Caffeine And Bone Loss

High daily caffeine intake can put people, especially women, at risk for bone loss,  Caffeine may decrease expression of the Vitamin D receptor and this may contribute to problems for bone formation and maintenance.  Abstract:

Of the various risk factors contributing to osteoporosis, dietary/lifestyle factors are important. In a clinical study we reported that women with caffeine intakes >300 mg/day had higher bone loss and women with vitamin D receptor (VDR) variant, tt were at a greater risk for this deleterious effect of caffeine. However, the mechanism of how caffeine effects bone metabolism is not clear. 1,25-Dihydroxy vitamin D(3) (1,25(OH)(2)D(3)) plays a critical role in regulating bone metabolism. The receptor for 1,25(OH)(2)D(3), VDR has been demonstrated in osteoblast cells and it belongs to the superfamily of nuclear hormone receptors. To understand the molecular mechanism of the role of caffeine in relation to bone, we tested the effect of caffeine on VDR expression and 1,25(OH)(2)D(3) mediated actions in bone. We therefore examined the effect of different doses of caffeine (0.2, 0.5, 1.0 and 10mM) on 1,25(OH)(2)D(3) induced VDR protein expression in human osteoblast cells. We also tested the effect of different doses of caffeine on 1,25(OH)(2)D(3) induced alkaline phosphatase (ALP) activity, a widely used marker of osteoblastic activity. Caffeine dose dependently decreased the 1,25(OH)(2)D(3) induced VDR expression and at concentrations of 1 and 10mM, VDR expression was decreased by about 50-70%, respectively. In addition, the 1,25(OH)(2)D(3) induced alkaline phosphatase activity was also reduced at similar doses thus affecting the osteoblastic function. The basal ALP activity was not affected with increasing doses of caffeine. Overall, our results suggest that caffeine affects 1,25(OH)(2)D(3) stimulated VDR protein expression and 1,25(OH)(2)D(3) mediated actions in human osteoblast cells.

Bone Structure Variation And Injury Risk

Does anatomical variation from person to person male some individuals more susceptible for particular kinds of injuries? Here is a study that says that glenoid bone structure can contribute to the risk of having anterior shoulder dislocation, abstract:

BACKGROUND:
Although increased retroversion of the glenoid has been shown to be an important factor in posterior instability of the shoulder, there are few studies reporting glenoid bone structure as a risk factor in anterior dislocation of the shoulder. This study aimed to compare glenoid version in patients with anterior dislocation of the shoulder and individuals in a control group with no shoulder problems before undergoing computed tomography and to assess a possible relationship between demographic characteristics and glenoid version angle.
METHODS:
The study group comprised 63 patients (12 women and 51 men; mean age, 35.71 years) with 1 or multiple unilateral anterior dislocations of the shoulder (dislocated group), whereas 63 individuals (11 women and 52 men; mean age, 35.38 years) with no history of shoulder complaints and no signs of instability constituted the control group. The glenoid version angle was measured on an axial cut of the computed tomography scan.
RESULTS:
The glenoid version angles on the dislocated side in the study group were significantly more anteverted than those of the dominant (P < .001) and nondominant (P = .023) shoulders of the control group. The version angles of dislocated shoulders significantly differed from those of nondislocated shoulders of both men (P = .041) and women (P = .049). There was no significant relationship between the glenoid version angle on the dislocated side and dislocation mechanism (P = .883), age group (P = .356), or number of dislocations (P = .971).
CONCLUSIONS:
Glenoid version is an important factor for the development of anterior dislocation of the shoulder.

You cannot change your inherent bone structure, but if you are aware of it – something that may be important particularly in athletes with a higher risk of certain injuries – you may take precautions to try and prevent those injuries for which you are particularly susceptible.

Cartilage Repair, Cell Signaling, And Osteoarthritis

Cartilage repair, aging, and osteoarthritis; new findings described here.  Cell signaling pathways are involved; modulating these pathways may be part of new, optimized treatments for this disease.  

