No previously published studies have reported on the placement and restoration of dental implants in a patient diagnosed with sarcoidosis. Patients with sarcoidosis may develop periodontitis as a manifestation of systemic disease and are therefore at increased risk of tooth loss. These patients are likely to want fixed dental prostheses, which may need to be supported by dental implants. The case presented is that of a 31-year-old female patient presenting with a missing maxillary central incisor and a sarcoidal process affecting the anterior maxilla, which had severely compromised the periodontium of the adjacent lateral incisor. The patient was successfully rehabilitated with an implant-retained prosthesis following a staged horizontal and vertical bone augmentation procedure. At the 4-year review, the implant restoration performed well with stable peri-implant bone levels. We conclude that dental implant rehabilitation in patients with sarcoidosis may be a predictable treatment option, depending on disease stability and concurrent systemic therapy, but these patients will require additional maintenance because of the possibility of an increased risk of peri-implantitis. The effects of sarcoidosis and its management on the success of dental implants are discussed to aid treatment planning for such patients.

Sarcoidosis is a granulomatous disorder of unknown etiology that can affect multiple organ systems.1  It is characterized by the formation of noncaseating granulomata, and although 20% of sufferers are asymptomatic, there is a 4% to 10% fatality rate due to pulmonary, cardiac, or central nervous system complications.2  The incidence of sarcoidosis ranges from 15 to 53 cases/100 000 and is higher among women3  and those of Afro-Caribbean decent.1  The peak age is 20 to 40 years, with a second peak occurring in individuals older than 50 years.2,4 

The pathogenesis of sarcoidosis is an uncontrolled and upregulated local cell-mediated immune response against an unknown “sarcoidal antigen.” The affected tissues are infiltrated by lymphocytes, monocytes, and macrophages, which secrete biological mediators (interleukin-2, interleukin-12, interferon-c, and tumor necrosis factor–α) that in turn induce the formation of noncaseating granulomata.5  Several infectious agents610  and environmental agents11  have been implicated; however, certain genetic polymorphisms are also involved,12  and these complex interactions likely influence the clinical manifestation, natural course, and response to treatment.13 

The disease may have an acute or chronic nature with general symptoms of dry cough, dyspnea and chest discomfort, fever, fatigue, anorexia, weight loss, polyarthritis, visual problems, and skin lesions; the latter frequently occur on the face.2  The skeletal system is affected in up to 39% of patients, with intraosseous lesions commonly involving the phalanges, metatarsals, and metacarpals.2,14  The head and neck region is affected in 10% to 15% of all cases of sarcoidosis, with the parotid salivary glands most commonly affected (3–4%15), resulting in enlargement and xerostomia, as well as the lacrimal glands, which may result in keratoconjunctivitis sicca. Sixty percent of minor salivary glands show noncaseating granulomata on biopsy in patients affected by sarcoidosis.2,16,17 

The diagnosis of sarcoidosis is usually established with a combination of clinical and histopathological features, but for many patients, systemic treatment is not necessary.18  Patients with symptoms are generally managed with corticosteroids,19  but alternative and adjunctive treatments for chronic or refractory disease include chloroquine, hydroxychloroquine, methotrexate, azathioprine, pentoxifylline, thalidomide, cyclophosphamide, cyclosporine, and inFLIXimab.1 

The aim of this article is to report on the rehabilitation of a patient, diagnosed with sarcoidosis, with a dental implant–supported prosthesis. The assessment, preprosthetic surgery, implant placement, restoration, and follow-up are described.

Examination and investigations

A 31-year-old female patient was referred to the Department of Restorative Dentistry of the Royal London Dental Hospital by her general dental practitioner for rehabilitation of the missing maxillary left central incisor (tooth 9) in March 2011 as she was unhappy with her current removable partial dental prosthesis.

She reported a history of an ectopic tooth No. 9, which was surgically exposed and bonded for orthodontic traction at the age of 10 years. The root underwent resorption, and the tooth was extracted at the age of 14. She had noticed a significant change in the alveolus around region No. 9 and was now also complaining of increased mobility in the maxillary left lateral incisor (tooth No. 10). The patient had been diagnosed with pulmonary sarcoidosis in January 2010 but was not undergoing active treatment. She was a nonsmoker and took no prescribed medications.

