Differential diagnosis of calcium pyrophosphate dihydrate deposition of the temporomandibular joint

Calcium pyrophosphate dihydrate (CPPD) deposition disease (pseudogout) of the temporomandibular joint (TMJ) is rare. It is characterized by the presence of crystal deposits that are birefringent under polarized light. Although these crystals are characteristically weakly birefringent, some other crystals such as those of calcium oxalate, synthetic steroids, and ethylenediaminetetraacetic acid are also birefringent. The differential diagnosis should therefore be based on a quantitative analysis of crystals or observation of the crystal structure in calcified sections. We present a case of CPPD deposition disease of the TMJ and report on the value of such an analysis to substantiate the diagnosis.     

Arthroscopic removal of nodules of synovial chondromatosis of the temporomandibular joint

In this report we describe a new method for removing nodules of TMJ synovial chondromatosis using arthroscopic surgery instead of open surgery. We used two steps during arthroscopy. In the first, we lavaged the cavity with sterile saline. In the next step, the second cannula was replaced with ethmoid forceps. Under arthroscopic guidance through the first cannula, all loose bodies were removed using the forceps. Since the loose bodies are not fragmented during this procedure, the time needed for removal is shortened. Based on this experience, we suggest the use of ethmoid forceps should be considered as an alternative procedure when nodules are unable to pass through the cannula by lavage with sterile saline.     

Clinical evaluation of the temporomandibular joint following orthognathic surgery--multiple logistic regression analysis

This study compares temporomandibular joint dysfunction (TMD) symptoms before and after bilateral sagittal split ramus osteotomy, and identifies predictive factors for the postoperative TMD symptoms by assessing the adjusted odds ratio using multiple logistic regression analysis. A consecutive series of 37 cases treated only with bilateral sagittal split ramus osteotomy were evaluated. New postoperative TMD symptoms appeared in 9 cases, preoperative TMD symptoms disappeared in 6 cases, and TMD symptoms were unchanged in 5 cases. The median period until the interincisal opening range attained 40 mm was 5 months (range, from 2 to 15 months). Age was a positive factor in patients with postoperative TMD symptoms, with an odds ratio of 1.43 (95 percent confidence interval, from 1.05 to 1.93). In addition, the maximum value of the bilateral setback distance of more than 9 mm was a positive factor of 6.95 (95 percent confidence interval, from 1.06 to 45.42). We concluded that surgical correction in skeletal malocclusion may affect temporomandibular joint dysfunction symptoms.     

Teeth contacting habit as a contributing factor to chronic pain in patients with temporomandibular disorders

Many different factors are known to cause and perpetuate the symptoms of temporomandibular disorders (TMD). However, the roles of parafunctional factors have not been clearly elucidated. We found one of these habits in the clinical setting. This parafunctional habit involves daily light touching of the upper and lower teeth, when the mouth is closed. We named this habit Teeth Contacting Habit (TCH). [OBJECTIVES] To investigate the following hypotheses: 1) TCH is associated with perpetuation of chronic pain of TMD patients; 2) TCH is associated with other behavioral factors. [METHODS] Two hundred and twenty-nine TMD outpatients with chronic pain were analyzed with multivariate logistic regression models. [RESULTS] TCH was found in 52.4% of patients. Patients with TCH and pain lasting for more than four months were less likely to experience improvements in pain at the first visit (OR = 1.944, p = 0.043). Other factors associated with TCH were as follows: unilateral chewing (OR = 2.802) and involvement in a precision job (OR = 2.195). [CONCLUSION] TCH can prolong TMD pain and is associated with other behavioral factors.     