Ageing processes play a major contributing role for the development of Osteoarthritis (OA). This prototypic degenerative condition of ageing is the most common form of arthritis and is accompanied by a general decline, chronic pain and mobility deficits. The disease is primarily characterized by articular cartilage degradation, followed by subchondral bone thickening, osteophyte formation, synovial inflammation and joint degeneration. In the early stages, osteoarthritic chondrocytes undergo phenotypic changes that increase cell proliferation and cluster formation and enhance the production of matrix-remodelling enzymes. In fact, chondrocytes exhibit differentiation plasticity and undergo phenotypic changes during the healing process. Current studies are focusing on unravelling whether OA is a consequence of an abnormal wound healing response. Recent investigations suggest that alterations in different proteins, such as TGF-ß/BMPs, NF-Kß, Wnt, and Cx43, or SASP factors involved in signalling pathways in wound healing response, could be directly implicated in the initiation of OA. Several findings suggest that osteoarthritic chondrocytes remain in an immature state expressing stemness-associated cell surface markers. In fact, the efficacy of new disease-modifying OA drugs that promote chondrogenic differentiation in animal models indicates that this may be a drug-sensible state. In this review, we highlight the current knowledge regarding cellular plasticity in chondrocytes and OA. A better comprehension of the mechanisms involved in these processes may enable us to understand the molecular pathways that promote abnormal repair and cartilage degradation in OA. This understanding would be advantageous in identifying novel targets and designing therapies to promote effective cartilage repair and successful joint ageing by preventing functional limitations and disability.

Wnt Signaling In Arthritis

http://www.mayoclinic.org/diseases-conditions/arthritis/home/ovc-20168903

A review on the role of Wnt signaling - often deregulated  in cancer particularly colon cancer - in arthritis can be found here. This is an example of the benefits of basic science research: first, by understanding Wnt signaling in general we better understand the diseases that exhibit aberrant forms of this signaling; second, by dissecting the finer details of how this signaling is controlled and what the downstream effects are, therapeutic interventions can be developed that targets this signaling to treat disease. Perhaps even preventive approaches can be devised as well. Arthritis may be another example of this pathway from lab bench to clinic. Abstract:

PURPOSE OF REVIEW:Arthritis defines a large group of diseases primarily affecting the joint. It is the leading cause of pain and disability in adults. Osteoarthritis (OA) affecting the knee or hip is the most common form among over 100 types of arthritis. Other types of arthritis include erosive hand OA, temporomandibular joint (TMJ) OA, facet joint OA, diffuse idiopathic skeletal hyperostosis (DISH), and spondyloarthritis (SpA). However, the specific molecular signals involved in the development and progression of OA and related forms of arthritis remain largely unknown. The canonical wingless/integrated (Wnt)/β-catenin signaling pathway could play a unique role in the pathogenesis of arthritis. In this review article, we will focus on the molecular mechanisms of Wnt/β-catenin signaling in the pathogenesis of OA and other types of arthritis.RECENT FINDINGS:Emerging evidence demonstrates that Wnts and Wnt-related molecules are involved in arthritis development and progression in human genetic studies and in vitro studies. Also, mouse models have been generated to determine the role of Wnt/β-catenin signaling in the pathogenesis of arthritis. Wnt/β-catenin signaling represents a unique signaling pathway regulating arthritis development and progression, and the molecules in this particular pathway may serve as targets for the therapeutic intervention of arthritis. Mediators and downstream effectors of Wnt/β-catenin signaling are increased in OA as well other forms of arthritis, including DISH and SpA. Through extensive investigations, including pre-clinical studies in transgenic mice and translational and human studies, the Wnt/β-catenin signaling pathway has been proven to play roles in bone and joint pathology by directly affecting bone, cartilage, and synovial tissue; further, these pathologies can be reduced through targeting this pathway. Continued investigation into the distinct molecular signaling of the Wnt/β-catenin pathway will provide additional insights toward the therapeutic intervention in arthritis.

Alternative Treatments For Musculoskeletal Pain

Physical therapists.  Citations for pictures at end of post.

Here is a refreshing article suggesting that instead of just prescribing medication, doctors should suggest exercise therapy and "psychosocial interventions" - a change from the 'quick fix" attitude of just popping a pill to solve very problem.  The conclusion of the abstract:

This review presents a comprehensive summary and critical assessment of current evidence for the treatment of pain presentations in primary care. The evidence synthesis of interventions for common musculoskeletal pain presentations shows moderate-strong evidence for exercise therapy and psychosocial interventions, with short-term benefits only from pharmacological treatments. Future research into optimal dose and application of the most promising treatments is needed.