Clinical examination (Figure 1) revealed a minimally restored dentition, a medium smile line, and thin gingival biotype. Tooth No. 10 was diminutive, grade 2 mobile, had 4-mm labial and 8-mm mesial gingival recession, and tested positive to sensibility testing. The edentulous region of No. 9 was wider than that of the maxillary right central incisor (tooth No. 8), and there was severe vertical and horizontal alveolar ridge deficiency in No. 9 region. Tooth No. 8 was of normal proportions with 2-mm mesial gingival recession. The maxillary left canine (tooth No. 11) was missing at the time of assessment, and the patient did not recall why. An acrylic tissue-supported partial removable dental prosthesis replaced tooth No. 9; the prosthetic tooth was 2-mm shorter than that of tooth No. 8 and had a large pink acrylic flange replacing the missing hard and soft tissues.

Figures 1–5.

Figure 1. At presentation. (a) Without prosthesis. (b). With prosthesis. (c) Horizontal bone deficiency. (d) Vertical bone deficiency. Figure 2. Preoperative periapical radiographs. (a, b) Ill-defined radiolucency in the anterior maxilla and almost 100% bone loss around tooth No. 10. Figure 3. Preoperative orthopantograph. Figure 4. Preoperative cone-beam computerized tomography with a radiographic stent in situ showing an osteolytic area consistent with intraosseous sarcoidosis. (a) Coronal slice. (b) Axial slice. (c) Sagittal slice though No. 21 position. (d) Sagittal slice though No. 10 region. Figure 5. Temporization. A metal-ceramic fixed resin-bonded dental prosthesis replacing teeth Nos. 9 and 10 following extraction of tooth No. 10; pink porcelain is replacing the missing hard and soft tissues.

Figures 1–5.

Figure 1. At presentation. (a) Without prosthesis. (b). With prosthesis. (c) Horizontal bone deficiency. (d) Vertical bone deficiency. Figure 2. Preoperative periapical radiographs. (a, b) Ill-defined radiolucency in the anterior maxilla and almost 100% bone loss around tooth No. 10. Figure 3. Preoperative orthopantograph. Figure 4. Preoperative cone-beam computerized tomography with a radiographic stent in situ showing an osteolytic area consistent with intraosseous sarcoidosis. (a) Coronal slice. (b) Axial slice. (c) Sagittal slice though No. 21 position. (d) Sagittal slice though No. 10 region. Figure 5. Temporization. A metal-ceramic fixed resin-bonded dental prosthesis replacing teeth Nos. 9 and 10 following extraction of tooth No. 10; pink porcelain is replacing the missing hard and soft tissues.

Close modal

Periapical radiographs (Figure 2), an orthopantomograph (Figure 3), and cone-beam computerized tomography (CBCT; Figure 4) were taken, which showed root resorption of tooth No. 10 and the maxillary left first premolar (No. 12) and evidence of an abnormal bone pattern in the anterior maxilla extending from the midline to tooth No. 12. This abnormal region had loss of definition of the cancellous bone and loss of the outline of both the buccal and palatal cortices. When reviewed by a consultant oral and maxillofacial radiologist, the appearance was considered to be consistent with previously described osteolytic areas affected by a sarcoidal process.2,17 

Treatment

A bone biopsy from region No. 9 was carried out by the Department of Oral Surgery, which, following histopathologic analysis, confirmed nonnecrotizing granulomatous inflammation indicating sarcoid changes in the maxillary bone.

The prognosis for tooth No. 10 was considered hopeless, and therefore it was extracted and the patient provided with a provisional metal-ceramic fixed resin-bonded dental prosthesis (RBP) replacing teeth Nos. 9 and 10, with teeth Nos. 8 and 12 as abutments (Figure 5).

Two months later, staged bone augmentation surgery was carried out (Figure 6). Cortico-cancellous bone allografts (RM·BB, Rocky Mountain Tissue Bank, Aurora, Colo) were used for vertical and horizontal augmentation of regions No. 9 and 10, with the 2 interproximal bone peaks at teeth Nos. 8 and 12 used as the vertical limit for the augmentation. The blocks were soaked for 10 minutes in an rhPDGF growth factor (Gem 21S, Osteohealth Company, Luitpold Pharmaceuticals, Shirley, NY) before stabilization with bone fixation screws. The overlying flap was deficient when attempting primary closure owing to the substantial increase in the horizontal and vertical dimension. Consequently, a porcine soft-tissue matrix (Geistlich Mucograft, Geistlich, Wolhusen, Switzerland) was used palatally in anticipation of possible flap dehiscence during healing. The flaps were approximated using a single horizontal mattress and multiple single interrupted sutures using 5-0 and 6-0 nylon and polytetrafluoroethylene sutures.

