors, opsonins, and transcription factors in macrophages from each tissue. Although the tissue of residence defined the core signature of macrophages, phagocytosis imprinted a distinct antiinflammatory profile. Phagocytic macrophages expressed CD206, displayed blunted expression of Il1b, and supported tissue homeostasis. Thus, phagocytosis is a source of macrophage heterogeneity that acts together with tissue-derived factors to preserve homeostasis.

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Phagocytosis imprints heterogeneity in tissue-resident macrophages.

Reducing dietary loading decreases mouse temporomandibular joint degradation induced by anterior crossbite prosthesis.

Background
Cartilage degradation is a typical characteristic of arthritis. This study examined whether there was a subset of phagocytic chondrocytes that expressed the specific macrophage marker, CD163, and investigated their role in cartilage degradation.

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The Identification of CD163 Expressing Phagocytic Chondrocytes in Joint Cartilage and Its Novel Scavenger Role in Cartilage Degradation

SUMMARY The aim of this study was to test the hypothesis that experimental and reversible changes of occlusion affect the levels of surface electromyographic (SEMG) activity in the anterior temporalis and masseter areas during unilateral maximal voluntary biting (MVB) in centric and eccentric position. Changes were achieved by letting 21 healthy subjects bite with and without a cotton roll between the teeth. The placement alternated between sides and between premolar and molar areas. The SEMG activity level was lower when biting in eccentric position without than with a cotton roll between teeth (P 0 AE05). In the anterior temporalis area, the balancing side SEMG activity was lower in eccentric than in centric but only in molar-supported biting (P =0 AE026). These results support that the masseter and anterior temporalis muscles have different roles in keeping the mandible in balance during unilateral supported MVB. Changes in occlusal stability achieved by biting with versus without a cotton roll were found

/pdf/semg-activity-of-jaw-closing-muscles-during-biting-with-u7y6pbpidu.pdf

SEMG activity of jaw-closing muscles during biting with different unilateral occlusal supports

Objectives To test whether changes in occlusal support differentially modulate masseter and anterior temporalis muscle electromyographic (EMG) activity during controlled maximal voluntary clenching Material and methods Forty-seven healthy subjects (32 M and 15 F, 229±13 years) were recruited Cotton-rolls were used to modify the occlusal contact relations and were positioned on the right, left, or both sides, and either in the molar or premolar regions, ie six different occlusal combinations Surface EMG activity was recorded bilaterally from the masseter and anterior temporalis area and normalized with respect to maximal voluntary clenching in the intercuspal position Analysis of variance and the paired t-test were used to test the data Results Normalized EMG activity was influenced by changes in cotton-roll modified occlusal support, and there were differences between muscles (p<0001) In general, EMG activity decreased in both muscles when occlusal support was moved from the molar to the pre

Influence of changing occlusal support on jaw-closing muscle electromyographic activity in healthy men and women.

Statement of problem. The temporomandibular joint (TMJ) disc is often observed to be thicker in temporomandibular disorder (TMD) patients. This clinical observation requires verification. Purpose. The purpose of this pilot study was to investigate whether the TMJ disc responds to dysfunctional occlusal changes by an increase in thickness. Material and methods. Twelve cadaver heads were divided into 2 groups, 1 with physiologically balanced occlusion (BO), 7 cadaver heads and 14 joints, and the other with physiologically nonbalanced occlusion (NO), 5 cadaver heads and 9 joints. The NO group had defining traits, such as reverse articulation or tightly locked occlusion. The latter is an occlusal relationship with drifted, tilted, and/or supraerupted teeth, often seen in patients who have lost posterior teeth. Histological sections from the lateral, center, and medial parts of the joints stained with haematoxylin and eosin were used for measuring the disc thickness. Student t tests and Bonferroni correction were used to compare groups (α=.05). Results. All 9 mean thickness values were higher in the NO than in the BO group. According to the t tests, the posterior band was thicker in the lateral ( P =.007) and center ( P =.015) sections, and the intermediate zone was thicker in the lateral section ( P =.008) in the NO than in the BO group. These differences were not significant after Bonferroni corrections. Conclusions. The results suggest that the TMJ disc has the ability to adapt to alteration of the space between condyle and fossa caused by occlusal changes. Further studies from larger groups should be undertaken. (J Prosthet Dent 2008;98:148-152)

Jian-Jun He

Papers

Reducing dietary loading decreases mouse temporomandibular joint degradation induced by anterior crossbite prosthesis.

The Identification of CD163 Expressing Phagocytic Chondrocytes in Joint Cartilage and Its Novel Scavenger Role in Cartilage Degradation

SEMG activity of jaw-closing muscles during biting with different unilateral occlusal supports

Influence of changing occlusal support on jaw-closing muscle electromyographic activity in healthy men and women.

The effect of physiological nonbalanced occlusion on the thickness of the temporomandibular joint disc: a pilot autopsy study.