Citations for pictures:

By _US_Navy_100723-N-7214P-020_Machinist's_Mate_Fireman_George_F._Avinger_practices_cone_drills_during_physical_therapy_in_the_Comprehensive_Combat_and_Complex_Casualty_Care_facility_at_Naval_Medical_Center_San_Diego.jpg: U.S. Navy photo by Mass Communication Specialist 1st Class Anastasia Puscian_US_Navy_090508-F-7885G-021_Staff_Sgt._Hugo_Reiner,_a_physical_therapy_craftsman_aboard_the_Military_Sealift_Command_hospital_ship_USNS_Comfort_(T-AH_20),_makes_a_wrist_brace_for_Teresa_De_la_Pena_during_a_Continuing_Promise_200.jpg: U.S. Air Force photo by Airman 1st Class Danielle GrannanUS_Navy_070917-N-8704K-072_Lt._Gwen_Smith,_attached_to_Military_Sealift_Command_hospital_ship_USNS_Comfort_(T-AH_20),_performs_physical_therapy_for_Marcus_Pryce_at_the_Arima_Health_Facility.jpg: U.S. Navy photo by Mass Communication Specialist 2nd Class Joshua Karsten_US_Navy_070706-N-8704K-101_Lt._Gwen_Smith,_attached_to_Military_Sealift_Command_hospital_ship_USNS_Comfort_(T-AH_20),_performs_physical_therapy_with_the_help_of_translator_Zoela_Armstrong_at_the_Paul_Brown_Arena.jpg: U.S. Navy photo by Mass Communication Specialist 2nd Class Joshua Karsten_US_Navy_081610-A-6522B-002_Physical_therapist_Lt._Cmdr._Mitchel_Ideue,_Officer_in_Charge_of_Inpatient_Services_at_Landstuhl_Regional_Medical_Center,_in_Landstuhl,_Germany,_gives_Army_Sgt._Charlie_McCall_a_physical_therapy_trea.jpg: U.S. Navy photo_US_Navy_091003-N-8960W-011_Gunner's_Mate_2nd_Class_Patrick_Cornwell_undergoes_an_exam_by_Lt._Cristi_Zohlen_to_document_his_shoulder_pain_in_the_physical_therapy_clinic_aboard_the_aircraft_carrier_USS_Nimitz_(CVN_68).jpg: U.S. Navy photo by Mass Communication Specialist Seaman Apprentice Robert Winn_US_Navy_020128-N-6077T-008_CVN_74_crew_member_receives_medical_treatment_aboard_ship.jpg: U.S. Navy photo by Photographer’s Mate 1st Class Kevin H. Tierneyderivative work: Jnyles (talk) - _US_Navy_100723-N-7214P-020_Machinist's_Mate_Fireman_George_F._Avinger_practices_cone_drills_during_physical_therapy_in_the_Comprehensive_Combat_and_Complex_Casualty_Care_facility_at_Naval_Medical_Center_San_Diego.jpg_US_Navy_090508-F-7885G-021_Staff_Sgt._Hugo_Reiner,_a_physical_therapy_craftsman_aboard_the_Military_Sealift_Command_hospital_ship_USNS_Comfort_(T-AH_20),_makes_a_wrist_brace_for_Teresa_De_la_Pena_during_a_Continuing_Promise_200.jpgUS_Navy_070917-N-8704K-072_Lt._Gwen_Smith,_attached_to_Military_Sealift_Command_hospital_ship_USNS_Comfort_(T-AH_20),_performs_physical_therapy_for_Marcus_Pryce_at_the_Arima_Health_Facility.jpg_US_Navy_070706-N-8704K-101_Lt._Gwen_Smith,_attached_to_Military_Sealift_Command_hospital_ship_USNS_Comfort_(T-AH_20),_performs_physical_therapy_with_the_help_of_translator_Zoela_Armstrong_at_the_Paul_Brown_Arena.jpg_US_Navy_081610-A-6522B-002_Physical_therapist_Lt._Cmdr._Mitchel_Ideue,_Officer_in_Charge_of_Inpatient_Services_at_Landstuhl_Regional_Medical_Center,_in_Landstuhl,_Germany,_gives_Army_Sgt._Charlie_McCall_a_physical_therapy_trea.jpg_US_Navy_091003-N-8960W-011_Gunner's_Mate_2nd_Class_Patrick_Cornwell_undergoes_an_exam_by_Lt._Cristi_Zohlen_to_document_his_shoulder_pain_in_the_physical_therapy_clinic_aboard_the_aircraft_carrier_USS_Nimitz_(CVN_68).jpg_US_Navy_020128-N-6077T-008_CVN_74_crew_member_receives_medical_treatment_aboard_ship.jpg, Public Domain, https://commons.wikimedia.org/w/index.php?curid=14511419