Figures 6 and 7.

Figure 6. Hard-tissue augmentation. (a) Muco-periosteal flap raised showing extensive vertical and horizontal bone resorption. (b) Vertical limits identified as interproximal alveolar crests. (c) Prepared allograft. (d) Stabilization with bone fixation screws. (e) Placement of porcine collagen matrix and membrane. (f) Primary closure. Figure 7. Flap dehiscence. (a) Two weeks postoperation. (b) Four weeks postoperation.

Figures 6 and 7.

Figure 6. Hard-tissue augmentation. (a) Muco-periosteal flap raised showing extensive vertical and horizontal bone resorption. (b) Vertical limits identified as interproximal alveolar crests. (c) Prepared allograft. (d) Stabilization with bone fixation screws. (e) Placement of porcine collagen matrix and membrane. (f) Primary closure. Figure 7. Flap dehiscence. (a) Two weeks postoperation. (b) Four weeks postoperation.

Close modal

The patient was prescribed co-amoxiclav 3 times per day (TDS) for 7 days, ibuprofen 400 mg TDS for 7 days, chlorhexidine 0.2% mouth rinse 4 times per day (QDS), and dexamethasone 10 mg, 8 mg, 6 mg, and 4 mg as a tapering daily dose. The provisional RBP was adjusted and recemented. As anticipated, flap dehiscence was noted 2 weeks later along the palatal edge of the flap, exposing the underlying soft-tissue matrix (Figure 7). However, the matrix healed uneventfully with full epithelialization during the ensuing 10 days.

After 5 months of healing time, the CBCT scan was repeated to confirm the volume of augmented bone (Figure 8). The bone width and height allowed planning of 2 implant fixtures (Straumann, Institut Straumann AG, Basel, Switzerland) to replace teeth Nos. 9 and 10 (Figure 9).

Figures 8 and 9.

Figure 8. Preimplant cone-beam computerized tomography (CBCT) demonstrating an increase in the volume of the alveolar ridge 6 months after staged augmentation. Because of the metal artifact from the bone screws, it was not possible to reliably measure the bone width. Incidentally, bone trabeculation now looks normal in comparison with the preoperative CBCT or periapical radiographs. (a–c) Axial slices. (d–f) Coronal slices. Figure 9. Digital implant planning with 4.1-mm diameter implant for tooth No. 9 and 3.3-mm for tooth No. 10 using CBCT taken 2 weeks before implant placement. (a) Sagittal slices with implant planning overlay at site No. 9. (b) Coronal slice with implant planning overlay for sites No. 9 and 10. (c) Axial slice with implant planning overlay for sites No. 9 and 10. (d) Sagittal slices with implant planning overlay at site No. 10. (e) Orthopantomograph view with implant planning overlay. (f) Three-dimensional reconstruction with implant planning overlay.

Figures 8 and 9.

Figure 8. Preimplant cone-beam computerized tomography (CBCT) demonstrating an increase in the volume of the alveolar ridge 6 months after staged augmentation. Because of the metal artifact from the bone screws, it was not possible to reliably measure the bone width. Incidentally, bone trabeculation now looks normal in comparison with the preoperative CBCT or periapical radiographs. (a–c) Axial slices. (d–f) Coronal slices. Figure 9. Digital implant planning with 4.1-mm diameter implant for tooth No. 9 and 3.3-mm for tooth No. 10 using CBCT taken 2 weeks before implant placement. (a) Sagittal slices with implant planning overlay at site No. 9. (b) Coronal slice with implant planning overlay for sites No. 9 and 10. (c) Axial slice with implant planning overlay for sites No. 9 and 10. (d) Sagittal slices with implant planning overlay at site No. 10. (e) Orthopantomograph view with implant planning overlay. (f) Three-dimensional reconstruction with implant planning overlay.