Immunohistochemical characterization of CD33 expression on microglia in Nasu‐Hakola disease brains

Nasu‐Hakola disease (NHD) is a rare autosomal recessive disorder, characterized by formation of multifocal bone cysts and development of leukoencephalopathy, caused by genetic mutations of either DNAX‐activation protein 12 (DAP12) or triggering receptor expressed on myeloid cells 2 (TREM2). Although increasing evidence suggests a defect in microglial TREM2/DAP12 function in NHD, the molecular mechanism underlying leukoencephalopathy with relevance to microglial dysfunction remains unknown. TREM2, by transmitting signals via the immunoreceptor tyrosine‐based activation motif (ITAM) of DAP12, stimulates phagocytic activity of microglia, and ITAM signaling is counterbalanced by sialic acid‐binding immunoglobulin (Ig)‐like lectins (Siglecs)‐mediated immunoreceptor tyrosine‐based inhibitory motif (ITIM) signaling. To investigate a role of CD33, a member of the Siglecs family acting as a negative regulator of microglia activation, in the pathology of NHD, we studied CD33 expression patterns in five NHD brains and 11 controls by immunohistochemistry. In NHD brains, CD33 was identified exclusively on ramified and amoeboid microglia accumulated in demyelinated white matter lesions but not expressed in astrocytes, oligodendrocytes, or neurons. However, the number of CD33‐immunoreactive microglia showed great variability from case to case and from lesion to lesion without significant differences between NHD and control brains. These results do not support the view that CD33‐expressing microglia play a central role in the development of leukoencephalopathy in NHD brains.     

Regulation of sterol carrier protein 2 (SCP2) gene expression in rat peritoneal macrophages during foam cell formation. A key role for free cholesterol content.

Sterol carrier protein 2 (SCP2) has been shown to be involved in intracellular transport and metabolism of cholesterol. However, there have been no reports concerning SCP2 in macrophages, the major source of atheromatous foam cells. We investigated whether SCP2 is present in rat peritoneal macrophages and determined the changes of SCP2 and its mRNA levels in macrophages during form cell formation induced by acetylated LDL (AcLDL). Immunoblot analysis and Northern blot analysis demonstrated that both SCP2 and its mRNA are expressed in rat peritoneal macrophages. Incubations with AcLDL caused a dose- and time-dependent increase of cellular esterified cholesterol, SCP2 and its mRNA in rat peritoneal macrophages. The inhibitor of acyl-CoA:cholesterol acyltransferase further enhanced AcLDL-induced increase of SCP2 protein and its mRNA. Incubations with 25-hydroxy cholesterol also caused a dose-dependent stimulation of SCP2 gene expression in macrophages, while incubation with maleylated BSA had no effect. These results suggest that the increment of cellular-free cholesterol is responsible for enhanced SCP2 gene expression in macrophages. The enhancement of SCP2 gene expression by AcLDL suggests that SCP2 may play an important role during foam cell formation induced by AcLDL which may be most important step for the atherosclerosis.     

An immunomodulating protein,Ling Zhi-8 (LZ-8) prevents insulitis in non-obese diabetic mice

Summary Ling Zhi-8 (LZ-8), a novel and recently discovered immunomodulatory protein having in vivo immunosuppressive activity, was tested for in vivo effect against Type 1 (insulin-dependent) diabetes mellitus in the non-obese diabetic mouse, the disease having immunologically mediated aetiology in this animal. LZ-8 had mitogenic activity in vitro towards spleen cells of the non-obese diabetic mice as previously shown towards those of DBA/2 mice. Intraperitoneal administration of LZ-8 twice weekly into the mice (10.3–12.6 mg/kg body weight) from 4 weeks of age prevented insulitis and an almost normal number of insulin producing cells were observed. Extreme insulitis and reduction of the number of insulin producing cells were observed in the pancreata of the untreated non-obese diabetic mouse. No cumulative incidence of diabetes mellitus was observed in the LZ-8 treated group, while cumulative incidences of 70% and 60% were observed in an untreated group followed up to 42 weeks of age when the incidence of diabetes was defined as a plasma glucose level of greater than 11 mmol/l and as a urine glucose level of greater than 2 +, respectively. T cell subset population analysis was performed to further investigate the action of LZ-8 on the non-obese diabetic mouse which revealed that LZ-8 treatment increased in L3T4⁺/Lyt-2⁺ ratio.