Close modal

In April 2013, implant placement was carried out 6 months after augmentation (Figure 10). Buccal and vertical graft resorption was noted; nevertheless, sufficient bone volume was maintained for implant placement in a prosthetically acceptable position despite preoperative severe ridge atrophy.

Figures 10–12.

Figure 10. Implant placement. (a) Preoperative view. (b) Healed bone graft prior to removal of fixation screws with both vertical and horizontal resorption. (c) Implant placement in an ideal buccopalatal position. (d) Fenestration and dehiscence around the implants. (e) Placement of particulate bone xenograft. (f) Placement of collagen matrix. Figure 11. Immediate postoperative radiograph showing good angulation and height 1 mm below the alveolar crest. Figure 12. Apically repositioned flap 3 months after implant placement. (a) Preoperative view. (b) Incision. (c) Partial-thickness flap. (d) Placement of allograft, which was stabilized with sutures but left completely exposed.

Figures 10–12.

Figure 10. Implant placement. (a) Preoperative view. (b) Healed bone graft prior to removal of fixation screws with both vertical and horizontal resorption. (c) Implant placement in an ideal buccopalatal position. (d) Fenestration and dehiscence around the implants. (e) Placement of particulate bone xenograft. (f) Placement of collagen matrix. Figure 11. Immediate postoperative radiograph showing good angulation and height 1 mm below the alveolar crest. Figure 12. Apically repositioned flap 3 months after implant placement. (a) Preoperative view. (b) Incision. (c) Partial-thickness flap. (d) Placement of allograft, which was stabilized with sutures but left completely exposed.

Close modal

The implants were placed 3 mm more apically than usual (6 mm from the gingival zenith of the adjacent tooth No. 8) to mitigate the possible risk from resorption of the vertically augmented site; the prosthetic outcome of longer clinical crowns had already been discussed with the patient. Bone-level implants (4.1-mm diameter, 10-mm long in region No. 9, and 3.3-mm diameter, 10-mm long in region No. 10) were placed, but crestal dehiscences on both implants and a fenestration in the region 9 implant were encountered; thus, simultaneous guided bone regeneration with deproteinized bovine bone (Geistlich BioOss, Geislich, Wolhusen, Switzerland) and porcine collagen membrane was performed. Tension-free primary closure was achieved with monofilament nylon sutures (Seralon, Serag-Wiessner, Naila, Germany).

Amoxicillin 500 mg TDS for 5 days and ibuprofen 400 mg TDS for 5 days were prescribed along with chlorhexidine 0.2% mouth rinse QDS. The provisional RBP was again adjusted and recemented.

A periapical radiograph taken 3 months after surgery and prior to implant exposure surgery confirmed the position of implants in relation to the prosthetic plan and alveolar bone above the level of implant shoulder (Figure 11).

Because of extensive coronal repositioning of the flap during the 2 surgeries and the extent of vertical augmentation necessary, sulcus deepening was carried out 3 months after implant placement (Figure 12). A split-thickness flap was raised and apically relocated, and a soft-tissue allograft (AlloDerm Regenerative Tissue Matrix, Acelity, San Antonio, Tex) was rehydrated in saline and cut to size to cover the exposed connective tissue bed. The provisional RBP was recemented.

Subsequently, the patient became pregnant and decided to defer further treatment until after the birth of her child, and so implant exposure surgery was delayed until October 2014 (Figure 13).

Figures 13–15.

Figure 13. Second-stage implant surgery 18 months after implant placement. (a) Split-thickness flap raised. (b) Implants exposed. (c) Tall healing abutments placed. (d) Closure. Figure 14. Provisionalization. (a) Initial provisional crowns. (b) Modifications to the provisional crowns and improved gingival contouring after 3 months. (c, d) Final modifications to the provisional crowns and gingival contouring after 6 months. Figure 15. Periapical radiograph during provisionalization, 3 months after implant placement. Note the well-fitting provisional crowns and bone remodeling at the implant-abutment junction.

Figures 13–15.

Figure 13. Second-stage implant surgery 18 months after implant placement. (a) Split-thickness flap raised. (b) Implants exposed. (c) Tall healing abutments placed. (d) Closure. Figure 14. Provisionalization. (a) Initial provisional crowns. (b) Modifications to the provisional crowns and improved gingival contouring after 3 months. (c, d) Final modifications to the provisional crowns and gingival contouring after 6 months. Figure 15. Periapical radiograph during provisionalization, 3 months after implant placement. Note the well-fitting provisional crowns and bone remodeling at the implant-abutment junction.

Close modal

Provisional composite resin screw-retained implant crowns were placed and adjusted during 3 subsequent appointments to modify the soft-tissue emergence profile (Figure 14). As anticipated, the implant clinical crowns were longer than the adjacent teeth with deficient interimplant papilla. A periapical radiograph showed the provisional crowns in situ and bone remodeling at the implant-abutment junction (Figure 15).

After a 6-month provisionalization period, definitive screw-retained linked crowns made from a milled cobalt chromium framework veneered with ceramic were fabricated with pink colored ceramic used on the cervical part of the prosthesis to conceal the interimplant papillary deficiency (Figure 16). A periapical radiograph (Figure 17) taken following definitive restoration showed well-maintained peri-implant bone levels, and the bone trabeculation appeared normal.

Figures 16–18.

Figure 16. Definitive restorations placed 6 months after implant exposure. (a, b) Final esthetic result. (c) Pink porcelain was used to replace the lost interdental papilla. (d) Occlusal view. Figure 17. Periapical radiograph at the fitting of the definitive restoration placed 6 months after implant exposure. Note the well-fitting linked definitive crowns and no loss in bone height. Figure 18. Periapical radiograph taken 15 months following the fitting of the definitive restorations and 3 years after implant placement.

Figures 16–18.

Figure 16. Definitive restorations placed 6 months after implant exposure. (a, b) Final esthetic result. (c) Pink porcelain was used to replace the lost interdental papilla. (d) Occlusal view. Figure 17. Periapical radiograph at the fitting of the definitive restoration placed 6 months after implant exposure. Note the well-fitting linked definitive crowns and no loss in bone height. Figure 18. Periapical radiograph taken 15 months following the fitting of the definitive restorations and 3 years after implant placement.

Close modal

Follow-up

During the most recent follow-up appointment, 4 years after staged bone augmentation and implant placement, the bone levels remain stable (Figure 18), and the patient remains satisfied with the esthetic and functional outcome.

Seventy-four cases of oral sarcoidosis have been reported in the literature,16,17,2023  with a female-to-male ratio of 1.5:1, a slight racial predilection to Caucasians, and ages ranging from 5 to 72 years (median, 37 years).20  Oral soft-tissue lesions have been reported as one of the first manifestations of systemic sarcoidosis,16,20,22,23  with the buccal mucosa being the most commonly affected site followed by the gingiva, lips, floor of the mouth, sublingual glands, tongue, palate, and submandibular gland.16,17,20,22 

The common clinical presentation is an asymptomatic localized submucosal swelling and well-circumscribed brown-red or violaceous papule, nodule, or finely granular macule. This makes the case reported unusual in that there were no visible changes to the oral mucosa. Other presentations include ulcers (which may become secondarily infected and symptomatic), fistulae, gingival inflammation, hyperplasia, and recession.2,16,17,20,22,2426 

As in the case presented, the maxilla and mandible may be involved,20,21,22,23,2529  with a higher incidence in the anterior maxilla and posterior mandible.20  Clinical manifestations of osseous involvement include loose teeth, pain radiating to the ears, and swelling. Nasal obstruction, nonhealing sockets, paresthesia, facial palsy, and a foul taste are also described.16,2023,26,27,29,30  Radiographically, these lesions appear as ill-defined radiolucencies that occasionally erode the cortex but do not cause expansion2,17 ; however, in rare cases, they may cause extensive destruction of the midface.31 

Up to 60% of orofacial lesions spontaneously resolve within 2 years. Symptomatic or progressing cases frequently respond to corticosteroid therapy, which may be administered intralesionally or systemically.2,16  Surgical excision of granulomatous swellings may be required,16  especially for intraosseous lesions such as in this case, which respond well to excision or curettage.22,23,28,29  Combined surgical and medical management has been described,25  as has extraction,26  splinting27  of mobile teeth, and even radiotherapy.30 

There have been no previous published accounts of the placement of dental implants in a patient diagnosed with sarcoidosis. Moretti et al21  described the management of a patient treated for peri-implantitis who presented with implants already placed into an iliac crest bone graft replacing teeth lost due to sarcoidosis affecting the periodontium. After periodontal treatment and over the 6-year follow-up described, during which the patient had 2 exacerbations of sarcoidosis both systemically and intraorally requiring steroid treatment, the implants lost 30%–50% of their bone support. This was despite the patient maintaining excellent oral hygiene and having 3–4 monthly maintenance visits at a postgraduate periodontal center.

Others have reported a diagnosis of periodontitis as a manifestation of systemic disease with regard to sarcoidosis, which is often rapidly progressing.14,24,29,32  Most confirmed the presence of a sarcoid process occurring in the periodontal tissues by histopathology.14,24,29  It seems plausible that this process could just as easily affect the peri-implant tissues as the periodontal ones, and therefore, the increased risk of peri-implantitis must be considered, discussed with the patient before treatment, and factored into any maintenance program.

As sarcoidosis is considered by some to be a foreign-body reaction, there may be concerns about the safety of implantation of a foreign material. Exposure to environmental titanium has been associated with increased risk of developing sarcoidosis, although this was by inhalation rather than implantation,17  with occupational exposure to titanium increasing the risk 3-fold (odds ratio, 3.15; 95% confidence interval, 1.02–9.68), although the sample in this study was only 8 affected subjects and 5 control subjects.33 

Patients who require systemic therapy for the management of their disease are likely to be taking corticosteroids,19  antimalarial agents, and immunosuppressants,1  and while there are no specific reports on the effects of medication for sarcoidosis on dental implant treatment, there is literature on the general effects of corticosteroids and immunosuppressants on dental implants. Animal studies3436  have shown a reduced removal torque of implants placed in the tibiae of rabbits given prednisolone, cyclosporin, and a combination of cyclosporin and nifedipine. One of these studies also placed implants in the rabbit's mandibles and found no difference in removal torque between those given prednisolone and the control animals, concluding that corticosteroids may not have such a significant effect on bone density and osseointegration in mandibular bone as they do in skeletal long bones.34  These studies must be interpreted carefully.

A case series reporting on the placement of dental implants in patients taking immunosuppressive medications following organ transplant reported that patients showed excellent results at 3 years37 ; however, a single patient followed up for 10 years had moderate vertical bone loss.38  Moy et al39  published retrospective data on the treatment of 1140 patients over a 21-year period, 78 of whom were taking corticosteroids, and no significant difference was found in the failure rate between those taking steroids and the rest of the cohort. To summarize, a review by Diz et al40  concluded that no convincing evidence has been published to demonstrate an increased dental implant failure rate in patients taking systemic corticosteroids or immunosuppression therapy.

This case has shown another example of how sarcoidosis can affect the bones of the head and neck and the effects this can have on the periodontium. Based on assessment and radiographic and histopathologic investigations, multiple rehabilitation options may be considered; any patient's suitability for these options must take into account the current activity status of the patient's sarcoidal process and any systemic therapies being employed.

Block allograft hard-tissue augmentation followed by implant placement with simultaneous guided bone regeneration and soft-tissue augmentation were successfully undertaken in this case; our outcome and follow-up results after 4 years show that the rehabilitation was successful, at least in the short term. Longer-term follow-up and studies with greater patient numbers are required to provide stronger evidence on this treatment modality in this patient group; however, recruiting a desirable number of patients is unlikely to be possible, and in such circumstances, low-level evidence in the form of case reports is of some benefit.

Abbreviations

    Abbreviations
     
  • CBCT:

    cone-beam computerized tomography

  •  
  • QDS:

    4 times per day

  •  
  • RBP:

    resin-bonded prosthesis

  •  
  • TDS:

    3 times per day

The authors thank Dr Jimmy Makdissi, Senior Clinical Lecturer and Honorary Consultant in Oral and Maxillofacial Radiology.

Martin James, Jay Matani, and Shakeel Shahdad declare no competing interests relevant to this article.

1. 
Baughman
R,
Lower
EE,
Du Bois
RM.
Sarcoidosis
.
Lancet
.
2003
;
61
:
1111
1118
.
2. 
Neville
BW,
Chi
AC,
Damm
DD,
Allen
CM.
Oral and Maxillofacial Pathology. 4th ed
.
Philadelphia
:
Saunders;
2015
.
3. 
Milman
N,
Selroos
O.
Pulmonary sarcoidosis in the Nordic countries 1950–1982: epidemiology and clinical picture
.
Sarcoidosis
.
1990
;
7
:
50
57
.
4. 
Newman
L,
Rose
C,
Maier
L.
Sarcoidosis
.
N Engl J Med
.
1997
;
336
:
1224
1234
.
5. 
Stehle
T,
Joly
D,
Vanhille
P,
et al.
Clinicopathological study of glomerular diseases associated with sarcoidosis: a multicentre study
.
Orphanet J Rare Dis
.
2013
;
8
:
65
.
6. 
Furusawa
H,
Suzuki
Y,
Miyazaki
Y,
Inase
N,
Eishi
Y.
Th1 and Th17 immune responses to viable Propionibacterium acnes in patients with sarcoidosis
.
Respir Investig
.
2012
;
50
:
104
109
.
7. 
Saidha
S,
Sotirchos
ES,
Eckstein
C.
Etiology of sarcoidosis: does infection play a role?
Yale J Biol Med
.
2012
;
85
:
133
141
.
8. 
Richter
E,
Greinert
U,
Kirsten
D,
et al.
Assessment of mycobacterial DNA in cells and tissues of mycobacterial and sarcoid lesions
.
Am J Respir Crit Care Med
.
1996
;
153
:
375
380
.
9. 
Popper
HH,
Klemen
H,
Hoefler
G,
et al.
Presence of mycobacterial DNA in sarcoidosis
.
Hum Pathol
.
1997
;
28
:
796
800
.
10. 
Kon
OM,
du Bois
RM.
Mycobacteria and sarcoidosis
.
Thorax
.
1997
;
52
(suppl 3)
:
47
51
.
11. 
Moller
DR,
Chen
ES.
What causes sarcoidosis
.
Curr Opin Pulm Med
.
2002
;
8
:
429434
.
12. 
Hattori
T,
Konno
S,
Takahashi
A,
et al.
Genetic variants in mannose receptor gene (MRC1) confer susceptibility to increased risk of sarcoidosis
.
BMC Med Genet
.
2010
;
11
:
151
.
13. 
Grunewald
J.
Review: role of genetics in susceptibility and outcome of sarcoidosis
.
Semin Respir Crit Care Med
.
2010
;
31
:
380
389
.
14. 
Suresh
L,
Aguirre
A,
Buhite
RJ,
Radfar
L.
Intraosseous sarcoidosis of the jaws mimicking aggressive periodontitis: a case report and literature review
.
J Periodontol
.
2004
;
75
:
478
482
.
15. 
Judson
MA.
The clinical features of sarcoidosis: a comprehensive review
.
Clin Rev Allergy Immunol
.
2015
;
49
:
63
78
.
16. 
Poate
TWJ,
Sharma
R,
Moutasim
KA,
Escudier
MP,
Warnakulasuriya
S.
Orofacial presentations of sarcoidosis: a case series and review of the literature
.
Br Dent J
.
2008
;
205
:
437
442
.
17. 
Motswaledi
MH,
Khammissa
RA,
Jadwat
Y,
Lemmer
J,
Feller
L.
Oral sarcoidosis: a case report and review of the literature
.
Aust Dent J
.
2014
;
59
:
389
394
.
18. 
Gibson
GJ,
Prescott
RJ,
Muers
MF,
et al.
British Thoracic Society, sarcoidosis study: effects of long term corticosteroid treatment
.
Thorax
.
1996
;
51
:
238
247
.
19. 
Paramothayan
S,
Jones
PW.
Corticosteroid therapy in pulmonary sarcoidosis: a systematic review
.
JAMA
.
2002
;
287
:
1301
1307
.
20. 
Suresh
L,
Radfar
L.
Oral sarcoidosis: a review of literature
.
Oral Dis
.
2005
;
11
:
138
145
.
21. 
Moretti
AJ,
Fiocchi
MF,
Flaitz
CM.
Sarcoidosis affecting the periodontium: a long-term follow-up case
.
J Periodontol
.
2007
;
78
:
2209
2215
.
22. 
Al-Azri
AR,
Logan
RM,
Goss
AN.
Oral lesion as the first clinical presentation in sarcoidosis: a case report
.
Oman Med J
.
2012
;
27
:
243
245
.
23. 
Cain
R,
Tamura
T,
Elhosseiny
A,
Vanisky
E,
Brundage
W.
Sarcoidosis presenting as a lytic lesion of the mandible
.
J Oral Maxillofac Surg
.
2012
;
70
:
2823
2828
.
24. 
Rubin
MM,
Sanfilippo
RJ,
Pliskin
A.
Maxillary alveolar bone loss in a patient with sarcoidosis
.
J Oral Maxillofac Surg
.
1991
;
49
:
1351
1353
.
25. 
Grimaldi
L,
De Santis
R,
Brandi
C,
D'Aniello
C.
Mandibular intrabony lesion as first sign of sarcoidosis: case report
.
Int J Oral Maxillofac Surg
.
2004
;
33
:
613
614
.
26. 
Verheijen-Breemhaar
L,
De Man
K,
Zondervan
RE,
Hilvering
C.
Sarcoidosis with maxillary involvement
.
Int J Oral Maxillofac Surg
.
1987
;
16
:
104
107
.
27. 
Hong
J,
Farish
S.
Intraosseous sarcoidosis of the maxilla: case report
.
Oral Maxillofac Surg
.
2000
;
58
:
435
439
.
28. 
Betten
B,
Stromme Koppang
H.
Sarcoidosis with mandibular involvement. Report of a case
.
Oral Surg Oral Med Oral Pathol
.
1976
;
42
:
731
737
.
29. 
Cohen
DM,
Reinhardt
RA.
Systemic sarcoidosis presenting with Horner's syndrome and mandibular paresthesia
.
Oral Surg Oral Med Oral Pathol
.
1982
;
53
:
577
581
.
30. 
Hoggins
GS,
Allan
D.
Sarcoidosis of the maxillary region
.
Oral Surg Oral Med Oral Pathol
.
1969
;
28
:
623
627
.
31. 
Klesper
B,
Schmelzle
R,
Donath
K.
Cutaneous manifestation of sarcoidosis (Boeck) with severe osseous destruction of the midface: a case report
.
J Craniomaxillofac Surg
.
1994
;
22
:
163
166
.
32. 
Makris
GP,
Stoller
NH.
Rapidly advancing periodontitis in a patient with sarcoidosis: a case report
.
J Periodontol
.
1983
;
54
:
690
693
.
33. 
Kucera
GP,
Rybicki
BA,
Kirkey
KL,
et al.
Occupational risk factors for sarcoidosis in African-American siblings
.
Chest
.
2003
;
123
:
1527
1535
.
34. 
Fujimoto
T,
Niimi
A,
Sawai
T,
Ueda
M.
Effects of steroid-induced osteoporosis on osseointegration of titanium implants
.
Int J Oral Maxillofacial Implants
.
1998
;
13
:
183
189
.
35. 
Sakakura
C,
Margonar
R,
Holzhausen
M,
Nociti
F
Jr.
Influence of cyclosporin A therapy on bone healing around titanium implants: a histometric and biomechanic study in rabbits
.
J Periodontol
.
2003
;
74
:
976
981
.
36. 
Duarte
P,
Nogueira Filho
G,
Sallum
E.
The effect of an immunosuppressive therapy and its withdrawal on bone healing around titanium implants: a histometric study in rabbits
.
J Periodontol
.
2001
;
72
:
1391
1397
37. 
Gu
L,
Yu
YC.
Clinical outcome of dental implants placed in liver transplant recipients after 3 years: a case series
.
Transplant Proc
.
2011
;
43
:
2678
2682
.
38. 
Heckmann
S,
Heckmann
J,
Julian
J.
Implant therapy following liver transplantation: clinical and microbiological results after 10 years
.
J Periodontol
.
2004
;
75
:
909
913
.
39. 
Moy
P,
Medina
D,
Shetty
V,
Aghaloo
T.
Dental implant failure rates and associated risk factors
.
Int J Oral Maxillofacial Implants
.
2005
;
20
:
569
577
.
40. 
Diz
P,
Scully
C,
Sanz
M.
Dental implants in the medically compromised patient
.
J Dent
.
2013
;
41
:
195
206
.